This pdf version of the /r/steroids wiki was compiled by u/Big_Papa_Bear_ on 11/9/2020

Overview
The /r/steroids wiki provides common knowledge on Anabolic-Androgenic Steroid (AAS) use as well as specifics
about the subreddit and our community.

Critical Thinking
Participation in this sub and with this habit requires one to execute critical thinking very well, to determine truth
from falsehood. Practice daily for best results.

Carl Sagan's Rules for Critical Thinking and Nonsense-

Detection
1. Wherever possible there must be independent confirmation of the “facts.”
2. Encourage substantive debate on the evidence by knowledgeable proponents of all points of view.
3. Arguments from authority carry little weight — “authorities” have made mistakes in the past. They will do so
again in the future. Perhaps a better way to say it is that in science there are no authorities; at most, there
are experts.
4. Spin more than one hypothesis. If there’s something to be explained, think of all the different ways in which
it could be explained. Then think of tests by which you might systematically disprove each of the alternatives.
What survives, the hypothesis that resists disproof in this Darwinian selection among “multiple working
hypotheses,” has a much better chance of being the right answer than if you had simply run with the first
idea that caught your fancy.
5. Try not to get overly attached to a hypothesis just because it’s yours. It’s only a way station in the pursuit of
knowledge. Ask yourself why you like the idea. Compare it fairly with the alternatives. See if you can find
reasons for rejecting it. If you don’t, others will.
6. Quantify. If whatever it is you’re explaining has some measure, some numerical quantity attached to it, you’ll
be much better able to discriminate among competing hypotheses. What is vague and qualitative is open to
many explanations. Of course there are truths to be sought in the many qualitative issues we are obliged to
confront, but finding them is more challenging.
7. If there’s a chain of argument, every link in the chain must work (including the premise) — not just most of
them.
8. Occam’s Razor. This convenient rule-of-thumb urges us when faced with two hypotheses that explain the
data equally well to choose the simpler.
9. Always ask whether the hypothesis can be, at least in principle, falsified. Propositions that are untestable,
unfalsifiable are not worth much. Consider the grand idea that our Universe and everything in it is just an
elementary particle — an electron, say — in a much bigger Cosmos. But if we can never acquire information
 from outside our Universe, is not the idea incapable of disproof? You must be able to check assertions out.
Inveterate skeptics must be given the chance to follow your reasoning, to duplicate your experiments and see
if they get the same result.

20 Most Common Logical Fallacies (aka: baloney detection)

In addition to teaching us what to do when evaluating a claim to knowledge, any good baloney detection kit
must also teach us what not to do. It helps us recognize the most common and perilous fallacies of logic and
rhetoric. Many good examples can be found in religion and politics, because their practitioners are so often
obliged to justify two contradictory propositions.

The twenty most common and perilous ones — many rooted in our chronic discomfort with ambiguity —
with examples of each in action:

1. Ad Hominem — Latin for “to the man,” attacking the arguer and not the argument (e.g., The Reverend Dr.
Smith is a known Biblical fundamentalist, so her objections to evolution need not be taken seriously)
2. Argument From Authority (e.g., President Richard Nixon should be re-elected because he has a secret plan to
end the war in Southeast Asia — but because it was secret, there was no way for the electorate to evaluate it
on its merits; the argument amounted to trusting him because he was President: a mistake, as it turned out)
3. Argument From Adverse Consequences (e.g., A God meting out punishment and reward must exist, because
if He didn’t, society would be much more lawless and dangerous — perhaps even ungovernable. Or: The
defendant in a widely publicized murder trial must be found guilty; otherwise, it will be an encouragement
for other men to murder their wives)
4. Appeal to Ignorance — the claim that whatever has not been proved false must be true, and vice versa (e.g.,
There is no compelling evidence that UFOs are not visiting the Earth; therefore UFOs exist — and there is
intelligent life elsewhere in the Universe. Or: There may be seventy kazillion other worlds, but not one is
known to have the moral advancement of the Earth, so we’re still central to the Universe.) This impatience
with ambiguity can be criticized in the phrase: absence of evidence is not evidence of absence.
5. Special Pleading, often to rescue a proposition in deep rhetorical trouble (e.g., How can a merciful God
condemn future generations to torment because, against orders, one woman induced one man to eat an
apple? Special plead: you don’t understand the subtle Doctrine of Free Will. Or: How can there be an equally
godlike Father, Son, and Holy Ghost in the same Person? Special plead: You don’t understand the Divine
Mystery of the Trinity. Or: How could God permit the followers of Judaism, Christianity, and Islam — each in
their own way enjoined to heroic measures of loving kindness and compassion — to have perpetrated so
much cruelty for so long? Special plead: You don’t understand Free Will again. And anyway, God moves in
mysterious ways.)
6. Begging the Question, also called assuming the answer (e.g., We must institute the death penalty to
discourage violent crime. But does the violent crime rate in fact fall when the death penalty is imposed? Or:
The stock market fell yesterday because of a technical adjustment and profit-taking by investors — but is
 there any independent evidence for the causal role of “adjustment” and profit-taking; have we learned
anything at all from this purported explanation?)
7. Observational Selection, also called the enumeration of favorable circumstances, or as the philosopher
Francis Bacon described it, counting the hits and forgetting the misses (e.g., A state boasts of the Presidents it
has produced, but is silent on its serial killers)
8. statistics of small numbers — a close relative of observational selection (e.g., “They say 1 out of every 5
people is Chinese. How is this possible? I know hundreds of people, and none of them is Chinese. Yours
truly.” Or: “I’ve thrown three sevens in a row. Tonight I can’t lose.”)
9. Misunderstanding of the Nature of Statistics (e.g., President Dwight Eisenhower expressing astonishment
and alarm on discovering that fully half of all Americans have below average intelligence);
10. Inconsistency (e.g., Prudently plan for the worst of which a potential military adversary is capable, but
thriftily ignore scientific projections on environmental dangers because they’re not “proved.” Or: Attribute
the declining life expectancy in the former Soviet Union to the failures of communism many years ago, but
never attribute the high infant mortality rate in the United States (now highest of the major industrial
nations) to the failures of capitalism. Or: Consider it reasonable for the Universe to continue to exist forever
into the future, but judge absurd the possibility that it has infinite duration into the past);
11. Non-Sequitur — Latin for “It doesn’t follow” (e.g., Our nation will prevail because God is great. But nearly
every nation pretends this to be true; the German formulation was “Gott mit uns”). Often those falling into
the non sequitur fallacy have simply failed to recognize alternative possibilities;
12. Post Hoc, ergo Propter Hoc — Latin for “It happened after, so it was caused by” (e.g., Jaime Cardinal Sin,
Archbishop of Manila: “I know of … a 26-year-old who looks 60 because she takes [contraceptive] pills.” Or:
Before women got the vote, there were no nuclear weapons)
13. Meaningless Question (e.g., What happens when an irresistible force meets an immovable object? But if
there is such a thing as an irresistible force there can be no immovable objects, and vice versa)
14. Excluded Middle, or False Dichotomy — considering only the two extremes in a continuum of intermediate
possibilities (e.g., “Sure, take his side; my husband’s perfect; I’m always wrong.” Or: “Either you love your
country or you hate it.” Or: “If you’re not part of the solution, you’re part of the problem”)
15. Short-Term vs. Long-Term — a subset of the excluded middle, but so important I’ve pulled it out for special
attention (e.g., We can’t afford programs to feed malnourished children and educate pre-school kids. We
need to urgently deal with crime on the streets. Or: Why explore space or pursue fundamental science when
we have so huge a budget deficit?);
16. Slippery Slope, related to excluded middle (e.g., If we allow abortion in the first weeks of pregnancy, it will be
impossible to prevent the killing of a full-term infant. Or, conversely: If the state prohibits abortion even in
the ninth month, it will soon be telling us what to do with our bodies around the time of conception);
17. Confusion of Correlation and Causation (e.g., A survey shows that more college graduates are homosexual
than those with lesser education; therefore education makes people gay. Or: Andean earthquakes are
 correlated with closest approaches of the planet Uranus; therefore — despite the absence of any such
correlation for the nearer, more massive planet Jupiter — the latter causes the former)
18. Straw Man — caricaturing a position to make it easier to attack (e.g., Scientists suppose that living things
simply fell together by chance — a formulation that willfully ignores the central Darwinian insight, that
Nature ratchets up by saving what works and discarding what doesn’t. Or — this is also a short-term/long-
term fallacy — environmentalists care more for snail darters and spotted owls than they do for people)
19. ** Suppressed Evidence, or Half-Truths** (e.g., An amazingly accurate and widely quoted “prophecy” of the
assassination attempt on President Reagan is shown on television; but — an important detail — was it
recorded before or after the event? Or: These government abuses demand revolution, even if you can’t make
an omelette without breaking some eggs. Yes, but is this likely to be a revolution in which far more people
are killed than under the previous regime? What does the experience of other revolutions suggest? Are all
revolutions against oppressive regimes desirable and in the interests of the people?)
20. Weasel Words (e.g., The separation of powers of the U.S. Constitution specifies that the United States may
not conduct a war without a declaration by Congress. On the other hand, Presidents are given control of
foreign policy and the conduct of wars, which are potentially powerful tools for getting themselves re-
elected. Presidents of either political party may therefore be tempted to arrange wars while waving the flag
and calling the wars something else — “police actions,” “armed incursions,” “protective reaction strikes,”
“pacification,” “safeguarding American interests,” and a wide variety of “operations,” such as “Operation Just
Cause.” Euphemisms for war are one of a broad class of reinventions of language for political purposes.
Talleyrand said, “An important art of politicians is to find new names for institutions which under old names
have become odious to the public”)

AAS Related Reading

The following material is presented on topics related to /r/steroids for educational purposes.

Books and Publications

1. ANABOLICS, 10th edition, William Llewellyn
2. A Compilation of Anabolic and Nutritional Supplements Steroids
3. Underground Steroids Handbook II, Daniel Duchaine
4. The Endocrine Society's Clinical Guide: Testosterone Therapy in Adult Men with Androgen Deficiency
Syndrome. ( PDF, Scribd )
5. Why are Steroids Illegal in the USA? (Scribd)
6. Testosterone: Action, Deficiency, Substitution, 3rd Edition (pp. 405-444). Cambridge University Press, New
York.Behre H.M., Nieschlag E., (2004). (PDF)
7. More
 Original Stories
1. A Pin Story
Laying in bed at the in-laws house and feeling lethargic after a long day of family activities; I get myself
up to go to the kitchen. I have to take care of this before bed.
This trip has really made me aware of my body dysmorphia as no one in the house is over 160 lbs and I'm
a pretty solid 205 of muscle, bone and organs. It's always obvious when traveling to other countries.
Most places that I go in this country, I'm the biggest guy there and typically in the best shape.
Meanwhile, I'm on a strict diet doing a cut cycle trying to get from 14% BF to 8%. Public bathrooms with
big mirrors are rough as everyone next to me looks small in comparison. I imagine them looking at me as
I look at some guys in my gym. Jesus Christ that guy is big. Sometimes it seems like people just move out
of your way.

I hover around the group until I can silently signal my SO that it's time to pin me. I head back to the room,
telling everyone good night and, like clockwork, she arrives 5 minutes later.

"Which side did you do last night?"

"I don't know, it's your job to track."
I feel my right and left medial glutes. "Right side today." I adjust myself onto the bed so that she has
access to my right ass cheek, hand her the alcohol wipe and hold the pin by the needle protector for her
to unsheath when ready. Like the professional she is, she finds the muscle, uses her petite hands to
measure the distances, quickly swabs and swiftly jabs. "That was a good one. Didn't feel a thing." I hope
she didn't hit any scar tissue.
There is really a lot of silence in the time it takes to push 2ml of viscous fluid down a 25g needle. It seems
to take forever; longer if you're high like I am now. It's almost all done, I can tell by the pressure. Here it
comes. Shit. It starts as a little itch, deep in your esophagus. It's almost negligible. It didn't start until the
end of the pin, shouldn't be that bad. Good night kisses and "I love you's" are exchanged as I hold in the
cough as long as possible. I never told her about Tren cough. The itch is creeping up my throat, becoming
unbearable. I make my way to the bathroom quickly as she disappears back to the group. The coughing
begins slowlly and my throat tenses up, no more swallowing for a bit, so I spit in the toilet instead. My
eyes are getting watery. The coughing escalates. I may puke.
The coughing is worse, but somewhat controlled, still spitting in the toilet and sink. I look in the mirror.
Tears are going down my face. I think I inhaled some saliva. I let out a round of coughs as I watch in the
mirror. Holy shit, my traps and chest look good when I cough. When will this end?

It's been about 2 minutes, but It's hard to say in high-time. The coughing turns violent.

Fuck, I may die this time.

How did I get into this situation?
 If someone read my truthful story about dying in this bathroom from Tren cough, they wouldn't believe
that anyone could be this stupid.

I start recounting how ridiculous it is.

You bought illegal drugs from an unground vendor.

You illegally had them shipped to you!?
You carried them to another country where they are illegal?
You secretly are injecting them at your family's house!?
And you're going to choke to death.
When will this coughing end?
How will it end?
All this risk, why are you such a dumb ass to die for this?

And just like that, it stopped; no more coughing. My throat still itches, but it's able to be ignored. I slowly
wipe up my eyes, clean the sink, flush the toilet and hope that no one heard me. I pause for a second to
listen and take a quick mirror check before exiting the bathroom.

When I see myself, I closely inspect my body.

"You are an undersized fatass. Time for bed."

I make my way back to the bedroom. The family is, apparently, unaware of my near death experience.
I'm tired. I need to fall asleep before Tren makes it impossible. One more pin left for this trip and all I can
do is hope that it goes better than this last one.

2. The Rage Story

Why do they make childrens beds so damn stiff? What the fuck is wrong with those people? Or maybe
something is wrong with me because I purchased this fucking thing. The tiny pillow on which I'm resting
my head is soaking wet from the sweat and oils that heavy Trenbolene usage incites. I flip the pillow
over, only to find that the other side is equally as wet. I have no recollection of having flipped it
previously. Fuck it. The pillow flies past my feet, hitting the wall with a nearly inaudible fwop and sinks to
the floor. Resting my head on the stiff mattress, I discover that it's wet as well and simply rest my head in
the wetness. At least it's not on my neck.
"Daddy, when is my next birthday?" Her tiny and excited voice piercing through the noise from the
party in the next room.
"Well, today was just your birthday party. Your real birthday is Tuesday and then you'll have another
one in a year. You need to sleep; It's late"
"Tomorrow?"
"No, in three days. The day after gymnastics. Now lets try to sleep." She has to be exhausted from all of
the activities today.
The noise from the next room consistently escalates, the volume of laughter and mumbled talk following
the graph of the number of wine bottles opened over time. I glance at the glowing yellow clock that also
serves as a nightlight. 10:27pm. I've been laying here for two hours trying to get her to sleep. My heart
begins pounding hard and fast, hands unsteady. I try to take my pulse, but can't really coordinate the
counting, timer and placement of my fingers on my neck for an entire minute. I decide to do a six second
estimate. Eleven. That puts me at 110 beats per minute, resting. Typically being bradycardia, this is
unwelcome news.

Remembering back to the previous weekend's fight with my SO when I smashed a bone china bowl on
our granite counter top, I recognize that my temper has higher peaks than usual. I have been removing
pieces of bone china from drywall all week and do not want to repeat it, especially not in front of family
and friends.

You're not going to say shit; Let it pass. Control your breathing, relax. I put my ever-present head set into
my ears, fire up Pandora and select the Mozart Piano Quartet channel. I can feel my heart beat in both of
my ears. My blood pressure is elevated. Focusing on my breathing and listening to the apropos song
"Intervention" by Helen Jane Long, I'm able to slow my heart rate down.

I wrap my arm around my tiny daughter and she rests her head on my bicep. A few songs pass and I
believe that she may have fallen asleep, unable to hear her breathing due to my head set.

"I don't want your arm." She moves to her own pillow. It's uncomfortable for her neck because of the
size.
The door to the hallway opens and the loudness of the party spills into the room, overtaking the music in
my head set. You're not doing shit. My heart rate begins to climb again. The noise continues to pour into
the room, seemingly louder and louder. They forgot to shut the door. JUST go shut the door. You're not
saying shit. I get up.
"Where are you going Daddy?"
"I'll be right back."
"Don't go."
"I'll be right back."
I exit the room and take the four steps to the hallway door. My SO and I lock eyes and, with a penetrating
stare, I swing the door shut harder than I intended. It slams and the noise from the party stops for a brief
second as the room sees me walk away. I hope they all got the point. My heart is racing again.
I lay back down into my spot on the bed that is nearly a puddle of sweat. Listening to the relaxing music
and focusing on my breathing for ten minutes, I'm unable to slow my heart rate. Physically feeling my
pulse in my ears, hands unstable and uncomfortable. This is fucked up. This is unusual. What would I say
at the hospital? I'd rather die here than go to the hospital, fuckit. I need this party to end. I text my SO.
"Come in here."
Laying there, still trying to control my heart rate, it continues to climb higher despite my efforts. I can
feel my body getting hotter. I call her. It rings up until the point that I think that it will go to voicemail
before she answers.

"Hello Honey." She's tipsy.

"Get in here."
"Ok."

She arrives in our daughter's room, nearly immediately. My heart is racing as if I were doing wind sprints.
I estimate it at 160 BPM, laying still on the bed.

"Why do we have to have an infant's birthday party last twelve hours?" I'm catching my breath as I talk,
unable to complete the sentence fully in one breath.
"What do you mean? It's only 11:00, it's just family and close friends."

She's standing back, away from the bed and me. I know that she can feel the heat and seriousness of my
stare through the darkness of the room.

"Shut it down. You have 15 minutes, or I will shut it down and kick every single person, including
family, friends and children, out of this fucking house." I'm nearly panting. Heart racing, hands shaking
underneath the covers.
"What is wrong with you? Why are you being like this?"

With the seriousness and implied finality of a military command I insist.

"Shut it the fuck down, or I will. Fifteen minutes, starting now." She sees me look at my phone for the
time. It's 10:57. I am going to go nuclear at 11:12. If the lights were on, my heartbeat would be visible,
moving the blanket which rests on my chest.
She turns and quietly leaves the room. I need to calm down before I have a heart attack. Maybe my last
electrocardiogram was wrong and I do have an abnormality. I do not fucking care, this party needs to
end. I can hear her announce the news to the room.
"He says that we have 15 minutes to end the party."

The disappointment of the group is verbal and strong.

"Why is he being like that?"

"It's only eleven o'clock."

She's trying to be quiet, but I hear her response.

"He's being mean again."

That fucking did it; I'm going to shut these fuckers up. I launch out of the bed, wearing only my boxer
briefs, and proceed to the kitchen. My body is red and hot, veins swollen and exposed, muscles engorged
with blood as I walk into the room of fifteen people. My heart wants to pound a hole through the front of
my chest wall. There is no way that I could utter a sentence right now without panting. Absolute silence
 befalls the room immediately as all eyes are on me for my next action. Fear can be felt in the air and a
few people shift in their chair, uncomfortably. With the stare of death, I go person to person making eye
contact as I walk, slowly and deliberately. Family members, in-laws, close friends, it doesn't matter. Dare
they say a fucking word and I'll explode. I'm prepared to lay waste to anything or anyone in my path.

No words, complete silence; staring at me in awe of the control that I took over the room. I walk to the
kitchen cabinet and open it, pulling out a large red cup that was stolen on some drunken night, from
some greasy diner. I proceed to the filtered water and fill up the cup, slowly, still looking people in the
eyes. Cup filled with water, I go to exit the room.

"Party. Over. Now."

It's as much as my racing heart would allow me to say. And without a single audible word, people leave
and family members go to bed. Jesus Fucking Christ, I was too close to making a huge mistake with loved
ones. Time for PCT.

3. Massive Attack
"If everybody jumped off a cliff," my father used to say, "would you?" This was a few years ago. It was
the summer a wild cougar killed a jogger in Sacramento. The summer my doctor wouldn't give me
anabolic steroids.

A local supermarket used to offer this special deal: if you bought fifty bucks worth of receipts, you could
buy a dozen eggs for a dime, so my best friends, Ed and Bill, used to stand in the parking lot asking
people for their receipts. Ed and Bill, they ate blocks of frozen egg white, 10-pound blocks they got at a
bakery supply house, egg albumin being the most easily assimilated protein. Ed and Bill used to make
these road trips to San Diego, then cross the border on foot at Tijuana to buy their steroids, their
Dianabol, and smuggle it back. This must've been the summer the D.E.A. had other priorities.

Ed and Bill are not their real names.

We were road-tripping down through California, and we stopped in Sacramento to visit some friends. At
this point the cougar was still running wild. This was the countryside, but not. The wilderness platted into
2.5-acre mini estates. Somewhere was a female cougar with cubs, squeezed in among the soccer moms
and swimming pools. This was less of a vacation than a pilgrimage from one Gold's Gym franchise to the
next along the west coast. On the road, we bought water-packed tuna and ate it dry, tossing the empty
cans in the back seat. We washed it down with diet soda and farted the length of Interstate 5.

Ed and Bill shot the pre-loaded syringes of D-ball, and I did everything else. Arginine, Ornithine, Smilax,
DHEA, saw palmetto, selenium, chromium, free-range New Zealand sheep testicle, Vanadyl, orchid
extract... At the gym, while my friends bench-pressed three times their weight, pumping up, shredding
their clothes from the inside, I'd hover around their giant elbows. "You know," I'd say, "I think I'm putting
on real size with this yohimbe bark tincture."
Yah, that summer.

The only reason they let me hover was for contrast. It's the old strategy of choosing ugly bridesmaids so
the bride looks better. Mirrors are only the methadone of body-building. You need an audience. There's
that old joke: "How Many Bodybuilders Does It Take to Screw in a light bulb?" Three: one to screw in the
bulb and two to say, "Really, dude, you look massive!" Yeah, that joke. That's not really a joke.

The Sacramento people we visited, on our way home from Mexico, we stopped by their house again, and
they pulled us inside and locked the doors. They were throwing a barbecue for some friends who'd been
away at a men's retreat. On this retreat, somebody explained, each man was sent out into the desert to
wander until he had a revelation. Now while the tiki torches flickered and the propane barbecue smoked,
one man stood clutching some kind of shriveled baseball bat. It was the desiccated skeleton of a cactus
he'd found on his quest, but it was more. "I realized," he said, "that this cactus skeleton was me. This was
my manhood, abrasive and hard on the outside, but brittle and hollow." Everybody else around the deck
closed their eyes and nodded. Except my friends, who turned the other way with their jaws clenched to
keep from laughing. Their huge arms folded across their chests, they elbowed each other and wanted to
walk up the road to see some historical rock. The hostess stopped us at the gate and said, "Don't! Just
don't." Clutching her wine cooler and looking into the darkness beyond the steam of the whirlpool and
the light of the tiki torches, she said a cougar had been prowling around.

The cougar had been right up next to their deck, and she showed us in the shrubs, a scattering of short,
coarse, blond hair. That year, everywhere we drove, that whole trip, there were already fences and
property lines and names on everything.

Ed juiced and lifted for a couple more years until he blew out his knees. Bill, until he ruptured a disk in his
back. It wasn't until last year when my father died, my doctor finally came across. I lost weight and kept
losing weight until he whipped out a prescription and said, "Let's try you on 30 days of Anadrol."

So I jumped off the cliff, too.

People squinted at me and asked what was different. My arms got a little bigger around, but not that
much. More than the size, the feeling was enough. Anadrol is an anabolic steroid, a synthetic derivative
of testosterone. Possible side effects include: testicular atrophy, impotence, chronic priapism, increased
or decreased libido, insomnia, and hair loss. One hundred tablets cost eleven-hundred bucks. Insurance
does not cover it. But the feeling does. Your eyes are popped open and alert. The way women look so
good when they're pregnant, glowing and soft, and so much more female, Anadrol makes you look and
feel that much more male. The raging priapism part - that was the first couple weeks. You are nothing
but the real estate between your legs. It's the same as those old illustrations in Alice in Wonderland
where she's eaten the cake marked "eat me" and frown until her arm sticks out the front door. Except it's
not your arm that sticks out, and wearing bicycle pants is totally out of the question.
About the third week, the priapism subsided or seemed to spread to my entire body. Weightlifting gets
better then sex. A workout becomes an orgy. You're having orgasms, cramping, hot, rushing orgasms in
your delts, your quads, your lats and traps. You forget about that lazy old penis. Who needs it? In a way
it's a peace, an escape from sex. A vacation from libido. You might see a hot woman ant think, "Grrrrrrr,"
but your next egg white omelet or set of squats are a lot more attractive.

I didn't go into this stupid. This is a kind of weird aside, but a friend in medical schoolmate me a deal that
if I introduced her to Brad Pitt, she'd sneak me in to help her dissect some cadavers. She met Brad, and I
spent a long night helping her disassemble dead bodies so first-year pre-med students could study them.
Our third cadaver was a 60-year-old physician. He had the muscle mass and definition of a man in his
twenties, but when we opened his chest, his heart was almost the size of his head. I held his chest open
and my friend poured in Formalin until his lungs floated. My friend looked at his freaking big heart, and
his equally freaky big dick, and she told me: testosterone. Self administered for years. She showed me
the coiled little wires and the pacemaker buried in his chest and told me he had a history of heart
attacks. About this time, a bodybuilder magazine ran an occasional little feature in its back pages, a
catch-up profile about a star bodybuilder from the 1980s. Back then, these stars posed and gave
interviews swearing they were blessed with great genetics and determination, they just worked hard and
ate well, they never used steroids. They swore. In the update features, these same guys were pale and
doughy, battling health problems from diabetes to cancer. And they admitted they had been using
steroids.

I knew all this, and I still jumped off the cliff.

My father was dead, Ed and Bill were a mess, and I was fast losing faith in tangible shit. Here I'd written a
story, a make-believe book, and it was making me more money than any real work I'd ever done. I had
about a 30-day window of free time between my book obligations and the opening of the Fight Club
movie. Here was a 30-day experiment, an updated Jack London adventure in a little brown bottle. My
friends didn't stop me. They only told me to eat enough protein to make the investment worthwhile.
Still, I didn't buy the 10-pound blocks of egg white. I never filled my fridge with rows and rows of foil-
wrapped boneless, skinless chicken breasts and baked potatoes the way Ed and Bill used to. I just took
the little white pills and worked out and one day in the shower, I noticed my nuts were disappearing.
Okay, I'm sorry. I promised a lot of friends I wouldn't go here, but this was the turning point. When the
old goose eggs shrink to ping-pong balls, then to marbles, then your doctor asks if you want a refill on
your Anadrol script, it's easy to say no. Here you are looking great, bright and alert, pumped and ripped
you're looking more like a man than you ever have, but you're less of a man where it counts. Besides, the
appeal of being a freaky, massive pile of muscle had already started to wane. Sure, at first it would be
fun, like owning a rambling Victorian mansion, but after the first couple weeks the constant maintenance
would eat up my life. I could never wander very far from a gym. I'd be eating egg protein every hour. All
this and the whole project would still collapse some day.
 I jumped off the cliff because it was an adventure. And for 30 days I felt complete. But just until the tiny
white pills ran out. Temporarily permanent. Complete and independent of everything. Everything except
the Anadrol. the woman in Sacramento, hosting that barbecue all those years ago, she'd said, "Those
friends of yours, they're crazy." Beside the swimming pool, the man cradled the brittle cactus skeleton of
his masculinity, the woman still stared at her clumps of bleached "cougar fur." Pumped and huge in their
tanktops, Ed and Bill disappeared, lumbering down the road. Out in the dark was the cougar. Or other
cougars.

Ed used to wear a T-shirt that said, "Fuck Moderation."

The hostess said, "Why do men have to do such stupid things?" "As long as America has a frontier,"
Thomas Jefferson used to say, "there will be a place for America's misfits and adventurers." Now Ed and
Bill are fat eyesores, but that summer, really dude, they were massive. A good pump, my father, the
Anadrol, all that's left is the intangible story. The legend. And okay, that thing about frontiers, maybe it
wasn't Thomas Jefferson, but you get the idea.

There will be cougars outside. It's such a chick thing to think life should just go on forever.

4. The Signal Story

Traveling around, as I always do, I just happen to be in Hawaii this week. I can’t get over this shit; it
chases me from place to place to place. Waking up from a sun drenched nap next to a pool that is built to
look like a beach, I immediately see another swole dude a few chairs over. I calculate his stats
immediately in my mind.

5’11, 210, 12-13%. Mad capped Delts, oversized traps, . . . definite gear user. I wonder what
his /r/steroids name is. That could be /u/Mak_Ultra.

Every time I find myself wondering if this swole dude in front of me is one of you.

Went to a Luau in Paradise Cove the other night. It has the standard girls in coconut bras and
metrosexual to manlet looking performers.

Anavar and Clen, for sure. Which /r/steroids member would he be? /u/roidie? Naah. Did I answer one of
this guy's questions?

Pretty high and, not quite, drunk the rest of the night, I sat around trying to figure out a signal that the
community could use to identify each other. With more sobriety, my senses sharpened and came to
reason.

Why the fuck would we signal each other? The conversations would be super awkward.
Ya, so, you're a member.
Dude, you look like your running some serious Tren with those sweats.
Nah man, it's just hot here.
 Awh, cool. Hey, I got a couple extra viagra and some dbol if you need it.
Alright, I'll hook you up with some legit Primo!
No one is going to fucking signal anyone and have those idiotic conversations. The fuck am I
thinking. Two slow taps on the head. That’s the stupidest idea in the world.
5. The Loss Story
”What will your cycle do to your sperm production?”
”I should be fine for the first 15 weeks or so due to the sequestration of testosterone by the gonads in
the presence of FSH.” She’s in the medical field, she’ll understand
”Are you sure? You know that I’m getting older. Chances are less.”
”It’ll be fine, nothing to worry about.”
The familiar flow of our negotiations proceed without flaw. A concern, followed by an explanation; A re-
iterated concern and a comfort. These things can become more deeply entrenched than the Donner Pass
in marriage. Each person knows what the other is doing, wether placating or telling the truth, it doesn’t
matter if a fight is avoided. She knows that I’m placating.

When the doctor opened the door, I could see that the room was tiny. It never helps my body
dysmorphia to be put into a very small room, with a very small woman to sit in a close quarters. I feel
oversized and uncomfortable, mutant-esque. We both enter the room and I squeeze by her, navigating
to the back where patients and family intuitively sit to hear the pertinent medical news. "Please, have a
seat." She promptly begins.
"As you know, your wife's endometriosis didn't get better by the six months of birth control or the
medication that was prescribed. Therefore we performed laparoscopic surgery to remove her right
fallopian tube."
"Yes."
"Well, while we were in there, we wanted to check the left fallopian tube to ensure it's health.
Unfortunately, it appears to have signs of endometriosis as well. She may not be able pass an ovum
through it and therefore pregnancy may be impossible. I would suggest an ink test to determine if a
non-assisted pregnancy is still possible."
"You mean, we may not be able to have more children without in-vitro?”
"Yes. The tests would give us more clarity."

She places the photographs that were taken onto the back lit glass panels so that we can view them. She
shows me the fallopian tube and points out the areas that it appears matted and flattened.

"If you're going to attempt to get pregnant naturally, do it quickly. You are both getting older and this
condition isn’t going to get any better.” I’m not sure that I want another child.
”Ok.”
She walks me through the post-surgical recovery process and what I should expect over the next few
days in terms of care for my wife. The printed pages of standardized recovery information, with the
important information circled in red, are handed to me and reviewed. She leads me back to the empty
recovery area where I sit and wait. Not long after my return, my wife is wheeled in on a gurney, looking
groggy, but awake. With no words, I give her a kiss and just look at her to assess her condition.

”Can I have some ice chips?”

The nurse quickly leaves to fetch them. As if the request was pre-planned to obtain some privacy for her
next question, she darts out. ”What did the doctor say?”
”Lets talk about it later, when you’re feeling better.”
”I’m fine, tell me.”
I recount what the doctor told me regarding her other fallopian tube, childbearing and the chance of
infertility. Her mood is visibly dampened. She really wants another. The nurse returns with the ice chips
during a long and contemplative pause. The business of the surgical recovery continues as the
conversation hangs in the air. It’s continuation is not triggered by a private moment, or a certain look or
feel; it’s triggered by a song.

Upon release and pick up at the patient exit, we hear the song “Do you want to build a snowman?” from
the movie “Frozen.” Somehow, the mood deepens and becomes more serious as the song progresses.
Anna sings the words, “We only have each other, it’s just you and me.” and the pressure releases.

”Do you think that we should do the ink test?”

”What would you want to do if it’s blocked?”
”I’m not sure.”
”Well, if it is blocked, we’d have to go through in-vitro.”
”I know, but don’t you think that we should see if it’s even possible?”
”I like trying, even if it can’t happen. If we’re not going to do in-vitro, there’s no need to have the test.”
The massive increase in libido while I’m on a bulk cycle ensures that the “trying” part of getting pregnant
is taking place, daily. On this bulk cycle I’m keeping my estrogen low which increases my libido even
more. Several weeks later, while cooking pancakes and bacon on a Saturday morning, I get the call from
the bathroom, “Honey, can you come here, please!?” There is an undertone of distress mixed with a
sprinkle of playfulness. “There’s something on the counter that you should see.” Looking around the
counter, I don’t see anything. ”The other counter.” I swing my head left to see the pregnancy test with
what looks like a “+” on it. Oh, shit. I grab it and double check the instructions. A + symbol means
pregnant.
Fuck, this is really happening. Here we go. You see, my previous cycle put a lot of stress on our marriage.
Fights, crying and a near divorce due to an interesting side effect that high doses of Trenbolone has for
me; it makes me stop tolerating bullshit. Trenbolone helped me say things that I had been avoiding for
years. Trenbolone helped push me to fix things that had been broken. And, unfortunately, Trenbolone
urged me to do it all at once. With my marriage on the rocks, I don’t want to have another kid. We are
still recovering from the damage that repairing things creates; wounds healing. Where I live today, a
man’s paternal rights to raise his child are unequal and easily removed. I could hear her lawyer in family
court already.
“He’s a drug user! Alcoholic. Injects steroids daily!”
“He’s been violent and broken things.”
“He scared all of our family and friends on our daughter’s birthday.”
“Smashed a porcelain bowl and almost hurt us.”
“He, . . .”
My missteps would be listed forever and I would never see either of my children again. The pregnancy
test represented risk in a way that nothing else could. At the same time, I was happy. My daughter would
have a sibling. My wife and I would have another intimate bonding time during her pregnancy. I would
have another child to love and love me. This time I have more experience and am better prepared for
this baby. Should be easy.
We hold each other in elation, thinking about the new child. For those few moments, miracles were
real. ”I took two tests at work yesterday and they were both positive.” Over time, the news settles in
and the implications start to present themselves. The money, time, and effort. The joy, bonding, love,
and happiness. The advantages of having a designated driver for ten months. The upcoming additional
stop every morning and evening. Sleepless nights and fun filled days.
The regime of doctors appointments begin and everything is fine. No morning sickness this time presents
a great relief. At about ten weeks the doctor begins using the doppler handheld ultrasound to hear the
child’s heartbeat. It can be difficult to hear, depending on the size, position, shape of the uterus, and
actual conception date of the fetus. When the doctor was unable to find the heartbeat at week ten, it
wasn’t a big deal. ”This is pretty common. Sometimes we just can’t find it. Nothing to worry
about.” She’s worried. By week fourteen, however, the heartbeat is typically apparent.
”We tried to check the heartbeat today, but couldn’t find it.”
”Ok. . ?”
”We immediately did an ultra-sound to check things further.” It’s not good. ”The ultra-sound
determined that it’s a blighted-ovum.”
”What does that mean?”
”It’s a fertilized egg that implanted into my uterus but didn’t develop for some reason or another.
Most often it’s due to a genetic defect.”
Being in the medical field often makes medical news less dramatic due to knowing how common these
things are and simple familiarity. The pace of my meal consumption slows to a crawl as my appetite
leaves me. Eating my salmon, brown rice and asparagus becomes more of a chore than usual. This
fucking bulk, I need to get this food in. I choke down the rest of my plate and make a 75g protein shake
with 40g of Waximaize. Shaking the blender ball cup vigorously due to the large amount of powder and
then chugging it makes that familiar bloated, filled up to my throat feeling apparent.
”What happens next?”
”It needs to be removed; I’m scheduled for a D&C next Monday.”
”Ok, I’ll take some time off.”

The conversation is all business, but I know that there’s pain there; She has wanted this for so long. That
night, we just hold each other in peace. The piercing quiet, soft stroking of her thumb in my hand, sweat
dripping down my legs where-ever two pieces of skin touch, and weary heavy-headedness make for a
difficult several hours. It’s hard to hold back my tears. It’s hard to not speak. There is nothing to say. I
eventually fall asleep before the sun rises. A few days later I am slowly engulfed by the realization.

Sperm have less motility while on steroids.

Sperm have less viability while on steroids.
Sperm have higher rates of genetic defects while on steroids.
My steroid use probably caused this.
Not only am I killing myself earlier, but I’m hurting my loved ones.
For what? To look good?
I’m hurting everyone around me for my aesthetics.
I’ve now sent my wife to surgery for visible abs.
I’m a horrible, selfish and vane asshole.
I deserve to die.
I remain with my head in my hands, on the ground, rigorously motionless, thinking these thoughts for
what seemed like hours. The guilt and shame filling my every cell, stealing what little self-worth I
maintained. If only the ceiling would collapse on me. Maybe this cycle will give me a myocardial
fibrillation. When my daughter returns home from school and jumps on top of me, I snap out of it. I
didn’t even hear her come in the house. I hug her tightly and go to greet my wife. She can tell that I’m
upset.
The next morning after my traditional cold shower, I need to pin for my bulk. Pinning after my shower is
a taciturn sacrament. The sacrament has a specific place for the implements, an order and cadence —
not today. The syringe's orange tip means that it’s delts day. When I finally get the pin unsheathed and
placed on my right delt, I set it on the skin slowly, intentionally. The thoughts from my time on the floor,
the previous day, fill my head. The pin, still pressing on my skin, hurting me with it’s sharp poke. You’ve
sent your wife to the hospital because of this. The pain of the needle on my skin is screaming at me to
pull it away. I see myself in the mirror. As usual, I inspect my body closely. You are an undersized
fatass. And, at that moment, the needle pierces my epidermis and sinks slowly into my muscle. With my
left finger and thumb I push the oil into my body, feeling that slight bit of pressure inside the muscle as it
enters.
 I pull the needle out slowly, guiltily. Fumbling with the sheath, I eventually cap it and hold it in my hand.
Overwhelmed with sorrow and pain, I stand there, over the sink, with my used steroid syringe in my
hand, crying. Untouched tears streaming down my face, chest heaving for gulps of air.

——————

As with any story, creative license is taken. This is a not an actual, literal account of what happened.
Liberties were taken with conversations, flow and almost everything in order to make it more
interesting, readable, emotional, and shorter.
6. The Dirty Bulk Story (video)
There was a time at the Old Westside gym where I couldn't gain weight to save my fucking life.

There was this dude who trained there who could just put on weight like fucking magic. He'd go from 198
to 308 and then to 275 and back down to 198. And he was never fat. It was amazing.

I finally asked him one day how he did it.

"You mean I never told you the secret to gaining weight? Come outside and I'll fill you in."

Now remember, we're at Westside Barbell. And this guy wants to go outside to talk so no one else can
hear. Think about that for a minute. What the hell is he going to tell me? This must be some serious shit
if we have to go outside, I thought.

So we get outside and he starts talking.

"For breakfast you need to eat four of those breakfast sandwiches from McDonalds. I don't care which
ones you get, but make sure to get four. Order four hash browns, too. Now grab two packs of
mayonnaise and put them on the hash browns and then slip them into the sandwiches. Squish that shit
down and eat. That's your breakfast."

At this point I'm thinking this guy is nuts. But he's completely serious.

"For lunch you're gonna eat Chinese food. Now I don't want you eating that crappy stuff. You wanna
get the stuff with MSG. None of that non-MSG bullshit. I don't care what you eat but you have to sit
down and eat for at least 45 minutes straight. You can't let go of the fork. Eat until your eyes swell up
and become slits and you start to look like the woman behind the counter."
"For dinner you're gonna order an extra-large pizza with everything on it. Literally everything. If you
don't like sardines, don't put 'em on, but anything else that you like you have to load it on there. After
you pay the delivery guy, I want you to take the pie to your coffee table, open that fucker up, and grab
a bottle of oil. It can be olive oil, canola oil, whatever. Anything but motor oil. And I want you to pour
that shit over the pie until half of the bottle is gone. Just soak the shit out of it."
"Now before you lay into it, I want you to sit on your couch and just stare at that fucker. I want you to
understand that that pizza right there is keeping you from your goals."

This guy is in a zen-like state when he's talking about this.

 "Now you're on the clock," he continues. "After 20 minutes your brain is going to tell you you're full.
Don't listen to that shit. You have to try and eat as much of the pizza as you can before that 20-minute
mark. Double up pieces if you have to. I'm telling you now, you're going to get three or four pieces in
and you're gonna want to quit. You fucking can't quit. You have to sit on that couch until every piece is
done.
And if you can't finish it, don't you ever come back to me and tell me you can't gain weight. 'Cause I'm
gonna tell you that you don't give a fuck about getting bigger and you don't care how much you lift!"

Did I do it? Hell yeah. Started the next day and did it for two months. Went from 260 pounds to 297
pounds. And I didn't get much fatter. One of the hardest things I've ever done in my life, though.

7. The Pituitary Story

"That motherfucker.”
I toss the paper and envelope onto the island. My doctor skipped a few check boxes on my blood work
order. Fuckit, checking them myself. I find a black pen and check the missing boxes.
☒ Estradiol
☒ Prolactin

Asking the doctor to mail me the blood order lets me review it and not have to go to a doctors office visit.
Getting the blood drawn takes ten minutes in the hospital. And, a few days later, I get a message from my
doctor to call him about the results. I decide to go there and just ask for a copy.

"Hi, I'm DL. I'd like a copy of my latest lab results."

"We can't give you a copy until the doctor signs off on them."
"What? They're the results from me, I paid for them." Be nice, she's probably just following bosses orders.
"The doctor still has to sign off on them and by state law we don't have to give them to you until he has
done that. Sit down and I'll be with you in a minute." da fuk

After about ten minutes, they bring copies of the results.

Test Amount Test Amount

TSH 3.4 Serum Test 586

T4 1.2 Free Test 159

T3 .80 Estradiol 59.8

HDL 40 Prolactin 23.1

LDL 170

I just glance at them and stick them in my bag, forgetting that they are even there. Before I make it home, I
get a call and glance at my phone.
 Dr. GP

I answer it and after a little small talk, he moves abruptly to the point of the call.

”DL, your results look ok. You need to start taking your statin again for the LDL until you can get your HDL
up into the 50’s or 60’s. The TRT dose seems to be working well, Thyroid is in range. Uhh, huh.
”There is one thing concerning here. Your elevated prolactin levels are very abnormal; I don’t see this
often. You’re going to need to go and have an MRI taken of your pituitary.”
”What’s that? I need to have a brain MRI?”
”Yes. Unfortunately. We need to see if there is anything going on in your pituitary gland. It is over-
producing prolactin and this usually indicates swelling and / or prolactinomas. It could be very serious, and
I want you to get this MRA as soon as you are able. Can you come and pick up the order?”
”Wait a minute. So, my pituitary may possibly be swollen, have a tumor, cancer or similar — causing it to
over-produce prolactin. What is the typical treatment for prolactinomas?”
”If that’s the case, which I’m not saying it is, you’ll need to see a neurologist and probably have your
pituitary gland removed. That’d put you on hormone replacement for the rest of your life.” Well, I’m
already there today.”
”Is there any way that opiates from my recent surgery could cause this?”
”I don’t believe so. Even if it did, we couldn’t determine it conclusively without the MRI. So, you need to
get this MRI immediately.”
Research, research, research, research, research, research, research, research, research, research, research,
research, research, research, research, research, research, research, research, research, research, research,
research, research, research, research, research, research
Prolactinomas

Prolactinomas develop when one of these normal cells develops a mutation that allows the cell to divide
repeatedly, resulting in a large number of cells that produce an excessive amount of prolactin. About 10
percent produce growth hormone as well as prolactin.

Symptoms

• Low Testosterone
• Decreased Sperm production
• Lethargy
• Loss of libido
• Loss of muscle mass and strength
• Decreased hematocrit

Fuck. I fucking have all of those when I’m not on TRT. Every symptom lines up and was there for three years
of not running gear, including not being able to impregnate my wife a second time. This explains so much of
 my life path, being on TRT, some of my decisions to use gear regularly to maintain muscle and strength. It fits
perfectly.

...

As I lay in a hospital bed, bare-assed, the neurosurgeon explains (for the fifth time).

”After you are comfortably put to sleep, we’re going to be entering your brain through your nose. We’ll
make a small incision, insert a probe, and visually verify what we saw in the MRI. If it is as we suspect, we’ll
be removing the pituitary. The nurses will give you all of the after care instructions and your medications
to take after surgery. Any questions?” I’ve researched this exhaustively at this point. I may still die.
”Nope. I understand.”
”Everything is going to be fine.”

As the doctor leaves the area, the anesthesiologist comes up.

”We’re going to be putting you to sleep now to go to surgery.”

”Ok, I’ve been told that I have a high tolerance. You may want to take that into consideration.”
”Yes, I was informed. Don’t worry, you’ll be out.”

I glance over at my wife who is grinning from having warned them. I just smile back. I’m trying to stay awake
as long as I can, to feel the effects. I want to feel the onset.

”Ok, will you count to 30 for me?”

”One… Two… Three… Four… Five…”

I faintly hear my wife’s voice, as she touches my arm softly.

”I lovvv”

——————

As with any story, creative license is taken. This is a not an actual, literal account of what happened. Liberties
were taken with conversations, flow and almost everything in order to make it more interesting, readable,
emotional, and shorter.

8. You Wanna Be A Freak?

I'm not banned. Tren does give you horrific sides.

But only at high dosages over long periods.

You wannabe a bodybuilder?

Everyone wants it..

Wanna be a freak?

Want to be a freak? You're in luck. I'm drunk and going to tell you but let's face it. You don't really want
this do you? Want to be a FREAK?

Really?

Want the girls dropping their jaw when you walk in the room? Want the guys saying WTF when they see
you? Want her down on her knees in front of you telling you how hot your abs look before she takes you
in her mouth?

Really?

Yeah, most guys do but they don't want to work for it. Face it. Most guys are lazy, don't want to sacrifice
and can't eat strict for a week. I'm not going to bullshit you guys in this thread. I will lay it all out but the
truth is we don't really want it bad enough. We say we do until we are45 minutes into our tenth cardio
session that week. WE say it until our muscles hurt so bad there are tears in our eyes and we give up. We
want it until we have to eat fish for the 4th time that day...I say I want it but I fucking love beer more, so I
drink...I say I want to be a FREAK but I don't want to work for it. I'm 10 weeks into a blast and my will
feels broken...I can't go on, or can I??? Do I really want this life? No time but time to train. Time to cook,
Time to grocery shop, Time to tan. Fuck!!! Not fish and shakes again...FUCK my life.

I walk past the mirror and catch a glimpse. MY oblique’s are chiseled. My veins look like spider webs all
over my body. I catch her looking at me at work, at the store, at the gym. Guys ask me what I'm on. I
can't take it. i'm on a FUCKING starvation diet and a shit load of cardio but that's not what they want to
hear. They want to hear what drugs to take...You PM me every fucking day. Same questions over and
over. ITS NOT THE DRUGS DUMMY!!! Or is it??? Yes and no. Can you take the sides?

Really??? 2 fucking weeks from now you will PM me again whining. I can't sleep. I can't eat like this. I
can't do that much cardio. I can't. I can't... THEN STOP PM'ing ME!!!! I can't help you. You don't fucking
want this! Just admit it! You don't fucking want this. Its hard. It hurts. You have no social life. You are in
the gym when your buddies are drinking beer. You are doing cardio when guys are lying on the couch.
You spend your last $50on protein powder and a bottle of prop. I know all this because I am you. I want it
for 2-3 months then I give up. Fuck 10 sessions of cardio a week. Fuck eating fish. Fuck taking pills so I can
sleep from all the insomnia from the TREN.
It’s ok. Get some sleep. Wake up and pin. Fuck I love to pin. Push in more oil. I love it. My lunches are
packed. Off to work. Train after work. Get the pump. Here they come. What are you on??? Not this
again...I'm on a crazy train. Fuck my life but fuck I look good and I can lift a shitload of weight. Go ahead,
fuck with me. I will make fast work of you...The tren is in my head. Is she cheating on me? How much
sleep did I get last night? 5hours max. Pin some GH and prop and tren. Fuck, I need some caffeine. Ok,
double espresso. Time to train.

So IF IF IF you can handle the work, cardio and diet not to mention the sides. Then what??? Drugs of
course.

You want that freaky bodybuilder look and your genetics are average like me??

Its actually quite simple but it takes a focus so strong and focused most give up in a few months if not
sooner

Fuck, where am I? Oh yeah the drugs. One word... Trenbolone. How lo0ng can you take it??? Don't cry to
me in 3 weeks when you can't sleep. I don't give a fuck. I can't sleep either. Time for some Xanax. Maybe
some whiskey. Most guys give up on tren right when its getting good. 9 weeks in and man your body is
changing. The girls want you. Give me some Cialis, prop and more tren...How high can I go. 1050mg tren
per week and I look in the mirror. Who is this??? I don't even look the same. I need some mast, maybe
some win, var, halo. Fuck I look like carved stone…I’m drunk but its all true. Do you want to be a freak?
Man the fuck up and start working for it bitch.

Prop, tren and an oral is a good start. The question is HOWLONG CAN YOU RUN THIS??? Tren at 9 weeks
1050mg per week and you are crazy. Eat, train, pin, sleep....over and over. I’m feeling insane just 6 more
weeks. Its 4months now..... Im sub 10% and huge. Not skinny. Huge and lean...How much longer can I go.
I want to look like the guy on the cover of the magazine. REALLY??? Eat some more fish and do some
more cardio...Fuck Fuck...

]Do you really want to be a freak??? Really..?

I walk past them every day at the gym. Same guys doing the same routine looking the exact same as they
did 3 months ago. Talking during sets and even while doing cardio. It isn't work, it's fucking social time for
them. I can't be social at the gym. I'm not built for it and I don't want it. I'm there to work, to train, to
push my body beyond what the average guy can do.
A few guys are there working like a bulldozer at a construction site. Heavy ass poundage's, sweat running
down and out of breath they push another rep. I see the pain in their faces and the strain on their bodies.
My turn mother fucker. Time to WORK. I warm up imagining the set before I do it. The steroids are
pulsing through my body. The tabs dissolved under my tongue. God how I love the taste of D-bol or
Anadrol while walking in the gym. I have been pushing the caffeine and getting in the food. I'm ready. I
don't pin pussy ass doses. I'm jacked to the max. A gram is child's play. I need to push in just a little more
oil.2200mg, 2500mg that week. Maybe a bit more. Fuck it, just fill the barrel all the way and shoot. I am
making changes everyday. I don't want to be the same. I can't be the same.

The steel is cold in my hands. I pump out a few fast sets. Load the weight up. Maybe I will get 4 reps.
Maybe 5. I look at the guy picking up a chick at the gym. He weighs a buck fifty. What a fucking joke. This
isn't a bar its a fucking place of employment. I'm here to WORK. Fuck the chicks. I don't need a girl right
now. I need to train. I lift the weight off and it feels heavy. I grind out 6 reps. Hell yeah! I'm just getting
started. OH fuck. Here comes some guy telling me how good I look. Looks like he has never trained a day
in his life. I ignore his questions and turn up my iPod. I'm trying to concentrate. Get the fuck away from
me my mind screams. I have to be cool. Don't want to get kicked out of the gym....again...I feel rage
inside me. Good. Channel it. Put it to use. Hit the set again. I don't want to be the guy who shows up and
goes through the motions. I want to make changes. God the pain is bad tonight. Lactic acid is heavy in my
muscles. Ok, enjoy the pain. Like it.Its good. Trick your mind. I like the pain. I want the pain. I'm grinding
out slow heavy ass reps. It burns but I tell myself its good. My rest between sets is minimal. I have done 5
sets but the guy talking to the chick has done none. Fuck he is tiny.

I walk over to the next bench and load up some more weights. I see a monster walking by. He is covered
in sweat. He nods. I nod back. Nothing is said. We are both in the same place. We are there to train not
talk. He asks for a spot with one word. spot? I nod and ask how many. He says 5 reps. He pushes out 8
with a few forced reps. My turn. The night goes by slow. Its work. Its hard but I have a pump. Time for
cardio. I take a piss and get on the treadmill. Bump up the incline and speed. The guy two machines
down is walking like he is strolling through the park. He's reading a fucking book. Hell, I can barely read
the numbers in front of me on the machine. I am feeling my lungs burn. Just 40 more minutes to
go...Fuck my life. Ok, go to that place in your mind far away. I look down and 15 minutes has gone by in
what seems like seconds. Good. Go to that place some more. I am absolutely covered in sweat. My shirt
looks like I pulled it out of a bucket of water. I finally finish and get off the treadmill.

Its late and I'm hungry. I feel dizzy. I walk out of the gym. and go get some food. Everyone is obese. I can't
believe how fat everyone is. They are pigs. I am in a world of fat people. How can these lazy fucks stand
it? I feel hate. Why do I hate these fat asses? Its weird but I feel like yelling at them to wake up. The girls
are looking at me again. One stops me and touches the ropes for veins in my arm and says nurses must
 love me when they draw my blood. Its funny but she is right. They do say that. I'm a freak. Its exactly
what I want. I'm walking art. My art. My sculpture. Its who I am....Just another day...a day of work to
become a FREAK

AAS Related Acronyms

Acronym Meaning Notes

Week 1 daily dose/Week 2 Example: 40/40/20/20 = 40mg per day for week 1, 40mg per
X/X/Y/Y daily dose/Week 3 daily day for week 2, 20mg per day for week 3, 20mg per day for
dose/Week 4 daily dose. week 4. Used in reference to Nolva, Clomid, or Torem PCT.

Anabolic-Androgenic
AAS
Steroids

Adrol Anadrol

AI Aromatase Inhibitor compounds that stop Gyno

An enzyme found in the highest amounts in the liver. Injury to

ALT Alanine transaminase
the liver results in release of the substance into the blood.

Low levels of AST are normally found in the blood. When

body tissue or an organ such as the heart or liver is diseased or
Aspartate
AST damaged, additional AST is released into the bloodstream. The
Aminotransferase
amount of AST in the blood is directly related to the extent of
the tissue damage.

Alternating between a bulk cycle with high AAS use and a

B&C Blast and Cruise
TRT cruise.

BMR Base Metabolic Rate

Dbol Dianabol

Deca Durabolin
Deca
(Nandrolone Decanoate)

DMZ Dymethazine

Delayed Onset Muscle

DOMS When your muscles get sore 2-3 days after exercising
Soreness

ED Every Day
Acronym Meaning Notes

EOD Every Other Day

E#D Every "#" Days. E3D = Every 3 Days: Take, skip two days, take.

Epi Epistane

Equipoise (Boldenone
EQ
Undecylenate)

Follicle-stimulating
FSH
hormone

Anabolic steroids or other

Gear things that are used during
a cycle

GH Growth Hormone

Side effect resulting from increased prolactin and/or estrogen

Gyno Gynecomastia
production

Halo Halotestin

Human Chorionic Luteinizing Hormone provided to facilitate production of

HCG
Gonadotropin testosterone by gonads

HGH Human Growth Hormone

Luteinizing hormone and Follicle-stimulating hormone to

Human Menopausal
hMG facilitate the production of testosterone and spermatozoa by the
Gonadotropin
gonads

Hormone Replacement
HRT
Therapy

IM Intra-muscular injection An injection that goes into the muscle tissue

LH Luteinizing hormone

Mast Masteron

PCT Post Cycle Therapy The method to recover from an AAS cycle.

Pins Syringes / Needles

PIP Post Injection Pain Pain felt in the area of an injection

 Acronym Meaning Notes

Drugs made for "research" purposes, very often highly

RC Research Chemical
underdosed

Subq Subcutaneous Injection An injection that goes into the fatty tissue

Sust Sustanon

Sdrol Superdrol

Tbol Oral Turinabol

Total Daily Energy The average amount of energy you need to do your daily
TDEE
Expenditure activities

Test Testosterone

Tren Trenbolone

Testosterone Replacement
TRT Using exogenous Test to mimic natural production levels
Therapy

Var Anavar

VG Ventro Glute A very common muscle in which to inject

Winny Winstrol

What Are Steroids?

The term “steroids” refers to a class of hormones with a classic polyphenol ring structure that are derived
from the cholesterol molecule. There are two types of steroids. They are often
confused: Anabolic and Catabolic. These two steroids serve different medical purposes.

Catabolic Steroids (Glucocorticoids)

A group of steroid hormones produced in the adrenal cortex or made synthetically. They have various
metabolic functions and are used to treat inflammation.

Glucocorticoids are utilized to treat:

1. Arthritis
2. Asthma
3. Autoimmune diseases such as lupus and multiple sclerosis
4. Skin conditions such as eczema and rashes
5. Some kinds of cancer

Side effects of glucocorticoids can include fat gain (particularly trunk), muscle atrophy, weakened bones, and
cataracts.

Anabolic Steroids (AAS)

A synthetic steroid hormone that resembles testosterone in promoting the growth of muscle. Such hormones
are used medicinally to treat some forms of weight loss and by some athletes and others to enhance physical
performance. The proper term for these compounds is Anabolic-Androgenic Steroids (AAS).

Use of anabolic steroids can have side effects which include:

1. Acne and cysts
2. Breast growth and shrinking of testicles in men
3. Voice deepening and growth of body hair
4. Heart problems, including heart attack
5. Liver disease, including cancer
6. Aggressive behavior
See Additional Sides

How Do Anabolic Steroids Work?

There is generally considered to be three mechanisms of action of AAS.

Firstly, by binding to the androgen receptor located in the cytoplasm, AAS stimulate protein synthesis in the
muscle. Secondly, they bind to the glucocorticoid receptor, blocking the catabolic actions of cortisol on
muscle (protein breakdown). Last, psychological effects include increased motivation and aggression, leading
to increased training intensity.

See Pharmacology of AAS

Are They Dangerous?

The general consensus is that if used properly, in conjunction with blood tests, AAS can be used safely.
However, the potential side effects can be extreme if they are used incorrectly. Most commonly, a lipid
profile imbalance which favors plaque deposition in the arteries occurs. The strict diet of most bodybuilders
means this is minimized by a low fat intake.

Liver problems can occur, particularly with the use of orals. Rare cases of hepatic peliosis (blood filled cysts in
the liver), more commonly known as a liver cancer, have been associated with oral AAS. While these cases
have been rare, it emphasizes the need for blood testing during a cycle.
 Gynecomastia can occur as a result of high levels of testosterone being partially converted to estrogen, the
main one being estradiol. The enzyme responsible for this conversion is aromatase, and can be inhibited by a
class of drugs called Aromatase Inhibitors (AI). However, a Selective Estrogen Receptor Modulator (SERM,
such as Raloxifine or Nolvadex) is also used because it blocks the estrogen receptor, rather than the enzyme.

Are There Any Long Term Effects?

AAS have been used in humans to improve performance since the 1930s. This was a crude extract from male
dog urine. Nazi paratroopers were thought to be the first to take testosterone for performance. In the fifties,
drug development company Ciba developed Dianabol—and the race was then on to find the best steroid in
terms of anabolic-androgenic dissociation.

The long history of use by many thousands of people has shown that if used reasonably, most people do not
experience any long-term effects. However, there is a distinct lack of research in this area, with the
occasional case study in the medical literature. The mass media likes to sensationalize the death of any past
steroid user.

The fact is, the most likely problem would be an increase in arterial plaque deposition as a result of an
unfavorable blood lipid levels. This does not affect all users, hence another reason for blood testing.

There is strong evidence to suggest that brief exposure to anabolic steroids might have long lasting
performance-enhancing effects:
• A cellular memory mechanism aids overload hypertrophy in muscle long after an episodic exposure to
anabolic steroids

Should I Begin Taking Anabolic Steroids?

The generally accepted criteria for starting the use AAS is as follows:

1. Research and obtain a very good understanding of what you are considering putting in your body PRIOR to
your cycle.
2. If you are under 25 years old it is possible to incur permanent damage from a cycle; there is also a greater
risk of unwanted side effects.
3. Do not run a cycle without having a PCT and an AI on hand. If you "can't afford" either, then you can not
afford to run a cycle.
4. The best first cycle is a simple first cycle. KISS. As more experience is gained and you learn how your body
reacts to gear, cycles can become more complex. Adding two previously unused elements to a cycle makes it
impossible to know which thing may be causing issues. Grow into your dose.
5. Steroids are magic. But just like any spell, this magic doesn't work without the right incantation. That
incantation, in this case, is a very good diet and exercise program. With these two in place, keep your
expectations reasonable and you'll be happy.
6. For your cycle duration, remain aware of how your body is reacting both physically and emotionally. If
something feels "off" or "not right", and it's not a known side, it probably isn't right. Typical beginner cycles
make people feel very good overall.

Can I Do This Naturally?

You will eventually reach a genetic potential maximum (calculate yours here) with regards to strength and
size. There are often people giving advice to "reach your genetic maximum potential first" before using gear.
Some at /r/steroids give and promote this advice, some do not. This advice is preference.
Information about how gear helps vs natural:
• Steroids vs Natural
• Natural Bodybuilder Cut Study
• Genetic Maximum Potential Models
• Chaos and Pain Question Genetic Maximums. (NSFW)
• Natural Muscle Building: A Look At Potential, Genetics & Arm Size

Why Young Men Should Not Take AAS

Originally by /u/hypnotoadIRL, updated by u/Decatest.

🚫🚫 🚫🚫 🚫🚫

“Anabolic steroids have been reported to induce psychiatric side effects such as aggression and depression.
Adolescence represents an extremely sensitive neurodevelopmental period to influence by detrimental
effects.”
– Side Effects of Drugs Annual
“AAS use by teenagers is a primary concern because of the potential side effects where remodeling of the
brain and behavioral maturation occurs.”
– Journal of Behavioral Processes
“AAS use impaired spatial learning and memory, and this effect was not rescued by exercise. The harmful
effects of AAS on learning and memory should be taken into account when athletes decide to use them for
performance or body image improvement.”
“Testosterone and anabolic steroids have been found to affect the central nervous system (CNS) in humans
and laboratory animals. The locations they affect include centers that regulate mood, sexuality and
aggression. People who use steroids in excessive doses often experience mood disorders that meet the
 criteria of psychiatric disease categories such as depression, anxiety, psychotic reactions and cognitive
deterioration.”
– Anabolic Steroids Cause Longstanding Changes in the Brain
Until you're around the age of 25,1, 2 your brain and endocrine system are still developing. This should be
obvious as you are still going through the end of puberty, getting acne, etc. During this time period,
supplementing with exogenous hormones is extremely dangerous.
Taking anything before you are completely finished with puberty can have negative side effects. While you
are maturing, your brain, organs, and cells are consistently gauging the overall development of your body.
When you introduce a foreign substance, you risk your body’s ability to truly judge how far along your
maturation is, resulting in the possibility of premature shutdown or stunting your growth and development
processes.

Be the adult you claim to be and make a good decision for your health. A man who has patience and
responsibility for his own life and health is vastly more masculine than one jabbing themselves with
hormones to get swole prematurely, damned be all the consequences.

Natural Blast
Your body is already pumping out blast levels of testosterone as part of the natural course of late
adolescence. It's the highest that it's ever going to be in your lifetime.

Why prematurely shut that down and ruin a great thing? You're essentially on free steroids right now. Don't
take that opportunity for granted and abort your own physiological development by injecting additional
variables that short-circuit the whole equation.

There's a serious potential for long-term side effects. People oft-say “I've stopped growing, so it's okay.” No:
it's not okay. The rest of you hasn't finished developing yet. There are many other potential side effects
besides simply your growth plates. Here are a few.

Brain Function, Memory, Alzheimers Disease

It's well known that hormones play a role in the development of cognitive brain function. Your
neuroendocrine system is still developing until the age of 25. Adding external hormones when your brain is
still developing can stunt normal development and maturation. All these effects are more serious in still-
growing and developing brain:

• Many steroids are neurotoxic.

• They lead to depression, memory loss and learning difficulties.

• They cause longstanding dysfunction in brain reward systems.

• They give rise to the accumulation of amyloid plaques, which leads to Alzheimers.

Do you really want to add these variables to a still-growing and developing brain? How can you know many
years down the road there won't be even more problems?

“Males who begin using anabolic steroids during teen years show increased impulsivity and decreased
attention compared to men who began using steroids in their adult years. In adolescent rats, anabolic steroid
exposure is associated with electrolytic imbalances, hyperactivity, anxiety, and increased sympathetic
autonomic modulation (e.g., fight or flight response) during adulthood, even when steroid use was
discontinued during adolescence. Adolescent males given anabolic steroids show increased aggression
even after steroid use is discontinued. These aggressive effects are paralleled by changes in levels of
serotonin and androgen receptors in the brain.”
“Chronic use of anabolic steroids has also been shown to cause dysfunction of reward pathways in animals.
Rats given twice daily nandrolone injections for four weeks showed loss of sweet preference (a sign of
reward dysfunction) accompanied by reductions of dopamine, serotonin, and noradrenaline in the nucleus
accumbens, a reward-related brain region. These effects persist for long after discontinuation of the drug.”
– NIDA. 2020, August 3. What are the risks of anabolic steroid use in teens?

Premature Closing of Growth Plates

This one is the most known about. Even if you think you've stopped growing, there still is a potential for
height increase over time. Scientists have found that growth plates don't fuse completely in some cases until
individuals are past 22. Don't be deterred just because you haven't grown taller in awhile. You grow out as
well as up. Do you want broader shoulders, or do you want to stay stuck with what you've got now?

Cancer, Liver, Kidney Disease

You hear all the time teenagers say “Well my friends it and they got big and nothing happened to them.”
Really? How do you know? Have they been to a doctor and had their liver and kidney values checked? Just
because a person looks okay on the outside, doesn't mean that they don't already host serious problems on
the inside. If treated improperly or in an untimely manner, liver and kidney damage can eventually be fatal.

Impotence
Your neuroendocrine system is still developing. Supplementing with hormones while you are still growing can
potentially cause permanent impotence and fertility issues in teenagers. When you add testosterone,
estrogen and a wealth of other synthetic androgens to your body it can cause problems with your normal
testicular growth and function. Remember, some of these effects are more than just temporary.
 Gyno, or “Bitch Tits”
Androgen usage in teens increases the risk of gyno. Gyno has already been known to happen naturally in
many teenagers because of fluctuating hormones. When you add more hormones to the mix, you
dramatically increase the problems. Remember once you have gyno, it's very hard to get rid of. Unless you
take the proper precautions up front, you'll have to resort to surgery and go under the knife.

Hair Loss, Acne, Prostate Dysfunction

All of these can be accelerated and aggravated with exogenous androgen use.

• Have you seen a 20-year old already going bald?

• What about permanent scarring from severe cystic acne?

• How about being unable to use the bathroom due to the excruciating pain involved in the process? It's not
pretty.

Don't think it can't happen to you.

Women & AAS

The side effects seen in women can be permanent. AAS can lower voice, facial hair growth, and induce
clitoral enlargement. For this reason, AAS administration to women must be used very cautiously—if at all.

References
A few references.

• Effects of anabolic-androgens on brain reward function

• Anabolic steroids cause longstanding changes in the brain
• 17β-trenbolone, an anabolic-androgenic steroid as well as an environmental hormone, contributes to
neurodegeneration
• The Impact of Nandrolone Decanoate on the Central Nervous System
• Nandrolone eleven times more damaging to blood vessels than testosterone
• Nandrolone Decanoate Induces Genetic Damage in Multiple Organs of Rats
• Voluntary exercise does not ameliorate spatial learning and memory deficits induced by chronic
administration of nandrolone decanoate in rats
— updated by u/Decatest —
 Tips For Interpreting Scientific Studies
The number one tip, is “Who stands to gain from this?” This is particularly relevant if you found the study
quoted by some supplement site, for example. You should also check at the end of the article to see if there
is any disclosure of conflict of interest from the researchers. There should also be information on the source
of funding. If it was funded commercially, and one or more of the authors have an interest, beware. Most
good journals will cite these things.
You can also look at the reputation of the journal itself. There is a ranking system or journals, but without
being a scientist, it is hard to know. For those wanting to read more see Impact factor.

Another factor of course is how relevant the research is. Was it in mice? Was it in elderly women? Was the
study well designed to test what you want to know?

One interesting area is the reference section. Here you can find yourself valuable information on studies that
might be more relevant to what you want. Throughout the text assertions are made that are backed up by
prior research. This is then referred to the reference section. Pubmed is wonderful at this as there are related
citations to the right side.

For example: Performance-enhancing drugs on the web: a growing public-health issue.

Links to research/references:

• Testosterone dose-response relationships in healthy young men

• Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen
treatment.

1 FREQUENTLY ASKED QUESTIONS (FAQ)

Compound Usage

wha

How much weight can someone expect to gain during the first cycle of steroids?
Provided dosing is sufficient, a steroid user can expect to make the most significant progress during their first
cycle. Although this will vary from person to person, it is not uncommon for someone to gain 20 pounds of
weight or more during a first cycle of AAS use. Some of this may be water retention, although a solid gain of
more than 10-15 pounds of muscle mass is possible.
Are the gains from steroid use temporary?
Yes, and no. Steroids can help you do two basic things with regard to muscle growth. First, they can allow you
to more rapidly reach your genetic limits for muscle growth. Provided you continue to train actively, eat
properly, and use an effective PCT program, you should be able to maintain at your genetic limit indefinitely.
So in this regard, the early gains do not have to be temporary.

Later, steroids can allow you to push well beyond your genetic limits. It is important to emphasize this, as
extreme physical development cannot be maintained long-term without the repeat administration of anabolic
substances. The body will always revert back towards its normal metabolic limits once AAS are removed. In
this context, some of the gains will not be permanent.

Steroids do permanently alter the physiology of your muscles by adding more cellular nuclei. With higher
nuclei content, each muscle cell can manage its volume more efficiently, which allows more rapid expansion.
Even after a long period of complete abstinence from training and AAS, the nuclei remain. This may provide a
“muscle memory” effect, allowing you to reach your genetic limit (perhaps a slightly extended limit) faster
than if you had never used AAS in the past. So in this regard, there are lasting benefits beyond the temporary
increase in muscle size itself.

Can steroids make me look like a professional bodybuilder?

If you have the underlying genetics to allow for this extreme muscle growth, this may be possible with a lot of
hard work and dedication. Genetics are a big factor in determining the ultimate limits to your physique, even in
an enhanced state. Many people use steroids and look very big and impressive because of it, but very few users
are able to make it to the stage of a professional bodybuilding show.

How dangerous is an isolated cycle of steroids?

Anabolic/androgenic steroids are among the safest drugs available, at least in a short-term sense. Fatal
overdose is not reasonably possible, and the negative health changes such as alterations in cholesterol, blood
pressure, hematocrit, and blood clotting (among other things) are very unlikely to manifest in serious bodily
harm or death after an isolated cycle. There are rare deaths from such things as stroke and liver cancer in short-
term abusers, but such occurrences are statistically extremely rare in light of the millions of people that use
these drugs. If you had to comparatively rate the acute risks of AAS abuse, they would be slightly higher than
marijuana, but far less than virtually all other illicit narcotics.

How dangerous is long-term steroid use?

The long-term use of steroids for non-medical reasons can be a unhealthy practice. It has been difficult,
however, to quantify the exact risk. The main issue is the fact that AAS abuse can promote heart disease, the
number one killer of men. Heart disease is a slow progressive disease, which may build for decades without
symptoms. Steroid abuse may accelerate the silent process of plaque deposition in the arteries, and also induce
other changes in the cardiovascular system that can increase susceptibility to stroke or heart attack. If death
finally occurs, however, it will be difficult for a medical examiner to pinpoint AAS as the cause; too many
variables play a role in the etiology of cardiovascular disease. The vast majority of deaths where AAS have
contributed go unreported for this reason. The exact mortality rates of long-term steroid abusers have, likewise,
been difficult to calculate. It is especially important to closely monitor cardiovascular disease and other health
risk factors if long-term steroid use is a practice you will follow.

Can steroids be used to enhance an athletic career safely?

The non-medical use of AAS by definition cannot be defined as a safe practice. However, it can be argued that
anabolic/androgenic steroids can be used with high relative safety, even over a period of many years. The
guidelines of steroid harm reduction are important to minimizing the negative health effects of these drugs.
Provided an individual follows these guidelines and is careful with drug selection, dosages, and durations of
intake, follows a diet low in saturated fats, cholesterol, sugar, and refined carbohydrates, actively trains with
both resistance and cardiovascular exercise, and uses cholesterol support supplements such as fish oils and
others during all cycles, it may be difficult in many cases to argue high tangible health risks. It takes a great
deal of involvement and planning to use AAS in this manner, which is always advised.

What are the safest steroids for men?

Testosterone, whatever the form, tends to be the safest steroid for men. When the dose remains within the
moderately supratherapeutic range, alterations in cardiovascular risks factors are noticed, but not extreme.
Some of this has to do with the beneficial cardiovascular effects of estrogen in men.

What steroids will not cause hair loss?

For those with a genetic predisposition to hair loss, all anabolic/androgenic steroids are capable of accelerating
the process. Slowing the onset of this during AAS use requires a focus on reducing relative androgenicity in
the scalp. This can be accomplished with the use of predominantly anabolic drugs. Alternately, moderate doses
of testosterone can be used with finasteride, a drug that reduces DHT conversion (and androgenic
amplification) in the scalp. Still, those genetically prone to hair loss can have problems with any steroid, and
are always advised to limit dosing, drug intake durations, and monitor effects on the hairline closely.

What are the safest steroids for women?

Women are generally most concerned h the virilizing (masculinizing) effects of anabolic/androgenic steroids.

The least virilizing agents are not in any way whatsoever those with the highest relative anabolic to
androgenic effect, such as nandrolone, oxandrolone, turinabol, and methenolone. Anabolic/Androgenic ratios,
while a useful measure to scientists, have little to no carryover in terms of virilization potential in women. In
fact, nandrolone—despite having an androgenic rating of only 37—is extremely virilizing in women.”
Care must always be taken, as all AAS are based on male sex steroids, and as such they can cause
masculinizing effects in women.

Do androgen receptors down-regulate?

Conclusions from Scientific Research

There is no scientific evidence to support the popular view that AAS use might be expected to result in
downregulation of the AR relative to receptor levels associated with normal androgen levels.

Conclusions from Bodybuilding Observations

While there are no studies showing downregulation in human skeletal muscle resulting from high-dose AAS
use, there are some studies in cell culture, and sometimes in vivo, which seem to indicate that downregulation
can occur, though not as a result of increase in androgen from normal to supraphysiological.

All of these studies, however, are flawed from the perspective of the bodybuilder wishing to know if
downregulation of the AR has ever been observed in any cell in response to increase of androgen from normal
to supranormal levels.

Upregulation in human muscle tissue, in vivo, is not directly proven but seems to fit the evidence and to
provide a plausible explanation for observed results.

Is there a limit to how muscular someone can get with unlimited gear?
Yes, myostatin inhibits extremely large growth in humans. It is speculated that some of the biggest
bodybuilders have mutations that cause them to produce very low levels of myostatin. Read more here.

What do the anabolic and androgenic reference numbers under the profile for each
steroid mean?
These numbers come from early studies measuring the effect of each steroid on certain muscle and sex organ
tissues of animals, usually mice. These numbers are useful for assessing the relative anabolic to androgenic
balance of each drug in humans. They are not as accurate at assessing the total muscle building potential of
each steroid, however, and should not be taken as absolute ratings of potency.

Can I just do a oral only cycle?

You can. Should you? Probably not. Oral steroids are still going to suppress your natural Test pretty hard. You
may find you don't feel the best or symptoms of low testosterone. if you choose to do a oral only cycle, you
should still look into getting a SERM (like Nolvadex/Clomid or the sorts) for a proper PCT, as well. You
should consider reading through this Wiki and potentially consider doing a real cycle, complete with
Testosterone, as you'll find better results, as well as feeling better overall too.
What about just a Prohormone or Designer Steroid cycle that I got at the store?
Again. You can. Should you? Probably not. Prohormones & Designer Steroids are going to suppress your
natural Test pretty hard. You may find you don't feel the best or symptoms of low testosterone. Prohormones
& Designer Steroids are no better (or even worse in some cases) than using a traditional oral steroid. The
supplemental PCT crap they sell with these Prohormones / Designer Steroids is predominantly bogus stuff and
if you choose to do a Prohormone / Designer Steroid cycle, you should at least look into getting a SERM
(like Nolvadex/Clomid or the sorts) for a real PCT. You should consider reading through this Wiki and
potentially consider doing a real cycle, complete with Testosterone, as you'll find better results, as well as
feeling better overall too.

Compound Handling

My Gear Crashed…How Do I Fix It?

Answer: Gear can crash due to storing the product in colder than recommended temperatures (or in
shipment)…or because the ratio of AAS to oil is out of balance (this can be either a manufacturer error or a
personal error if home brewing). This does not damage the steroid. In order to correct the problem, simply run
the vial under warm water until the products reverts back to its normal state. Clean with alcohol swab after
drying off.

My Gear Has Particles Floating In It?

Answer: You can choose to either dispose of the product or you can re-filter it by using a Whatman filter.
While opinions will differ on this subject, the opinion of re-filtering is still available and a suitable solution in
many cases, assuming the product is not badly polluted. In cases where it is apparent that the product is very
poor quality and contains a large amount of foreign material, it would be wise to dispose of the product. This
should not occur with reputable UGL’s and will never occur with Pharm-grade versions, although an
occasional speck may occur with UGL products here and there and is usually not a big deal.

I need to travel during my cycle/blast/cruise. What do?

Answer: A solution would be to switch over to testosterone Undecanoate. With a half life of 20 days, it makes
for an excellent and risk free choice.
You could also frontload your choice of cypionate/enanthate ester for a shorted trip. Use Steroid Plotter to plan
it out. However, the rapidly dropping levels of this choice make it difficult to manage estrogen properly.
 Cycle Complications

When I go to donate blood they ask about steroid use. Am I possibly harming someone
else?
The primary concerns for steroid users giving blood are infectious disease transmission. Given that users self-
administer injections there is a concern about knowledge of proper needle handling and use. People with HIV /
AIDS or Hepatitis should not give blood.

Reference

I got sick while on cycle. What do?

Assuming it's not just "Test Flu", you have two choices. Cruise on a low dose or PCT. Of course a lot of
factors play in with if you got sick near the beginning, in the middle, or near the end. In the beginning most
will opt to cruise instead of "PCT-ing" so early. In the middle most will opt to cruise instead of "PCT-ing" and
cutting the cycle so short. Near the end can be tricky. Most still choose to cruise and potentially extend the
cycle longer than originally intended, but if it's really close to the end some may choose just to go ahead and
PCT. Obviously this all depends on the severity of your illness. Also if it's something that you'll get over
within a week, most will just continue their dosages as normal.

I'm getting unbearable back / shin / calf / etc. pumps. What can I do?
The first line of action should be:

• Taurine (3-10g pre-workout, you may also add 3-5g AM/PM depending on when you workout)

• Magnesium (200-500mg pre-workout, you may also add 200-500mg AM/PM depending on when you
workout)

• Potassium (200-300mg pre-workout, you may also add 200-500mg AM/PM depending on when you workout)

• Upping your water intake (1-2 gallons ED)

If none of this helps, anecdotally, Cialis (10-15mg ED) has been known to help.

Injecting

My Injection Spot Is Red, Itchy, Or Sore?

Answer: Get to a doctor for some antibiotics if it is red, itchy, or hot. If it is simply sore and/or swollen it is
probably going to be okay see: Post Injection Pain (PIP). If in doubt, get some antibiotics; a common thing to
tell your doctor is that you injected B12.
 Is It Normal To Bleed After An Injection?”
Answer: Yes, it is common to occasionally nick a vein close to the surface of the injection site, which will
cause blood to leak from the surface. The amount of blood which can seep from an injection site can be
anywhere from a drop or two, to a very light stream which slowly flows down that body part. Even in the event
a larger vein is hit when doing an injection, this type of bleeding is relatively easy to stop and will not pose any
harm to the individual.

Is Aspirating Required?
Answer: Many AAS users do not aspirate when injecting. It is considered a bit of an out-dated methodology,
but it never hurts to do it.
According to the CDC:
Aspiration - Aspiration is the process of pulling back on the plunger of the syringe prior to injection to ensure
that the medication is not injected into a blood vessel. Although this practice is advocated by some experts, the
procedure is not required because no large blood vessels exist at the recommended injection sites."
STTI International Nursing Research Congress Vancouver, July 2009:
"Aspiration is not indicated for SC injections."

"Aspiration is not indicated for IM injections."

Organizations which state aspiration is not necessary:
• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)
References located at the bottom of the page.

Does Injecting Build Up Scar Tissue?

Answer: Yes, repeated Intramuscular injections can cause the muscle to build up scar tissue. Generally there is
no inflammation or inclusion in the tissue. In an effort to minimize scar tissue build up, users will rotate
through many injection sites. If you're interested, here is a case study of a woman in an extreme case, it
includes stained muscle biopsies

How Do I Open Ampules?

Answer: Ampules can be aided in opening by scoring (some ampules come pre-scored). Scoring is a process
in which in a fine line is ground away around the neck of the ampule. Scoring makes it much easier to snap the
top of the ampule off without breaking the vial and spilling the oil. Normally, a scoring tool is used for this
process, although sometimes knives or other objects can be used.
An amp opener can be used, which is the fastest and the least time consuming methods.

If you don't have an ampule opener. Grasp the ampule between thumb and forefinger of one hand. Move liquid
from the neck to the body of the ampule by tapping (thumping) the ampule sharply. Using gauze pad (or
similar), grasp stem (the part above the neck) with other hand. Break stem away from you and discard
safely. This is a very helpful video that shows the process

Lastly, the tape-method can be employed, as well. The tape method involves taping the entire vial all the way
up to the neck line. Several layers of tape should surround the vial, so that it is properly secured. The point of
taping the vial is two-fold. One purpose is to prevent the contents of the ampule from spilling, should the
ampule break somewhere other than the neckline. The other purpose is to reinforce the ampule, so that it is
more likely to break at the neckline. One can combine both the tape method and the scoring, which is the best
way to ensure that the oil contained in the ampule will not be spilled.

Can I Re-Use Syringes?

Answer: Absolutely not. You should never take a needle which has entered the body and re-insert it back into
a steroid product, as this can result in bacteria build-up and cause potential future infections.

How Fast Should I Inject?

Answer: As a general rule, 30 seconds per mL/cc.

Is It Dangerous To Inject Small Air Bubbles?”

Answer: No, a small amount of air will do no harm. Air bubbles injected into muscle tissue is of no concern.
Even if the individual were to thread a vein and inject the entire contents of the syringe into the vein, the small
air bubbles contained within it would be the least of that person’s worries. In reality, several cc’s of air would
have to be injected directly into a vein all at once, in order to cause cardiac arrest. Even injecting 2-3 cc’s of air
directly into a muscle would be largely inconsequential. Of course, such an action is not recommended, but
you get the point.

Ancillaries

Q: Can Nolvadex (Tamoxifene) and Arimidex (Anastrozole) be used together?

A: Yes, they can when needed. Taking Arimidex with Nolvadex decreases the serum concentration of
anastrozole by 27%, but has no effect on the pharmacodynamics of either
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362190/
In conclusion, the results of this study confirm that anastrozole does not affect the pharmacokinetics of
tamoxifen when the two drugs are given in combination to post-menopausal women with early breast cancer.
In addition, the oestradiol suppressant effects of anastrozole appear unaffected by tamoxifen.
http://publications.icr.ac.uk/629/
As a result of (a) the lack of effect of anastrozole on tamoxifen and DMT levels and (b) the observed fall in
blood anastrozole levels having no significant effect on oestradiol suppression by anastrozole, we conclude
that the observed reduction in anastrozole levels by tamoxifen is unlikely to be of clinical significance when
anastrozole and tamoxifen are administered together.
The actual ATAC trial that this information comes from. Pharmacokinetic details can be found here
http://www.nature.com/bjc/journal/v85/n3/pdf/6691925a.pdf
"...the observed fall in blood anastrozole levels having no significant effect on oestradiol suppression by
anastrozole, we conclude that the observed reduction in anastrozole levels by tamoxifen is unlikely to be of
clinical significance when anastrozole and tamoxifen are administered together."*

Q: Can Nolvadex (Tamoxifene) and Letrozole be used together?

A: Yes, they can when needed. Just be aware that taking Letrozole with Nolvadex decreases the serum
concentration of Letrozole by 35-40%.
https://pdfs.semanticscholar.org/e492/c9fb67a771779ac3be19faf14ea3b458e03a.pdf
Pharmacokinetic analyses of the combination of tamoxifen and letrozole have revealed that these drugs
interact, resulting in letrozole concentrations approximately 35-40% lower than when letrozole is used alone.
...
...letrozole has no impact on tamoxifen concentrations.

Q: Does Aromasin need to be taken with fat?

A: It works better when taken with a high fatty meal, yes.
http://www.rxlist.com/aromasin-drug.htm
Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in
water
http://www.rxlist.com/aromasin-drug/indications-dosage.htm
the recommended dose of AROMASIN is 50 mg once daily after a meal.
http://www.drugs.com/monograph/aromasin.html
High-fat meal increases plasma exemestane concentrations by approximately 40%.
http://labeling.pfizer.com/showlabeling.aspx?id=523
Absorption: Following oral administration of radiolabeled exemestane, at least 42% of radioactivity was
absorbed from the gastrointestinal tract. Exemestane plasma levels increased by approximately 40% after a
high-fat breakfast.
http://www.drugs.com/monograph/aromasin.html
Dosages >25 mg daily not shown to provide substantially greater suppression of plasma estrogens but may
increase adverse effects
HGH

Does using HGH shut down natural HGH production?

Answer:
The mechanism by which chronic exposure to hGH leads to tolerance, dependence, and a withdrawal
syndrome is unclear and does not involve the suppression of hormone secretion. During the nadir of growth
velocity, which follows the withdrawal of prolonged drug therapy, serum GH levels remain normal, as do
serum IGF-I and IGF-binding protein-3 levels (4). Moreover, endogenous pulsatile secretion of GH resumes
within days even after long-term hGH therapy (7).

http://press.endocrine.org/doi/full/10.1210/jcem.87.8.8721

General

Does ejaculation reduce my testosterone levels?

Temporarily, yes, it does. However, not ejaculating will eventually decrease the levels even more. For peak
levels, only ejaculate every seven days.

A research on the relationship between ejaculation and serum testosterone level in men.
http://www.ncbi.nlm.nih.gov/pubmed/12659241
The purpose of this study is to gain understanding of the relationship between ejaculation and serum
testosterone level in men. The serum testosterone concentrations of 28 volunteers were investigated daily
during abstinence periods after ejaculation for two phases. The authors found that the fluctuations of
testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however,
a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular
fluctuation was observed following continuous abstinence after the peak. Ejaculation is the precondition and
beginning of the special periodic serum testosterone level variations, which would not occur without
ejaculation. The results showed that ejaculation-caused variations were characterized by a peak on the 7th day
of abstinence; and that the effective time of an ejaculation is 7 days minimum. These data are the first to
document the phenomenon of the periodic change in serum testosterone level; the correlation between
ejaculation and periodic change in the serum testosterone level, and the pattern and characteristics of the
periodic change.

Are American military personnel tested for steroids?

Steroids are not part of the standard drug panel. However, users should be aware that their superiors have the
ability to order steroid-specific testing if an individual is suspected of using. PCT drugs will also not appear on
the test.
Can steroids increase the size of my penis?
hGH: It is very likely that it can and will with prolonged usage.
Effect of human growth hormone therapy on penile and testicular size in boys with isolated growth
hormone deficiency: first year of treatment.
http://www.ncbi.nlm.nih.gov/pubmed/6406387
The response of genital and gonadal growth during the first year of treatment with human growth hormone
(hGH) was studied in 20 boys with isolated growth hormone deficiency (IGHD) (11 of hereditary origin and 9
sporadic cases). Prior to hGH treatment, 13 of the 15 prepubertal boys had a penis length below the normal
mean, 3 of which were more than 2 SDS below the mean. The boys with hereditary IGHD had a greater deficit
in penile size than did the sporadic cases. hGH treatment improved the penile length in all but two boys aged
14 and 15 yr, and led to growth up to normal size in the three boys with very small penises. Three of the
hereditary IGHD patients had subnormal testes and all of the other prepubertal boys had a testicular volume in
the normal range. hGH treatment increased testicular size, particularly in the prepubertal boys. Of three
additional untreated adults with IGHD, one had a subnormal-size penis and two had penises of low-normal
size. Our findings constitute further evidence that hGH deficiency is associated with decreased penile growth
and, to some extent, decreased testicular size, and that hHG treatment improves the growth of the genitalia and
gonads. Since these effects were also observed in prepuberty, it seems that not all the hGH or, rather,
somatomedin effect on sex organs is androgen mediated.
Testosterone: There is evidence that in infants and young children that it can increase size.
Congenital hypogonadotropic hypogonadism and micropenis: effect of testosterone treatment on adult
penile size why sex reversal is not indicated.
http://www.ncbi.nlm.nih.gov/pubmed/10228293
Micropenis is commonly due to fetal testosterone deficiency. The clinical management of this form of
micropenis has been contentious, with disagreement about the capacity of testosterone treatment to induce a
functionally adequate adult penis. As a consequence, some clinicians recommend sex reversal of affected male
infants. We studied 8 male subjects with micropenis secondary to congenital pituitary gonadotropin deficiency
from infancy or childhood to maturity (ages 18 to 27 years). Four patients were treated with testosterone before
2 years of age (group I) and four between age 6 and 13 years (group II). At presentation, the mean penile
length in group I was 1.1 cm (-4 SD; range, 0.5 to 1.5 cm) and in group II it was 2.7 cm (-3.4 SD; range, 1.5 to
3.5 cm). All patients received one or more courses of 3 intramuscular injections of testosterone enanthate (25
or 50 mg) at 4-week intervals in infancy or childhood. At the age of puberty the dose was gradually increased
to 200 mg monthly and later to an adult replacement regimen. As adults, both group I and II had attained a
mean final penile length of 10.3 cm 2.7 cm with a range of 8 to 14 cm (mean adult stretched penile length for
Caucasians is 12.4 2.7 cm). Six of 8 men were sexually active, and all reported normal male gender identity
and psychosocial behavior. We conclude that 1 or 2 short courses of testosterone therapy in infancy and
childhood augment penile size into the normal range for age in boys with micropenis secondary to fetal
testosterone deficiency; replacement therapy at the age of puberty results in an adult size penis within 2 SD of
the mean. We found no clinical, psychologic, or physiologic indications to support conversion of affected male
infants to girls. Further, the results of this study do not support the notion, derived from data in the rat, that
testosterone treatment in infancy or childhood impairs penile growth in adolescence and compromises adult
penile length.
Role of parenteral testosterone in hypospadias: A study from a teaching hospital in India
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183705/
Additionally, a father decided to treat his infant son with Testosterone for increased penis size.

Are fat cells ever lost?

The number of fat cells in your body is set in childhood and early adolescence. Those fat cells will shrink or
expand to hold more fat as required.

http://www.ncbi.nlm.nih.gov/pubmed/18454136
Obesity is increasing in an epidemic manner in most countries and constitutes a public health problem by
enhancing the risk for cardiovascular disease and metabolic disorders such as type 2 diabetes. Owing to the
increase in obesity, life expectancy may start to decrease in developed countries for the first time in recent
history. The factors determining fat mass in adult humans are not fully understood, but increased lipid storage
in already developed fat cells (adipocytes) is thought to be most important. Here we show that adipocyte
number is a major determinant for the fat mass in adults. However, the number of fat cells stays constant in
adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of
adipocytes is set during childhood and adolescence. To establish the dynamics within the stable population of
adipocytes in adults, we have measured adipocyte turnover by analysing the integration of 14C derived from
nuclear bomb tests in genomic DNA. Approximately 10% of fat cells are renewed annually at all adult ages
and levels of body mass index. Neither adipocyte death nor generation rate is altered in early onset obesity,
suggesting a tight regulation of fat cell number in this condition during adulthood. The high turnover of
adipocytes establishes a new therapeutic target for pharmacological intervention in obesity.

Why do steroids make your traps and shoulders pop out that much?
There are more androgen receptors in those areas. Related study.

2 MEDICINAL USE OF AAS

Due to the culturally engrained stereotype of AAS use, medicinal use of AAS has just recently began to be
investigated. This page seeks to document areas where AAS may be beneficial to patients with disease.
Anxiety

There is a large amount of anecdotal evidence that increased Testosterone levels can assist with anxiety
relief.

Cerebral Palsy

Consensus seems to be forming that hGH is beneficial for use for Cerebal Palsy patients.

Is treatment with growth hormone effective in children with cerebral palsy?

Dev Med Child Neurol. 2004 Aug;46(8):569-71.

http://www.ncbi.nlm.nih.gov/pubmed/15287249
Children with cerebral palsy (CP) often have poor linear growth during childhood, resulting in a diminished
final adult height. Here we report a female with CP and short stature but without growth hormone (GH)
deficiency who exhibited increased growth during treatment with GH. We also report two other children with
CP who were treated with GH: one female with a history of leukemia, and a male with Klinefelter syndrome.
These two children were both found to be GH-deficient by insulin provocative GH testing and responded to
treatment with increased growth rate. Growth improved to a greater extent in the two children with
apparent GH deficiency. In summary, it is felt that GH therapy might be beneficial for children with CP and
warrants further investigation. Growth hormone deficiency in two children with cerebral palsy.

Dev Med Child Neurol. 1995 Nov;37(11):1013-5.

http://www.ncbi.nlm.nih.gov/pubmed/8566448
The authors describe two children with cerebral palsy and linear growth failure secondary to growth
hormone deficiency. One of the children was successfully treated with growth hormone replacement
therapy. His linear growth velocity increased from 3cm/year before therapy to 8.3 cm/year during the first
two years of therapy. Potential complications such as worsening orthopedic status did not occur.
Psychosocial benefits were noted. The authors conclude that growth hormone deficiency may play a role in
linear growth failure in some children with cerebral palsy and that some of these children may benefit from
growth hormone therapy.
Growth hormone deficiency and cerebral palsy
http://www.dovepress.com/articles.php?article_id=5238
Cerebral palsy (CP) is a catastrophic acquired disease, occurring during development of the fetal or infant
brain. It mainly affects the motor control centres of the developing brain, but can also affect cognitive
functions, and is usually accompanied by a cohort of symptoms including lack of communication, epilepsy,
and alterations in behavior. Most children with cerebral palsy exhibit a short stature, progressively declining
from birth to puberty. We tested here whether this lack of normal growth might be due to an impaired or
deficient growth hormone (GH) secretion. Our study sample comprised 46 CP children, of which 28 were
male and 18 were female, aged between 3 and 11. Data obtained show that 70% of these children lack
 normal GH secretion. We conclude that GH replacement therapy should be implemented early for CP
children, not only to allow them to achieve a normal height, but also because of the known neurotrophic
effects of the hormone, perhaps allowing for the correction of some of the common disabilities experienced
by CP children.
Growth Hormone Therapy Improves Bone Mineral Density in Children with Cerebral Palsy: A Preliminary
Pilot Study
http://press.endocrine.org/doi/full/10.1210/jc.2006-0385
Context: Cerebral palsy is associated with osteopenia, increased fracture risk, short stature, and decreased
muscle mass, whereas GH therapy is associated with increased bone mineral density (BMD) and linear
growth and improvement in body composition. Objective: We conducted a pilot study to evaluate the effect
of 18 months of GH therapy on spinal BMD, linear growth, biochemical markers, and functional measures in
children with cerebral palsy.
Design and Setting: The study was a randomized control trial, conducted from 2002–2005 at the University of
California, Los Angeles, Orthopedic Hospital’s Center for Cerebral Palsy.
Patients: Patients included 12 males with cerebral palsy, ages 4.5–15.4 yr. Intervention: We compared 18
months of GH (50 μg daily) vs. no treatment. Primary Outcome Measures: Spinal BMD (dual-energy x-ray
absorptiometry scan), height, growth factors, and bone markers were assessed.
Results: Ten subjects (five in each group) completed the study. Pre- and post-average height z-scores were
−1.47 ± 0.23 and 0.8 ± 0.2 (GH-treated group) vs. −1.35 ± 1.26 and −1.36 ± 1.27 (control group) (Δ sd score,
0.67 vs. −0.01; P = 0.01). Average change in spinal BMD z-score (Δ sd score corrected for height) was 1.169 ±
0.614 vs. 0.24 ± 0.25 in the treated and control groups, respectively (P = 0.03). Osteocalcin, IGF-I, and IGF-
binding protein 3 levels increased during GH therapy. There was no change in quality of life scores as
measured by the Pediatric Orthopedic Disability Inventory.
Conclusions: This small pilot study suggests that 18 months of GH therapy is associated with statistically
significant improvement in spinal BMD and linear growth.

Collagen Synthesis

Testosterone decreases collagen synthesis, reducing the strength, flexibility and structural integrity of skin
and joints. There are ways to mitigate this. Boldenone (Equipoise), Methenolone (Primobolan), Nandrolone
(Deca), oxandrolone (Anavar) and human growth hormone (hGH) each enhance collagen synthesis, which
helps to offset testosterone's negative impact.
Options

Procollagen III is a primary indicator used to determine the rate of collagen synthesis:

• Boldenone at 3 mg/kg increases procollagen III by approximately 340% within one week.
• Nandrolone at 3 mg/kg a week increases procollagen III levels by 270%.
• Primobolan at 5 mg/kg increases collagen synthesis by ~180%.
• HGH at 6 iu/day increases the collagen deposition rate by around 250% in damaged collagen structures.
• Stanozolol boosts collagen production40340-9/full) and mRNA.
• Anavar is prescribed post-surgery and has hundreds of scientific studies demonstrating increased collagen
synthesis, accelerated wound healing and enhanced recovery.
• Estrogen plays an integral role in keeping tendons and joints strong.
— Contributed by u/Decatest

COPD

It doesn't appear that AAS are effective for COPD.

http://www.ncbi.nlm.nih.gov/pubmed/18684793
Patients with severe chronic obstructive pulmonary disease (COPD) commonly develop weight loss, muscle
wasting, and consequently poor survival. Nutritional supplementation and anabolic steroids increase lean
body mass, improve muscle strength, and survival in patients enrolled in comprehensive rehabilitation
programs. Whether anabolic steroids are effective outside an intensive rehabilitation program is not known.
We conducted a prospective, double-blind, placebo-controlled, 16-week trial to study the benefits of
anabolic steroids in patients with severe COPD who did not participate in a structured rehabilitation program.
Biweekly intramuscular injections of either the drug (nandrolone decanoate) or placebo were administered.
Sixteen patients with severe COPD were randomized to either placebo or nandrolone decanoate. The placebo
group weighed 55.32 +/- 11.33 kg at baseline and 54.15 +/- 10.80 kg at 16 weeks; the treatment group
weighed 68.80 +/- 6.58 at baseline and 67.92 +/- 6.73 at 16 weeks. Lean body mass remained unchanged, 71
+/- 6 vs. 71 +/- 7 kg in placebo group and 67 +/- 7 vs. 67 +/- 7 in treatment group, at baseline and 16 weeks
respectively. The distance walked on 6 min was unchanged at baseline, 8 weeks, and 16 weeks in placebo
(291.17 +/- 134.83, 282.42 +/- 115.39, 286.00 +/- 82.63 m) and treatment groups (336.13 +/- 127.59, 364.83
+/- 146.99, 327.00 +/- 173.73 m). No improvement occurred in forced expiratory volume in one second,
forced vital capacity, maximal inspiratory pressure, maximal expiratory pressure, VO(2) max or 6-min walk
distance or health related quality of life. Administration of anabolic steroids (nandrolone decanoate) outside
a dedicated rehabilitation program did not lead to either weight gain, improvement in physiological function,
or better quality of life in patients with severe COPD.

Cystic Fibrosis

This thread has some information

Hepatitis C

Sexual dysfunction in males with chronic hepatitis C and antiviral therapy: interferon-induced functional
androgen deficiency or depression?
Hypogonadism

See Testosterone Replacement Therapy (TRT)

Immune therapy

http://www.medibolics.com/litref2.htm

Multiple Sclerosis

Not to be confused with glucocorticoid use to treat inflammation produced by MS, anabolic steroids also can
play a role.

Users Letter
Dr. Terry Wahls discusses dietary treatment of MS in a TED Talk.

Need access to these:

The treatment of multiple sclerosis with anabolic steroids

Results of combined administration of anabolis steroids in patients with multiple sclerosis

Post Traumatic Stress Disorder (PTSD)

Joe Rogan Experience #574 - Dr. Mark Gordon, Matthew Gosney & Jason Hall (TL;DW - Doctor is treating
PTSD patients with hormone therapy) - [139:56]

3 TESTOSTERONE REPLACEMENT THERAPY (TRT)

Welcome to r/steroids' wiki on testosterone replacement therapy (TRT). This wiki explores TRT for treating
low testosterone (aka low T).
For a medical reference, see The Endocrine Society's "Clinical Guide: Testosterone Therapy in Adult Men with
Androgen Deficiency Syndrome." ( Original PDF | Scribd )

Categorization of Low Testosterone (T)

Before we get into testosterone replacement therapy for treating low T, let’s look at the categories of male
hypogonadism (low T).

Primary Hypogonadism
This type on low T is caused by a problem with your testicles. The testicles are still receiving the message
from the brain to produce testosterone, but the testicles aren't working properly and cannot produce enough
 testosterone. This form of hypogonadism is usually due to injury to the testicles or radiation exposure from
chemotherapy.

Secondary Hypogonadism
This type of low T is caused by a problem with you pituitary or hypothalamus, two glands in the brain that tell
the testicles to produce testosterone. Basically, the messaging system is broken. [As a side note, physicians
and online references generally group pituitary and hypothalamus problems together. If they don’t, problems
with the pituitary may be referred to as secondary hypogonadism and problems with the hypothalamus may
be referred to as tertiary hypogonadism.]

Secondary hypogonadism is far more common than primary hypogonadism and many more things can cause
it. It can be caused by pituitary or hypothalamic disorders or a pituitary tumor. Fortunately, only about 0.25%
of these pituitary tumors are cancerous, the rest are benign. But, they still may effect testosterone
production. Secondary hypogonadism may also be caused by obesity, diabetes, and the use of certain
medications.

Lastly, normal aging may cause secondary hypogonadism. The truth of the matter is that aging gradually
wears down all the systems of the body. One system that gets particularly worn down is the messaging
system for the production of testosterone. As a result, testosterone levels gradually decline with age. This
natural decline in testosterone production leads to the prevalence of low testosterone in middle-aged and
older-aged men. It is estimated that between 20-40% of older men have low testosterone and/or suffer from
symptoms associated with low T.

Symptoms of Low Testosterone

Some advertisements for testosterone replacement products may lead you to believe that simply feeling
tired or cranky is a sign of low T. In reality, symptoms tend to be more involved than that. Regardless of your
age, low T symptoms can include:

• Erectile dysfunction, or problems developing or maintaining an erection

• Other changes in your erections, such as fewer spontaneous erections
• Decreased libido or sexual activity
• Infertility
• Rapid hair loss
• Reduced muscle mass
• Increased body fat
• Enlarged breasts
• Sleep disturbances
• Persistent fatigue
• Brain fog
• Depression

Many of these symptoms can also be caused by other medical conditions or lifestyle factors. If you’re
experiencing them, make an appointment with your doctor. They can help you identify the underlying cause
and recommend a treatment plan.

What is TRT?

Testosterone replacement therapy (TRT) is the administration of testosterone to men to treat low T. It is a
prescription treatment overseen by a physician. The main goal of therapy is to reestablish normal
testosterone levels. Physicians typically aim to reestablish a testosterone level between 500 ng/dL and 1000
dg/nL.

Men sometimes confuse anabolic steroid usage (testosterone cycles) for the purpose of bodybuilding with
TRT. TRT uses normal, physiological dosages to increase low testosterone levels back to normal levels. The
testosterone preparation is taken regularly, oftentimes for the rest of an individual’s life. On the other hand,
testosterone cycles for the purpose of bodybuilding use above normal, supraphysiological dosages to
increase testosterone levels above normal for a period of time. Users of testosterone cycles for the purpose
of bodybuilding typically cycle on and off testosterone to give their bodies a break from these
supraphysiological testosterone levels.

• A Guide to Hypogonadism - National Library of Medicine

• Androgen Replacement Therapy - Medscape
• Testosterone Therapy in Adult Men - Endocrine Society
• Testosterone Replacement Therapy - Elite Men's Guide
• Testosterone Wiki - Testosterone Subreddit

Getting On TRT

To get a prescription to go on TRT, you're going to have to get blood work that shows that you have low
testosterone. The blood work will at a minimum measure your total testosterone level. It may also measure
your free testosterone and sex hormone binding globulin levels. Any test providing all three values will
provide more information than the total testosterone level alone, so ask for the most comprehensive test
possible.

The test requires a blood sample to be taken from a vein. The best time for the blood sample to be taken is
between 7 a.m. and 10 a.m because testosterone levels fluctuate throughout the day and early morning tests
offer the most reliable results. A second sample is often needed to confirm a result that is lower than
expected.

Additional tests of use include a measurement of LH (luteinizing hormone) levels, FSH (follicle stimulating
hormone) levels, prolactin levels, and a full thyroid panel.
• Testosterone Testing - LabTestOnline
• Testosterone Testing - MedLinePlus

Finding a Doctor; Getting Blood Work

TRT has really only recently gone mainstream. Some physicians know quite a bit about it; some know very
little. Some physicians wholeheartedly support it; some look at it very skeptically. Most will be somewhere in
the middle. Thus, it’s important to find a physician that you feel comfortable with and that has a good
understanding of and respect for TRT.

If you suspect you have low testosterone because you have some symptoms of low T, start by talking about
these symptoms with your doctor. Then, ask your doctor for a simple blood test to measure your
testosterone levels. If your doctor won’t perform a blood test, either get a different doctor or get some blood
work done yourself. Plenty of companies now offer hormone panel testing services Any Lab Test
Now, DirectLabs, DiscountedLabs, ZRT Laboratory. While you can’t get a TRT prescription from them, you can
arm yourself with the results by figuring out whether or not your levels are low.

Here are the different doctors that you can see that most often treat men with low testosterone (ordered by
ease of access and knowledge of TRT). In any case, a male doctor is more likely to prescribe testosterone than
a female doctor:

• Low T Centers/Men’s Health Clinics – These clinics specifically cater to testing for and treating men with low
testosterone. They charge a monthly fee for access to physicians. Insurance may or may not cover these
providers, so check. (Companies with the most locations are Low T Center, BodyLogicMD,
and LowTestosterone.com). Note: These centers and clinics do not prescribe testosterone to any man that
comes in complaining of low testosterone symptoms. They perform blood tests and only prescribe
testosterone therapy to men with clinically diagnosed low testosterone.
• Anti-Aging/Longevity Clinics – These clinics typically also prescribe HGH as well as other hormones. They are
expensive because they typically only take cash and do not charge to insurance.
• Naturopathic Doctors (NMDs) – Some are licensed to prescribed hormones; some are not. If they are licensed
to prescribe hormones, they are likely to prescribe TRT fairly easily. They are often cheaper than anti-aging
clinics, but may not work with insurance, so check.
• Endocrinologists - Can be covered by insurance; some specialize in TRT, but some are not as knowledgeable
about TRT. They also help manage diabetes and obesity. If you have diabetes and/or are obese, they can help
with both issues.
• Urologists - Often treat low testosterone and other related men’s health issues like sexual dysfunction. If you
have sexual dysfunction issues, they can help with both issues.
• General Practitioner/Primary Care Manager – They may treat you if they are comfortable with prescribing
testosterone and comfortable with you. They are also the most likely not to have a good deal of knowledge
of or experience with TRT.
Understanding your Blood Work Results
The normal range for total testosterone levels in men is approximately 300 ng/dL to 1050 ng/dL. There is no
absolute consensus among different medical organizations for the exact cutoff for low testosterone. In
general, the cutoff ranges from high 200s to low-to-mid 300s ng/dL. This range is over a broad age range and
there is no “normal” testosterone level based on age that men can look to as a reference.

The official recommendations of the major professional organizations are:

Organization Suggest Total Testosterone Level for Treatment

2010 guidelines suggest 300 ng/dL as a common threshold for symptoms in

many men, but state that “the threshold testosterone level below which
The Endocrine Society symptoms of androgen deficiency and adverse health outcomes occur and
testosterone administration improves outcomes in the general population is
not known”.

American Organization 2002 guidelines suggest men with symptomatic hypogonadism and a total
of Clinical testosterone level of less than 200 ng/dL may be potential candidates for
Endocrinologists therapy.

European Association
< 350 ng/dL
of Urology

Japanese Urological 2008 guidelines suggest that total testosterone be ignored and diagnoses be
Association made purely from free testosterone.

As mentioned above, your free testosterone level is as important, if not more important, as the total
testosterone level. The normal range for free testosterone in men is 5 ng/dL to 21 ng/dL. It should be noted
that labs use different assays and methodologies to measure free testosterone levels. A free testosterone
(direct) test will yield values outside of the above range if you try to convert the values. In this case, use the
reference range for free testosterone provided by the lab. Compare your lab results directly to the lab
provided range to assess where you stand. For example, AnyLabTestNow provides a free (direct ) range of 35
to 155 pg/mL (3.5 to 15.5 ng/dL).

Two important points should be noted regarding the normal range for testosterone. First, the normal range
for testosterone is quite large. One man can have nearly three to four times the testosterone as another man
and both men can be considered “normal”. The size of the change in testosterone levels over a lifetime can
be just as important as the actual clinical value for the development of low T symptoms. While low T is
generally defined as total testosterone below 300 ng/dL, men with levels above this cutoff value may still
experience symptoms of low T because they experience big individual declines over their lifetime. Some men
start to experience the symptoms of low testosterone at merely low-normal levels; anecdotal reports include
some men suffering symptoms of low testosterone at levels as high as 450 ng/dL.

Second, testosterone levels naturally decline. Total testosterone levels decline nearly 30% between the ages
of 25 and 75. Free testosterone levels decline nearly 50% between the ages of 25 and 75. But, the normal
range is applied to both a 25-year-old and a 75-year-old man. There is no clinically “normal” testosterone
level based on age that men can look to as a reference. Some studies do measure average total and free
testosterone with age, so that you can compare your levels with the average study levels. Elite Men’s
Guide Normal Testosterone Levels article provides more detail on testosterone levels.

Common TRT Prescriptions

Testosterone
There are a few different forms of testosterone for TRT. These forms can be broken down into four
categories: 1) injectable oil-based testosterone, 2) testosterone gels/creams, 3) testosterone lozenges, and 4)
implantable testosterone pellets. The two most common forms are injectable oil-based testosterone and
testosterone gels. Testosterone may also come in transdermal patches or troches, but both forms are not
used often.

Right now, there are no FDA-approved oral pill forms of testosterone in the US. In general, oral pill forms may
cause liver damage and should be avoided for TRT. The only safe oral form for long-term use is testosterone
undecanoate, which again is not available in the US. For men outside the US, it is marketed under several
brand names including Andriol, Undestor, and Nebido among others.

Most docs will first recommend Testosterone in the following forms and generally (but not always) in this
order:

Gels/Creams

Testosterone gels deliver testosterone through daily skin applications. The gels consist of a hydro-alcoholic
base medium with 1 or 1.62% active testosterone. These formulations deliver 25, 50, or 100 mg of
testosterone per day. This form of testosterone is relatively new with the first testosterone gel introduced in
2000. As such, most gels are sold under a brand name only and are typically more expensive than generic
injectable testosterone cypionate and enanthate. Androgel, Axiron, Fortesta, Testim, and Vogelxo. Recently,
generic versions, such as Bio-T-Gel have become available.

Recently, testosterone gel usage has surpassed injectable testosterone usage for TRT. Approximately 60% of
TRT users use testosterone gels, while 35% use injectable testosterone (according to Endo Pharmaceuticals
FDA filing for Aveed). Gels will likely be the first recommendation by any physician. It’s important to know
that the surge in their usage may be largely attributed to the heavy advertising by the pharmaceutical
companies promoting these gels not the actually effectiveness of these gels.
Overall, gels mimic the natural release of the body, but many men complain that testosterone gels do not
fully raise T levels back up to normal desired levels. Experience has shown that some patients may never
absorb enough testosterone from gels to improve symptoms of low T.

Pros: Easy to use; dosage can be easily modified; many available gels; mimic physiological release Cons:
Expensive; inconsistent dosage; can rub off on others; doesn't work well if you sweat a lot; must be applied
daily; may not raise levels to desired levels.
Products: Androgel, Axiron, Bio-T-Gel, Fortesta, Testim, and Vogelxo
Dosage: 2.5-10 grams of gel spread over the application site daily

Injections

Testosterone injections involve the injection of oil-based testosterone into the muscle (usually the thighs,
glutes, or deltoids). The testosterone is then absorbed via the muscle into the blood stream over time.
Intramuscular testosterone preparations have been the mainstay of testosterone replacement therapy since
the 1950s, and they are one of the most popular forms of testosterone for TRT.

The two most common forms of injectable testosterone are testosterone enanthate (TE) and testosterone
cypionate (TC). TE and TC are modified forms of testosterone. Specifically, they have an ester molecule
attached to the T molecule. This attachment slows the absorption of testosterone and increases the half-life.
Due to their long half-lives, both TE and TC provide a sustained release of testosterone into the bloodstream.
The most commonly recommended dosing regimen for TRT is 100 mg to 200 mg every one to two weeks. If
your doctor tells you to inject every other week, half the dose and inject every week. Lower dosages injected
more frequently lower the fluctuations in testosterone levels between injections. For more info on
testosterone esters, see r/steroids A Primer on Esters.

Overall, injections of testosterone enanthate and testosterone cypionate are inexpensive and safe. Since
both forms have been around for so long, generic versions of these medications are available. Most men that
use injectable testosterone for TRT swear by it because they get T levels back to normal and deliver results.

While injectable testosterone is safe, know about two potential drawbacks. First, T injections can cause
fluctuations in T levels following administration. Following an injection of testosterone enanthate or
testosterone cypionate, T levels exceed normal physiological levels for the first 2 to 3 days. They then steadily
decline to levels below physiological levels just prior to the next injection. To minimize this issue, just shorten
the interval between T injections and lower the dose proportionally to minimize this cyclical nature of highs
and lows. (See the dosage instructions) Second, injectable testosterone increases red blood cell production
more than other forms of testosterone. To address this potential side effect, just get regular check-ups with
your doctor after starting TRT to monitor red blood cell levels. Then, your doctor can address any issues
preemptively.
 Of note, the FDA recently approved a new injectable testosterone ester (testosterone undecanoate) called
Aveed by Endo Pharmaceuticals. Like testosterone enanthate and cypionate, testosterone undecanoate has
an ester attached to it. Unlike testosterone enanthate and cypionate, which need to be injected every week
or every other week, testosterone undecanoate needs to be injected once every 10 weeks. Studies show that
testosterone injections of 750 mg Aveed maintain normal levels between 300 and 1000 ng/dL for up to 10
weeks.

Pros: Inexpensive; consistent dosage; easy to adjust dosage. Cons: Need to inject; some doctors may not
want you to inject on your own; T levels may fluctuate if you inject infrequently; may experience injection
site pain.
Products: Testosterone cypionate (generic); testosterone enanthate (generic); testosterone undecanoate aka
Aveed (branded product by Auxilium Pharmaceuticals, Inc.)
Dosage: 100 – 200 mg every one to two weeks. If your doctor tells you to inject every other week, half the
dose and inject every week. Lower dosages injected more frequently lower the fluctuations in testosterone
levels between injections. For injecting info, see r/steroids Safe Injecting Technique
• Testosterone Cypionate - FDA AccessData
• Testosterone Enanthate - FDA AccessData
• Aveed Full Prescribing Information - Endo Pharmaceuticals Inc.

Pellets

Testosterone pellets are implanted underneath the skin in the subdermal fat layer by a physician. The pellets
slowly release a steady infusion of hormone into the body testosterone as they dissolve over the course of
three to six months.

Pros: Easy to use; need to administer very infrequently; no risk of transfer. Cons: Needs to be surgically
inserted and removed; may extrude/push out of your skin on their own; difficult to adjust dosage once
implanted.
Products: Testopel (branded product by Auxilium Pharmaceuticals, Inc.)
Dosage: 6-8 pellets implanted every 3-6 months
• Testopel Full Prescribing Information - Auxilium Pharmaceuticals Inc.

Nasal Gel

Testosterone nasal gel is administered into each nostril three times a day every day.

Pros: Convenience; ease of use

Cons: Must be taken three times per day, every day, preferably at the same time each day. Additionally, it
failed to restore testosterone levels to normal in 10% of men in the phase 3 clinical trial.
Products: Natesto ((branded product by Endo Pharmaceuticals, Inc.)
Dosage: One spray in each nostril three times per day (5.5 mg per spray; 33 mg per day)
• Natesto by Endo Pharmaceuticals
• Natesto Full Prescribing Information

Lozenges

Transbuccal testosterone lozenges are placed under the tongue or against the surface of your gums. The
lozenges release testosterone, which is then absorbed through the mucous membranes of the mouth. The
lozenge lasts for 12 hours after which time it must be replaced with another lozenge for a total of two
lozenges per day.

Pros: Less liver toxicity than oral forms because it is absorbed through the gums not swallowed. Cons: Must
be kept in the mouth all day; may aggravate gums.
Products: Striant (branded product by Auxilium Pharmaceuticals, Inc.)
Dosage: 2 lozenges per day
• Striant Full Prescribing Information - Auxilium Pharmaceuticals Inc.
• FDA Patient Insert on Striant
If you can get injections, do it. Everybody on /r/steroids will recommend the same. When the doc
recommends the gel/cream you can mention that you're worried about it getting on your girlfriend or kids
and they'll usually understand. You may also want to mention that you tend to sweat a lot or that you hear
it's less effective and more expensive than injections. For /injection locations and information, see the Wiki.

HCG/HMG
HCG is injected either intra-muscularly or subcutaneously. It can be used alone or in conjunction with
Testosterone. Dosage varies, but can be 250-1000iu injected 2x per week. Higher doses of HCG (greater than
1000iu per week) can possibly cause HCG-insensitivity, rendering it mostly ineffective after prolonged use.

HMG is very similar to HCG, the key difference being that HCG acts as a synthetic LH (luteinizing hormone).
hMG contains the real hormones the body produces, because of this it can stimulate the testes without risk
of desensitizing the testes to LH. For this reason, if using hMG or HCG long term, hMG would be the safer
option. However, hMG is often significantly more expensive than HCG.

Testosterone vs. HCG

Testosterone is the most common, but has the potential to cause infertility and testicular atrophy during TRT
use. HCG can be used in it's place or in conjunction at low doses to maintain fertility and testicular size.
Whereas testosterone directly puts exogenous testosterone into your blood stream, HCG tells your body to
create more endogenous testosterone.
Clomid
Clomiphene is sometimes used in place of testosterone/HCG. It is sometimes used in an attempt to restart
HPTA, as well. Like HCG, it helps TRT-users maintain fertility. However, it can sometimes have unwanted side
effects. It comes in an oral form and dosage can be 25-50mg ED, but may be tapered down based off BW.

Aromatase Inhibitors (AIs)

Testosterone can be converted in estrogen via the aromatase enzyme. Consequently, taking testosterone via
TRT may increase estradiol levels. Most men on TRT dosages will not experience high estradiol levels.
However, some genetically susceptible men may experience high levels. These high estradiol levels may lead
to symptoms of high estrogen such as fluid retention and gynecomastia. As such, it is important to routinely
test estradiol levels during TRT.

If estradiol levels are found to be too high, the most common treatment is Anastrozole (Arimidex) or
Aromasin. Arimidex inhibits the aromatase enzyme, and thus it inhibits the conversion of testosterone to
estrogen. Common medication and doses are 0.25-0.5mg Arimidex E3-7D or 12.5-25mg Aromasin E3-7D
(depending on estrogen levels and response).

Normal estrogen range is about 7-42 pg/mL. Most users on this sub report that they feel best when they're at
20-30. However, many on this sub also feel that an AI isn't needed until/unless you notice symptoms of high
estrogen.

Medication Dosages-General
Most docs have a "standard" dosage for each medication that they start you at (that will vary slightly from
doc to doc). Some docs may adjust these doses after a month or so of use depending on your BW results and
how tell them your mood and libido respond.

HCG and TRT

HCG is commonly co-prescribed with testosterone. Practically speaking, HCG is prescribed primarily to men
looking to maintain fertility during TRT. Some physicians and testosterone clinics argue that all men taking
testosterone should also take HCG because HCG helps enhance the effects of testosterone therapy. There is
no consensus, however, on using HCG for this purpose.

To begin, The Endocrine Society’s Clinical Guidelines for Testosterone Therapy do not recommend for the use
of or against the use of human chorionic gonadotropin (HCG) during testosterone therapy. They basically do
not offer any opinion either way.

With that being said, some physicians and some low testosterone centers/clinics do prescribe HCG along with
TRT, especially for maintaining fertility.
 HCG is an FDA-approved drug, and it is recommended by the American Association of Clinical
Endocrinologists as the first therapy for the treatment of low sperm production. As such, some physicians
prescribe HCG alongside testosterone therapy to maintain fertility in men during TRT.

Why does testosterone therapy cause infertility in men? Exogenous testosterone shuts down the body’s
natural production of testosterone by the testes. Testosterone levels in the body remain normal because of
the exogenous testosterone but testosterone levels within the testes drop below normal. Since sperm
production requires high levels of testosterone within the testes, testosterone therapy reduces sperm
production. In some men, this reduction may be enough to cause fertility issues. Be aware of this potential
side effect and discuss your options with physician if you are looking to conceive a child.

Besides stopping TRT or lowering the dosage, one potential way to maintain fertility during TRT is to take
HCG. In men, HCG stimulates the testes to produce testosterone, which raises the intratesticular
testosterone level and allows for the production of sperm.

According to the American Association of Clinical Endocrinologists Clinical Guidelines HCG should be the
initial therapy of choice for increasing sperm production for at least six to twelve months. Therapy with HCG
is generally begun at 1,000 to 2,000 IU injected intramuscularly two to three times a week, and it is taken
alongside testosterone. Also, two studies with men specifically on testosterone replacement therapy show
that 500 IUs every other day also maintains normal sperm production.

If sperm production has not been initiated within six to twelve months of therapy with HCG, the AACE
recommends that administration of FSH in a dosage of 75 IU injected intramuscularly three times a week
along with the HCG regimen. After six months, if sperm are not present or are present in very low numbers
(<100,000/mL), the human menopausal gonadotropin (or FSH) dosage can be increased to 150 IU
intramuscularly three times a week for another six months.

It should be noted that HCG must be properly stored because it is a peptide not a discrete molecule, like
testosterone. Typically HCG comes in the form of a powder in a sterile ampule to prolong its shelf life. In
order to use, HCG must be reconstituted/remixed with bacteriostatic water.

In general, HCG should be kept in the refrigerator away from food. If unmixed, the shelf life of HCG is
generally up to 18 months in the refrigerator. If mixed, the shelf life of HCG is up to 2 months in the
refrigerator. If unrefrigerated, unmixed HCG typically only lasts 60 days, whereas mixed HCG typically only
lasts 48 hours.

What to Expect While On TRT

The First 1-3 Months

• Doctor visits: Most docs will have you come in every couple of weeks for the first 2-3 months and then once
every year.
• Time to notice effect: You can notice some effects on libido within the first few hours (although it may be
placebo). Effects on mood may take more like 2-3 weeks.
• Mood Effects: Increase in energy and overall a better sense of well-being.

• Libido Effects: Greater desire for sex. More frequent erections, especially during sleep.

• Negative Side Effects: In this time, you'll probably get some night sweats. You may also get some acne
breakouts. You probably won't notice a whole lot of other negative effects at this point.

3-Months and On
• Fewer doctor visits
• Night sweats and acne should decrease
• First 1-3 days after injection, you'll feel great. Next 4-8 days you'll feel good. The next 8-14, you'll still
probably feel slightly better than before you started. That's why I recommend E7D injections or more
frequent--it evens it out so you feel great consistently.
• Mood is likely more consistently good.
• Libido effects may be slightly less than in the first 1-3 months, but still a big improvement.
• Somewhat Common Positive Effects: Some TRT-users also may experience a loss of fat, increased muscle,
Increase in strength, a deeper voice, and increase in facial and body hair.
• New Negative Side Effects: It's possible that you might experience high estrogen at this point, so watch out
for estrogen sides. If you experience increased headaches, nipple lactation, or worsening vision, talk to a
doctor; this could indicate a pituitary tumor that is increasing in size due to the medication.

General Tips While on TRT

• Get blood work. It's the only way to confirm low T and whether or not estrogen and/or prolactin are causing
side effects.
• Keep a daily log of your injections, your sex drive, and your mood. It can be useful to show to a doctor if
you're trying to argue for/against adjusting medication. Plus, it can help determine if you're actually
experiencing effects of the medication since the change is generally pretty gradual.
• If you have problems telling other people you're on TRT that you'd like to open up to: remember that this
isn't much different than having poor eyesight and getting glasses or lasik. You have abnormally low
testosterone. The medication is helping you be "normal." That being said, some people may still view it as
steroids and you won't be able to say anything to sway them. Depends on the person you're telling.

Injection Tips

• Z-Track injection method is helpful, but not 100% necessary.

• Quad injections are easy, but many prefer ventrogluteal.
• You may also want to consider subcutaneous injections. They use a smaller needle and the absorption rate is
a little slower, evening out your T levels.
Subcutaneous injection is excellent for TRT purposes. Subcutaneous injection sites.

The subcutaneous that I refer to here is not the same as an IM injection "leaking" and doesn't have the
associated pain. An intentional sub-q injection is actually into the subcutaneous fat. It tends to form a small
nodule which is easily absorbed. An injection which leaks gets between the muscle fascia and the
subcutaneous fat. It absorbs more slowly and causes more irritation.

The easiest sites to use are near the umbilicus (belly button) or in the oblique fat pads (love handles) for e3d
injections. It's easy to see what you are doing and both hands are available. Because of this, it's much easier
than IM for regular small injections and just as effective. If the volume is 0.3 cc or less, it's completely
painless and doesn't leave any visible signs unless you are very lean. At around 10% one may need to stop
using the belly sites and stick to obliques. Even with 2 sites, each will be completely absorbed before you
return to it.

There is less discomfort than IM. With good gear (eg: pharma) there is no PIP. It might sting for a few minutes
but that's it.

A 29G 1/2" slin pin with 0.5cc syringe is a good size. They are low dead space needles, meaning there is less
wasted gear. The only downside is that drawing can take a while, but since it's such a low volume it doesn't
really add up to much time.

For instructions on doing the shots, watch this video: SUBCUTANEOUS TESTOSTERONE INJECTIONS - THE
CUTTING EDGE WITH DR. JOHN CRISLER

The video and shows the belly and oblique sites.

Dr. Crisler recommends a 5/8" 25G needle. I had some leakage with a larger needle and the syringe / needle
had a larger dead space that wasted gear. I'm much happier with 29G. His fears about a high-pressure jet are
unfounded due to the viscosity of the oil.

Coming Off TRT

You may want to come off of TRT for a number of reasons (cost, sick of pinning, no longer wanting to be
swole, etc). If it's solely for fertility concerns, you may not need to (see info above about HCG/HMG/Clomid).
Otherwise, you'll want to make sure that you don't come off cold turkey and instead do an actual PCT.
Coming off cold turkey, you risk having your HPTA remain shut down, tanking your test, and suffering
depression, ED, and other low T side effects. See the Wiki for TRT-specific PCT recommendations.

Benefits of TRT

Testosterone replacement therapy in men with low testosterone produces many positive benefits. These
benefits can be broken down into conclusive benefits and inconclusive benefits. Conclusive benefits are
benefits that are relatively certain, whereas inconclusive benefits are benefits that are not certain.
 Conclusive Benefits: Testosterone replacement therapy has consistently shown to positively alter body
composition. It increases muscle mass (via increased muscle synthesis) and decreases fat mass (via increased
fat lipolysis), especially abdominal fat mass. It also slows or even reverses the loss of bone mineral density
due to aging. TRT also increases libido.

Inconclusive Benefits: Testosterone replacement therapy may also improve sexual function (improve erectile
function), improve mood, reduce depression. However, TRT has not been shown to conclusively improve
erectile function and mood. The primary reason why TRT may not help with erectile dysfunction or
mood/depression is because both conditions can be related to one or more of many potential underlying
medical conditions unrelated to testosterone levels. Without addressing such underlying conditions,
testosterone alone will likely not improve erectile dysfunction or mood/depression.

Side Effects of TRT

The following are potential side effects of TRT.

• Polycythemia – Polycythemia occurs when red blood cell production increases too much. Testosterone
stimulates the production of red blood cells. Thus, TRT may increase red blood cell levels beyond normal.
High red blood cell levels cause the blood to thicken and clot, which can potentially lead to a stroke.
Oftentimes, if red blood cell production rises to dramatically, TRT dosages must be lowered or stopped.
Additionally, your physician may perform a phlebotomy (a withdrawal of blood to lower red blood cell levels).
The risk appears to be higher with IM preparations and may be due to the supraphysiologic levels that are
seen with infrequent injections.

• Infertility – TRT interrupts the body’s normal release of testosterone. It also impairs the production of sperm.
While infertility is usually reversible, it is important for men who wish to preserve their fertility to talk with
their physician prior to commencing TRT.

• Sleep Apnea – TRT may worsen sleep apnea in men who have been previously diagnosed.

• Gynecomastia – TRT may alter the balance of testosterone and estrogen in the body in certain men. Some
men’s bodies metabolize testosterone in estradiol more readily than normal. This aromatization causes the
breast tissue to swell. It is important to address any issues with gynecomastia quickly. Unfortunately, medical
treatment of gynecomastia that has persisted beyond a year is often ineffective. Gynecomastia Wiki -
Gynecomastia Subreddit

• Fluid Retention - Fluid retention may occur in the arms and legs at the beginning of therapy. It generally
resolves after the first few months of treatment.

• Alteration of Lipid Levels - Testosterone therapy may adversely affect cholesterol levels, slightly lowering HDL
cholesterol and slightly raising LDL cholesterol. Most cases of adverse affects to cholesterol deal with
supraphysiological doses of testosterone, not replacement doses.
 The Endocrine Society Clinical Practical Guidelines detail the conditions in which testosterone administration
is associated with a high risk of adverse outcome and in which testosterone should not be administered:

Very high risk of serious adverse outcomes

• Metastatic prostate cancer
• Breast cancer
Moderate to high risk of adverse outcomes
• Unevaluated prostate nodule or induration
• PSA >4 ng/ml (>3 ng/ml in individuals at high risk for prostate cancer, such as African-Americans or men with
first-degree relatives who have prostate cancer)
• Hematocrit >50%
• Severe lower urinary tract symptoms associated with benign prostatic hypertrophy as indicated by AUA/IPSS
>19

• Uncontrolled or poorly controlled congestive heart failure

• TRT Side Effects - Medscape

Related Posts

Word of caution to the naturally low-T crowd.

/u/sixxsix creates this entry
After 1 year on TRT
The Epically Long TRT Story
10 pins in and smiling
The journey to good TRT
4 Months starting TRT TRT is amazing
10 Things to look for in a doctor for TRT
Subcutaenous Test Injection Sites - Self Experiment (For Science)

Studies

Subcutaneous administration of testosterone. A pilot study report.

CONCLUSION: Therapy with weekly subcutaneous testosterone produced serum levels that were within the
normal range in 100% of patients for both peak and trough levels. This is the first report, which demonstrated
the efficacy of delivering weekly testosterone using this cheap, safe, and less painful subcutaneous route.
4 ANABOLIC STEROIDS AND THE LAW
United States law prohibits the possession of anabolic steroids without a legal medical prescription,
imparting severe penalties (including fine and/or imprisonment) for those that choose to violate these laws.
Under influence of U.S. government officials, World Anti-Doping Agency (WADA) members, and public
criticism following numerous doping scandals, a growing number of countries are following the U.S. by
adopting their own laws against the possession of anabolic steroids and other sports doping drugs. In many
cases similar severe criminal penalties have been enacted. The following section discusses in more detail
various national laws that concern the personal use of anabolic steroids and other related drugs.

United States

Anabolic steroids have been classified as controlled substances in the United States since 1991, with passage
of the Anabolic Steroid Control Act of 1990 (Pub. L. No. 101-647, Sec. 1902, 104 Stat. 4851, 1990). This law
makes it a criminal offense to sell, distribute, manufacture, or possess anabolic steroids without proper legal
authorization. The outlined penalties for possession without a legal prescription include a maximum of 1 year
of imprisonment and/or a minimum fine of $1,000. This may be increased to 2 years of imprisonment and/or
a $2,500 minimum fine for individuals with a prior drug conviction. Note that this law was amended in 2005
following passage of the Anabolic Steroid Control Act of 2004. The new law added 26 new steroid compounds
to the list of controlled substances, and also removed the legal requirement that a compound be proven
anabolic in humans before it can be added. This “promotes muscle growth” clause was the key roadblock to
removing many of the “legal steroids” of the late 1990s and early 2000s.

State vs. Federal

Criminal laws against the possession of anabolic steroids exist at both the federal and state level in the U.S.
Depending on the circumstance, an individual may be charged with a steroid related crime by either the
federal government or the state government where the crime took place. Unless the crossing of state lines
was involved, most criminal prosecutions for steroid related crimes take place at the state level in accordance
with state laws. Most often the state laws mirror federal statutes very closely although this is not always the
case. There can also be a great deal of variability in how punishments are determined between one state and
another. If you are not obtaining medications legally through a physician’s prescription, it is advisable to
study the steroid laws closely, particularly those of your individual state.

Austria

The possession of anabolic steroids is not a criminal act according to Austrian law. In 2008, Austrian
government officials announced intent to place criminal penalties on steroid possession.
Australia

It is a criminal act to import, supply, use, or possess anabolic steroids in Australia without a prescription from
a medical practitioner, dentist, or veterinarian (Poisons and Drugs Act Amendment of 1994). The outlined
penalties for possession without a legal prescription include a maximum of 6 months of imprisonment and/or
a fine of $5,000.

Belgium

It's a criminal act to manufacture, transport, acquire, or possess doping substances including anabolic
steroids, human growth hormone, and erythropoietin.Penalties for selling is imprisonment ranging from 1
month to 5 years and a fine that ranges from 3000 to 100,000 euros. Penalties for transport, import, export,
possession, usage and manufacturing are one of the penalties for selling instead of both (either
imprisonment or the fine). If you are found to possess one of said substances it is equaled to using. Some of
the substances you are allowed to use and possess of course if you have a prescription. Belgium also "muscle
profiles". “Muscle profiling” is the practice of identifying suspected anabolic steroid users based simply on
their appearance, then arresting them on that basis and forcing them to submit to urine tests.

Canada

Anabolic steroids are included in the Canadian Controlled Drugs and Substances Act as Schedule IV
substances. It is illegal to sell, manufacture, or import anabolic steroids into Canada without proper legal
authorization. Possession of anabolic steroids for personal use is not a criminal act.

Czech Republic

In 2008 it became a criminal act to manufacture, import, export, store, or distribute anabolic steroids in the
Czech Republic. The potential penalties include a maximum of 3 years in prison. It is not a crime to possess
steroids for personal use.

Denmark

In Denmark it is a crime to manufacture, import, export, market, dispense, distribute, or possess doping
substances including anabolic steroids, human growth hormone, and erythropoietin without proper medical
or scientific reason (The Act on Prohibition of Certain Doping Substances No. 232 of 21 April 1999). The
potential penalties for possession include a maximum of 2 years in prison.

France

In 2008 it became a criminal offense to manufacture, transport, acquire, or possess doping substances
including anabolic steroids, human growth hormone, and erythropoietin in France. The potential penalties for
possession include a maximum of 5 years imprisonment and/or a 75,000 Euro fine.
Greece

The possession of anabolic steroids is not a criminal act according to Greek law. In 2008, government officials
announced intent to place criminal penalties on steroid possession in Greece.

Israel

In Israel, under the provisions of the Pharmacy Ordinance, it is prohibited to import anabolic steroids that are
not approved by the Ministry of Health, and their sale without a physician’s prescription is prohibited. The
Division of Enforcement and Inspection in the Ministry of Health is working with elements of customs and the
police to locate and seize anabolic steroids that are illegally imported and/or manufactured in Israel. The
Division is also working for the prosecution of traders and vendors of these substances. Offenders also face
tax evasion charges (on sales value of steroids).

New Zealand

It is a criminal act to import, supply, use, or possess anabolic steroids in New Zealand without a prescription
from a medical practitioner. As it so happens, steroids fall broadly under the Medicines Act as opposed to the
Misuse of Drugs Act. The Misuse of Drugs Act is what defines drugs as Class A,B or C etc, and decides which
punishments should be given to their sale or use. Some Medicines also fall under Both Acts as they are
deemed to have a high risk of abuse potential, or are considerably more dangerous. If you are caught with
steroids or other medicines in your possession without a prescription, or you are selling them without
permission you could face potentially years in prison or thousands of dollars in fines.

Norway

It has always been illegal to import, export and sell anabolic steroids in Norway. The Medicinal Products Act
was amended on June 14, 2013 & in force as of July 1, 2013, to make the use and purchase of anabolic
steroids illegal, as well.

Sweden

In Sweden it is a crime to import, manufacture, transport, sell, possess, or use doping substances such as
anabolic steroids and growth hormone without proper legal authorization (The Swedish Act prohibiting
certain doping substances (1991,1969). The potential penalties include a maximum of 2 years in prison.
Possession for personal use is usually regarded as a petty offense and given a maximum penalty of 6 months
imprisonment.

United Kingdom

Anabolic steroids are controlled as Class C substances under the Misuse of Drugs Act 1971. There is no
possession offense, but it is illegal to manufacture, supply or possess/import/export steroids with the intent
 to supply, without a license to do so. The maximum penalty for these offenses is 14 years in prison and/or a
heavy fine. The “supply” offense can mean something as simple as sharing anabolic steroids with someone
else, even if you don’t sell them. There were changes to UK steroid law as of April 23, 2012 that pertained to
importing anabolic steroids. Following advice from the ACMD, anyone wishing to import these drugs from
outside the UK will have to do so in person (“personal custody”). It will no longer be permitted to buy
steroids and associated drugs from outside the UK, through internet and mail order sites and have the
products delivered. There has been a great deal of pressure in recent years from the U.S. and World Anti-
Doping Agency to place criminal penalties on the possession of anabolic steroids without a prescription.

References

1. Llewellyn, William, Anabolics 2010, 2003-4

2. https://www.health.gov.il/English/Topics/PharmAndCosmetics/pharm_crime/Pages/steroids.aspx
3. http://www.israelnationalnews.com/News/Flash.aspx/270013

5 TALKING POINTS
/u/MittRomneysCampaign wrote (original):

So far, I have had two discussions that went very well that involved layperson subreddits.

I like the way these discussions went because few of the responses were outright dismissive (something like
"lol ok juicehead" without even listening to you would be dismissive), and to the extent they were opposing
steroids, they were based on misinformation -- not outright contempt for the idea. But once this misinformation
was corrected, the commenters/voters seem largely receptive.

I am linking these with "np" because the last thing we need is a "roid rage brigade."

1. Futurology: https://np.reddit.com/r/Futurology/comments/3afjpa/the_male_pill_is_coming_and_its_going_to_
change/csccdrq
2. SubredditDrama: https://np.reddit.com/r/SubredditDrama/comments/3btepe/i_simply_say_name_one_single_i
nitiative_feminism/csprvow

You and I both know that most of these drugs are fine. So we're on the same page. I don't need to convince you
because I'd be preaching to the choir.
 Any time you are talking with a layperson about steroids, you need to try to avoid saying anything that paints
you as a Roid User Stereotype.

If you are too angry, you can be accused of "roid rage" and instantly dismissed, because they will think "if I
take it I will act like this guy." We all know roid rage isn't a thing, but they don't. So your job is to convince
them rational people exist who use these things.

If you come off as too enthusiastic, you run the risk of looking like a junkie. People think steroids = needles =
heroin = steroids are as harmful as heroin. It doesn't matter if they're wrong. They think it and they vote.

So, rules of conversation that are important in everyday civilized discussion become even more
important when trying to make the case that a hormone attributed to anger and destruction should be legal.

1. Try your best not to swear or seem angry. If you do swear, make sure it's very strategic swearing. If you do
seem angry, make sure it comes off as a professional kind of outrage, like a doctor who is outraged that a
beneficial treatment is not allowed -- because that's what doctors would do if TRT were outright illegal.

2. Make sure to NEVER insult your opponent. Only respond to their reasons, and respond to their reasons with
evidence. Don't say "you have no idea what you're talking about" or "you're an idiot" or anything like this. If
avoiding these things makes you seem like a robot, that's fine. It's preferable to seeming angry. If you are so
angry you can't have the discussion any more, POLITELY leave.

3. At the same time, don't be condescending. Normal people already feel threatened by you because you lift. And
I'm pretty sure this applies to 99% of this board because for however much you don't think you lift, normal
people really really don't lift. Regardless of how silly it is, "bigger than me" means "person who could maybe
beat me up" in caveman logic. The last a regular person needs is a lecture from a person who is both stronger
AND smarter than them.

But how you frame anabolics matters a lot too, so here's an unassorted list of points to remember and/or
emphasize:

Don't say "steroids." Say "male hormones."

Yes, I realize that steroids are male hormones, and YOU realize that steroids are hormones, but the average
person barely knows anything about this, and hasn't bothered to make the connection that testosterone = male
hormone = steroid. You have a limited amount of time to convince people, usually, so make sure you don't lose
their attention.

Mention that estrogen is a steroid also, and in the birth control pill
Many women take the pill and advocate for its availability. The reasoning I use is something like "estrogen is a
steroid, it's just not an anabolic steroid, because it's not a male hormone, and male hormones tend to help build
muscle."
The average person does not realize that estrogen = steroid, and that testosterone = steroid, just that
testosterone happens to be a steroid that builds muscle.

You will get a lot of support from women who find this hypocritical. Many women I've talked to don't realize
that estrogen is in the birth control pill, so they don't bother to think "hey, my sex hormones help me not get
pregnant, so why wouldn't giving men their sex hormones help them not impregnate me?" I've been able to
convince a lot of the women I know this way. (The women I associate with are pretty open-minded, but still.
They'd be against it if I hadn't said anything.)

Frame testosterone in terms of birth control.

I realize that testosterone is not primarily used as birth control, but it has been used as such before. Trestolone
is also useful to mention, because of how it's been used for birth control purposes and can also be used for
muscle-building.

Avoid the "cheating" debate by mentioning that athletics would be unfair even if
they were drug free.
I'm just going to copy-paste this: "the anti-cheating stance is a losing battle since (a) it's been a losing battle for
decades, tests are extremely beatable and (b) athletes are already at some kind of genetic advantage anyway if
they're winning. They'd have to be -- the number of things you can do to make yourself better at a sport is
finite, while genetic variation will continue all the way along the top level. (Examples of this variation include
factors like your predisposition to building muscle, your natural testosterone levels, your maximum vo2max,
and so on.) ... The idea that drugs give an unfair advantage and genetics don't would be true assuming equal
genetic advantage, but when you're looking at the highest levels of the sport you're looking at the athletic
height of 7 billion people, which is a ton of genetic variation to pool from. Reducing all advantages period
would be a really losing battle, so it's more consistent to just say "athletes will take these anyway, so let's see
what they can do when they don't have to hide it."

Mention that steroids already were legal for a long time without many
consequences, and that criminalizing them produces consequences of its own.
This is what I said: "Arnold did steroids more safely because the drugs were legal and he knew what he was
getting. When you don't know the product you're getting, there is a much greater risk of dilution, contaminants,
etc. Also, this isn't like, say, LSD, which was a craze then was illegal pretty much everywhere before we could
even study it. We have a pretty good idea of what it'd look like if these drugs were legal again because they
were before, and they still are legal in something like a dozen countries and decriminalized in others."
Mention that the AMA, FDA, NIDA, NIH, and DEA actually testified in opposition
to the inclusion of male sex hormones under the Controlled Substances Act.
Most people are under the impression that steroids are illegal for health reasons, and not for sporting reasons.

When I say things like this, most people give me weird looks, because they are still under the impression that
drug laws are scaled to drug harm: "The primary roadblock to male birth control is that they all involve male
sex hormones like testosterone. Ergo, you can take these to be better at sports. If you can take them to be better
at sports, this is a fast-track to their criminalization. So the issue isn't really developing male birth control, it's
developing male birth control that doesn't help you be better at sports."

Mention the inconsistencies in scheduling as support for this being about sports.
Metenolone is grouped with testosterone and trenbolone, despite metenolone being extremely unharmful and
trenbolone being harmful in at least some respects. The only commonality they have is that they benefit an
athlete. If these drugs were illegal for purely health reasons, they'd be in different schedules.

Mention that testosterone is produced by your body, so it must be safe at some

doses.
Most women I've talked to don't know that they have testosterone. When I say "your testosterone levels", they
look at me with this blank expression on their face like they didn't know that was possible.

Attack the category "anabolic steroid" for being misleading in this kind of
discussion.
The category "anabolic steroid" is as useful to assess safety/unsafety as "pain-killer" is, because "pain-killer"
includes both ibuprofen and heroin. Saying "anabolic steroids are harmful" is like saying "painkillers are
harmful." Well, yes, some are, in certain dosages, but as a category? No.

Mention that drug laws do not have to correspond to drug harm.

Here is a comparative drug harm chart by David Nutt. Steroids rank toward the bottom.

Virtually everyone is aware that cannabis is mostly harmless. They think steroids are toward the top of harm,
so this is a clear discrepancy in perception. If you stress that they're less harmful than cannabis, this will
change perceptions.

Try to use chemical names instead of steroid slang.

Saying "tamoxifen" or "clomifene" might be annoying, but you sound more credible to regular people when
you do this. If you say "you can treat side-effects with tamoxifen, HCG, and an aromatase inhibitor" you sound
immensely more believable than a person who says "you won't get sides if you PCT with HCG and pop some
nolva or clomid." If this sounds pretentious to you or you never talk this way, just roll with it.
You will need to prioritize some steroids and throw others under the bus.
Think about the most harmless hormones we can take. Those are the steroids you should be advocating for.

So: testosterone, nandrolone, methenolone (primo), oxandrolone (anavar), and maybe MAYBE
methandrostenolone (dbol).

But testosterone comes first, then nandrolone/methenolone/anavar, then everything else.

DO NOT try advocating for making tren or halo legal. This is suicide. People will google trenbolone and say
"wtf, they give this to cattle? and you're putting that in your body?" OR someone will mention that tren killed
Zyzz which will lead to a discussion about what really killed him, and so on.

I'm in favor of making all of this shit legal or at least decriminalized, but you will not win this battle by having
an all-or-nothing approach. You need to take the most defensible stance you can take and "legalize cattle
hormones that killed some 22 year old" is not that.

Even if you run tren, I'm not judging you. Just don't mention tren or act like tren is great. Focus on the basics
and the stuff with the least side effects.

Stress that since you already have estrogen and testosterone in your body, there
are "roids" in your body.
This is why testosterone is the hormone you need to focus on the most.

When people think of steroids, they think of that shit they give Bane to make him instantly monstrous.

It's very difficult to, with a straight face, oppose a hormone that's in your body as we speak.

Other useful links

Why roid rage is a myth: http://examine.com/faq/what-is-roid-rage.html
About the SAC: http://www.steroid.com/The-Steroid-Control-Act.php

Anyway, it's possible to convince laypeople that these hormones are fine. In a perfect world, we could just give
everyone a textbook and have them learn how these drugs work, so then they'd say "what's the big deal?" --
but, no one is going to read that textbook, so you need to do the convincing.

It's very possible. You just need to avoid certain pitfalls when making your arguments and make sure to stress
certain points over others.

I hope this helps, because all of us benefit.

 6 THE CYCLE
Typical AAS usage comes in pre-planned lengths of time that a person is taking any compounds. The idea is to
achieve a set of goals and then allow the body to get back to stasis and ensure that there are no medical
issues before doing it again. There is also some controversy about possible decreased effectivity of long term
use of AAS use. Cycles range in lengths from short (8 weeks) to long (20 weeks).

There are several different items that need to be understood to execute a good cycle.

A decent summary post in That Pastebin.

Pre-cycle Check list

The following check list has been created to help new users ensure that all bases are covered.

1. Cycle goals: What are your goals for the cycle? The goals of the cycle are imperative to planning a complete
cycle with compounds, length and recovery.
2. Eating plan: How many calories are you planning per day? If you're cutting, will you re-feed? How often?
3. Exercise plan: Generally, your recovery period after exercise will decrease. This will allow more physical
exertion while on cycle. Try to take advantage of this to get the most out of your cycle and plan more time in
the gym.
4. Blood work: The hallmark of all safe cycles, blood work is required to ensure user safety.
Pre-cycle: It is strongly recommended that blood work be done before a cycle to ensure good health and to
obtain an accurate measure of pre-cycle testosterone production.
On-cycle: Depending on the length of your cycle and trust in your source, you may want to get blood work
done while on cycle. This would verify that gear is working correctly and ensure that you remain in good
health.
Post-cycle: After PCT, newer users or users with unknown sources should get blood work done to ensure a
return of natural testosterone production.
5. Gear list: What gear needs to be purchased? Consider planning to purchase a little more than needed as
accidents (dropping a vial, etc) happen.
6. AI list: Different cycles require different AI's. It's always recommended to have one on hand, even if not
actually used during cycle. If you cannot afford an AI, you cannot afford to run a cycle.
7. PCT List: Your natural production of testosterone will, more than likely, cease during cycle. A definitive plan
needs to be put into place to ensure a return to stasis and normal testosterone production after cycle.
8. Pins, storage and disposal: How many pins do you need? How will you store them? How will you dispose of
them? Find out how to legally dispose of your pins.
9. Questions: During cycle you will probably gain a lot of mass. You may have friends and family ask how you
are doing it. Be prepared to answer these questions.
10. Clothes: Yes, you'll probably need some new ones while on cycle.

Planning the Cycle

When planning your cycle, you will need to know how much of each substance you will be using for the
entire duration of the cycle. It can greatly help to plot your blood levels of the various compounds.

Calculating Total Amount Needed

1. To calculate the total amount needed to be purchased:

X mg desired * number of days / week(s) * number of weeks total = total amount needed

2. Calculate the total mg per vial:

total ml * #mg / ml = total mg per vial

3. Then calculate the vials needed:

total needed / mg per vial = total vials

4. Round up and add one to be sure:

total vials, rounded up +1 = total purchase amount

Example

1-12 Test Prop 150mg EOD

Source provides 10 ml vials of 100mg / ml Test Prop.

1. To calculate the total amount needed to be purchased:

150 mg * (7 injections / 2 weeks) * 12 weeks = 6,300 mg total needed

2. Calculate the total mg per vial:

10 ml of 10g mg/ml vial = 10 ml * 100mg /ml = 1000 mg per vial

3. So for a Test P cycle, 150 mg, EOD:

6,300 mg / ( 1000mg / vial ) = 6.3

4. Round up and add one to be sure:

(6.3 round up =) 7 + 1 = 8 total vials needed

 Calculating Dosage
Most vials come in 10ml vials. The label will typically tell you the number of milligrams per milliliter (mg / ml).
For example, a vial of Testosterone Propionate can come in a 10ml vial with 100mg / ml. That means that the
entire vial contains 1000mg of the substance. If you want to inject 150mg of the substance EOD, you will
inject 1.5ml.

X mg desired / (N mg / ml) = Total ml needed per injection.

For a Testosterone Propionate vial at 100 mg / ml and a user wanting 150mg E0D:

150mg / (100 mg / ml) = 1.5 ml

For a Testosterone Ethanate vial at 250 mg / ml and a user wanting 150mg E2D:

150mg / (250 mg / ml) = .6 ml

Finding A Source

As is posted everywhere, this forum is not the appropriate place to look for a source. We regularly ban
people for asking source questions or discussing source information. There are multiple other ways to find a
source.

• The best sources are usually found through trusted friends and gym members. They have experience with the
gear from the source and first hand knowledge of it.

• Many forums have advertisements from sources and / or rating systems. Do a great deal of research before
proceeding. Most forums or websites that have source advertisements or similar are receiving money to run
their operations from the sources.

• Internet search engines are littered with sources although their legitimacy is unknown.

Purchasing
Most sources will want buyers to use Western Union for purchases. This is especially true when using a new
source. As you become more familiar with the source, they may allow you to use different payment methods.
Western Union will require identification for any transfer of over $600 or if you have done more than two
transfers in a year. The policies for identification have been getting more strict and are likely to require
identification for any transfer or pick up.
Shipping
Domestic shipping using USPS (if in the USA) is, generally, considered to be the best and most secure method
to receive your gear. Domestic shipping using FedEX or UPS is considered to be more risky as they check
packages much more often due to a much lower number of packages handled.

International shipping will, typically, be shipped in multiple shipments, depending on the order size. The
sources keep the total weight of the package low to avoid increased scrutiny.

Most sources charge a flat rate to ship your order.

http://www.reddit.com/r/steroids/comments/1vieqn/rsteroids_what_do_you_do_to_minimize_your_risk/
How the USPS works

Packaging
Sources will package the compounds in a discrete package that doesn't have much labeling and doesn't
reveal any information about what is being shipped. Good sources will bubble wrap the compounds and tape
them securely. Great sources will double pack the compounds so as to make tampering much more evident.
Packaging is very important so as to ensure that there are no leaks or reason for a postal inspector to further
review your shipment.

Receipt
Shipments do not require a signature and are to be left at the shipping address. Do not sign for
packages. Some very cautious individuals will accept the shipment and leave it unopened in their house for
two weeks before opening it. The theory is that the recipient can deny that it is theirs if the package remains
unopened and not touched. It is unknown if this is a successful strategy as we have not heard of a case where
a person is individually targeted for receipt of AAS.

Controlled Delivery

A controlled delivery is when law enforcement has targeted an individual suspected of receiving an AAS
shipment. They will typically attempt to deliver the package to the person to whom it is addressed and get a
signature for the package delivery. This is not a common occurrence, however, it is becoming more common.

Seizure Letter

There are cases when a shipment is seized by Customs or the Postal Inspector as they have detected AAS in
the packages. Typically, a letter will be sent to the shipping address giving the recipient the opportunity to
come into the customs office to pick up the package and verify legal receipt. If you receive a letter of this
nature, unless you have a legitimate prescription for the compounds ordered, it is best to ignore the letter.
 It is very important to note that, once one of these letters has been received, that the recipient's name and
address are typically flagged and further shipments are more rigorously inspected. It is best to not attempt to
receive AAS at the same location any further.

Post from a steroid-friendly LEO

Long time lurker and felt the need to clarify a bit on legal concerns with steroids. Some of this information
isn't new but it's more accurate than what I've seen said here.

• Steroids are SORT OF on LEO radar. Most agencies focus their limited resources on harder drugs, violent
crimes, and other social crimes.

• Steroids are rarely the sole cause of an investigation. They mainly come up if you're caught distributing
product locally, possess it visibly while traveling, or is seen while searching as a result of a "more serious"
warrant.

• No matter what, USPS cannot open your package. If it tears open what is visible to the eye is fair game. Do
note, though, that the average post office employee just does not care.

• Darknet Markets are subject to more scrutiny because (generally) they're harder drugs. Weed is typically the
easiest to spot because some vendors poorly pack it - leading for the smell to escape. Steroids cannot be
smelled by us or dogs, and can be packed very safely (especially since the vials are quite strong).

• There are many, many millions of packages moving daily. No one has the time to examine packages, nor the
inclination. Customs will seize caught packages 95+% of the time. They cannot pass down every single thing
that is caught to local LEO. It's a waste of time and resources.

• Another poster wisely commented on how there are testosterone clinics shipping you controlled substances
in the mail, legally. This is true. While they have a legal license to do so, it does reflect on how unlikely
domestic packages are investigated. The reason sources like internet pharmacies get away with sending you
those substances is NOT simply because Customs doesn't care (the importation of prescription drugs is illegal,
though lowly scheduled), it's because Customs/Feds/LEO cannot know what you have a prescription for
without doing a long, long investigation. It's not worth their resources to investigate something like this.
You're safe ordering these substances.

• Police will ALWAYS say they're coming after the customers after a source is busted. That's entirely a scare
tactic. Common sense - why would LEO announce a bust and then say "we're coming for you" ? People would
just clear house. And that's what they hope - people will get nervous and toss their gear.

• IT DOES NOT MATTER IF YOU SIGN FOR A PACKAGE OR NOT What matters is POSSESSION. LEO CAN, AND
HAS, JUST LEFT A PACKAGE IN A MAILBOX FOR YOU TO TAKE IN. Importantly, POSSESSION LEADS TO A
WARRANTED SEARCH, BUT DOES NOT MEAN YOU ARE GUILTY. I highly advise EVERYONE to clear house when
 ordering steroids. If you are subject to a search over the one package what will get you in trouble is if you
have illegal drugs/paraphenalia in your house. They DO NOT have a case against you if you have a clean
house. They WILL try to scare you - but seriously do NOT say anything. A lawyer will have your case dropped.

• Sources - you're at risk, but not as much risk as people want you to believe. People typically get caught
because they sell locally, have people picking up their stuff get caught and rat you out, or are investigated
after large powder orders (small orders won't have people investigate you, but you'll be on their radar). I
would highly advise ALL sources use BTC and drop WU/MG. Too much to risk there.

• Silly thing but it is wise - when ordering, in your emails tell the source you're going to ship it to a friend's
mailbox and will take it from his box without him knowing. Then tell him to include a note saying "[Your
name] if you see this, give it to [friend's name]" within the box. This is a VERY good thing to do. If it's not
caught, you're fine. If it ends up being caught for a 1 in a billion chance, it looks like it was a decoy and helps
your case a TON.

• PGP is not as important as people think. As long as both parties use an encrypted email (and connect with a
VPN, TOR, TAILS, whatever) you're fine. This is because if they get access to the webmail all information is
decrypted either using automatic PGP decryption (eg: Countermail) or locally on their computer (somewhere
this information is going to be stored). In my opinion - domestic and international, for personal ordering, is
perfectly safe. International they'll just seize unless you're ordering large powder. I would clean house while
ordering and don't say a word because they'll have no case against you.

Blast and Cruise

Some users decide that they do not want to waste time with PCT, and instead want to keep using steroids for
a longer period. What they will then do is run a cycle (blast), and then run a TRT dose (cruise). This allows the
body to heal from the stress placed under it during the blast, allowing the liver/kidneys to rest and letting
their cholesterol normalize. Once they are back within healthy parameters, they may then proceed to do
another blast.

This allows you to avoid going through PCT, which in and of itself is rather harsh on the body. This also
prevents the muscle loss often seen in PCT. There are downsides, of course. You will likely be either infertile
or have a very low sperm count during this period, and the longer you stay on the higher the chances are of
you staying that way should you PCT. These cases are rare, but it has happened.

7 YOUR FIRST CYCLE

So, you got interested in steroids and are now trying to figure out where to start. Beginners have one
rule: KISS.
That stands for Keep It Simple, Stupid. The more chemicals you toss in at once, the bigger your chances of
going down in a flaming fireball. A big, bloated, gyno-y fireball. BUT most potential side effects can be
avoided entirely if the cycle is followed correctly and the proper precautions are taken.
Contrary to what a lot of people say, /r/steroids does not believe that you have to have reach your full
natural potential before running a cycle. What is recommend is that you have a good amount of experience
and knowledge when it comes to training and nutrition and that you start off fairly lean – It is recommend
that you are under 15% body fat and ideally closer to 10%.

This wiki page will include how to administer the steroids, recommended doses and durations, how to
prevent and counteract side effects, and what you can expect to gain from your first cycle.

Can I Just Do An Oral Only Cycle?

You can. Should you? Absolutely not. Oral steroids are going to suppress your natural Testosterone
production hard. You need to take them together with a dose of testosterone to replace your natural
production, which will be shut down. Without a testosterone base, you will feel weak, tired, depressed,
low libido, erectile dysfunction, muscle loss and weakness—all the symptoms of low testosterone. As you
won't have any testosterone to support the muscles you're building, you'll lose all your newfound, hard-
earned gains just after you've gotten them. If you choose to do a orals-only cycle against all sound advice,
you should look into getting a SERM (like Nolvadex/Clomid or the sorts) for a proper PCT, as well. You should
consider reading through this Wiki and doing a real cycle, complete with Testosterone, as you'll find better
results, as well as feeling better too.

What About A Prohormone Or Designer Steroid Cycle That I Got At The Store?
Again. You can. Should you? Probably not. Prohormones & Designer Steroids are going to suppress your
natural Test pretty hard. You need to take them together with a dose of testosterone to replace your
natural production, which will be shut down. Without a testosterone base you may find you don't feel the
best or you feel symptoms of low testosterone. Prohormones & Designer Steroids are no better (or even
worse in some cases) than using a traditional oral steroid. The supplemental PCT crap they sell with these
Prohormones / Designer Steroids is predominantly bogus stuff and if you choose to do a Prohormone /
Designer Steroid cycle, you should at least look into getting a SERM (like Nolvadex/Clomid or the sorts) for
a real PCT. You should consider reading through this Wiki and doing a real cycle, complete with Testosterone,
as you'll find better results, as well as feeling better overall too.

The Basic Bulk

The Basic Bulk, that is recommend, is a 12–20 week cycle of Testosterone while running a moderate calorie
surplus with emphasis on gaining as much lean muscle tissue as possible and progressively adding weight to
your lifts.
 Testosterone is a powerful tool, if used correctly and can put a good +12–15lbs of LEAN mass on you
(excluding water and fat gain) over the course of 16 weeks. It is also a relatively mild compound and causes
little to no issues with side effects. Again, most potential side effects can be avoided entirely if the cycle is
followed correctly and the proper precautions are taken.
Read Other Users Experiences With Testosterone:
• 1st Compound Experience Thread
• 2nd Compound Experience Thread

When purchasing your AI (Aromatase Inhibitor) and SERMs (Selective Estrogen Receptor Modulator) it is
advised to buy pharmaceutical grade products when possible. Your Testosterone can be pharmaceutical
grade or from an underground lab (UGL). Just make sure you do plenty of research of the brand before you
spend any money to make sure they have good reviews.

REMINDER: This forum is not the place for you to do research or request source information.

What You Will Need

Essentials
• Testosterone Enanthate or Cypionate - 4 x 10 mL Vials (generally dosed 250-300mg per mL)
• An Aromatase Inhibitor (AI) like Arimidex or Aromasin
• PCT Medication
|--- /r/steroids Recomended PCT
• Syringes and Needles
|--- Luer Lock Syringes
|--- 21g Needles (1" to 1.5") for drawing
|--- 25g Needles (1" to 1.5") for injecting Glutes
|--- 25g Needles (1") for injecting anywhere else (Not necessary if only injecting Glutes.)
|--- Alcohol injection swabs

Optional Items
• An Oral Steroid
• HCG (Learn more on the PCT wiki page)
|--- Bacteriostatic Water
• SERM in case of a gyno flair-up
|--- Raloxifene
or
|--- Nolvadex
 Why 4 Vials of Testosterone?
On a lot of forums the first cycle advised to new steroid users is 10-12 weeks. 10 weeks is slightly too little. 12
weeks is fine, but you will have Test left in the vial. For this reason, you may go up to 16–20 weeks. Given this
is your first cycle and will likely yield some of the most dramatic results, (assuming diet, training and rest are
on point) you want to strike a balance between maximizing your gain and minimizing the time it will take to
recover from the cycle and any potential side effects. It is always recommended to at least PCT for your first
cycle vs. Blast & Cruise.

Testosterone Enanthate Or Testosterone Cypionate?

What's The Difference?
Approximately nothing. Definitely nothing that is going to make a difference in choosing one or the other for
our purposes. Read the specifics below:
• The ester weights are almost identical, with Cypionate being ever so-slightly heavier.
Meaning there is ever so-slightly more actual testosterone hormone (~1%) in Enanthate.
• The terminal half-life is also almost identical.
Enanthate is 4.5 days.
Cypionate is 5 days.
This will result in ever so-slightly more stable bloods with Cypionate.
• For some, they may experience a slight difference in potential Post Injection Pain (PIP). This is due to
Cypionate having a higher melting point than Enanthate, making Cypionate more prone to being able to
cause PIP. This all depends on how your Testosterone was brewed by your source/supplier. Read more on
Post Injection Pain (PIP): Here.
Please See Our Esters Wiki Page: Here

Arimidex or Aromasin?
You should read the AI portion of The Estrogen Handbook, as well as the compound profiles for each, and
make that choice on your own. Arimidex's compound profile: Here. Aromasin's compound profile: Here.
If you choose Arimidex: Just be aware the blood levels of Arimidex can drop a bit when used alongside
Nolvadex. (In case of a gyno flair-up - see more below)
If you choose Aromasin: BE SURE TO TAKE IT WITH FATS

How Much AI Do I Need?

How much AI is required can vary from person-to-person, as a guide it advised you get bloodwork to dial in
your dose. You will basically need to use trial and error to find your ideal AI dose to get your Test:Estrogen
balance at your personal ‘sweet spot’. MOST users will find .5 mg of Arimidex or 12.5 mg Aromasin E3D or
E3.5D to be a good starting dose. Some may need more frequent (EOD) dosing or some may even need less
than E3.5D; this is really something that varies person-to-person too much.
 In The Estrogen Handbook, it gives an idea of side effects for both low and high Estrogen levels which may
help you gauge an idea of where you’re at should you become confused and not want to have bloods
taken, BUT blood work will be the only way to know 100%.
It is HIGHLY UNLIKELY that you will need this dose on 500mg of Testosterone, but it is suggested to have
enough to run the Arimidex 1mg EOD or Aromasin 25mg EOD, this will give you more than what you
realistically should need. REMEMBER: Get bloodwork to dial in the AI dose you may need.

When Should You Start Your AI?

There are two different trains of thought:

1. Dose preventatively (i.e., before you get high bp, spicy nips, etc.)
2. Dose only when you start to notice sides (acne, bloating/water retention, high blood pressure, nips that are a
bit zesty)
To be cautious, we will cover when you should start preventatively. We are also going to be presuming that
this is your first cycle and as such we will be going by what’s outlined on this wiki page. However,
the preferred method is only to take an AI only when sides necessitate.

Estrogen (E₂) is highly anabolic, cardioprotective and neuroprotective, and essential for normal physiological
functioning. Crashed E₂ sides are far worse than the inverse, and estrogen should be proportionally high just
as test, so long as sides don't get out of hand. Gyno takes weeks to develop, and new gyno can effectively be
taken care of with SERMS while continuing the cycle.

What We Know
Testosterone Peaks

Testosterone will peak shortly after your first injection. See below:

• Test E has been shown to peak as soon as ~6-10hr after injection[1](https://imgur.com/a/ECYhEXk2)

• Test C has been shown to have pharmacokinetics very similar to the pharmacokinetics of testosterone
enanthate, with peak testosterone serum concentrations shortly occurring after injection.[1][3]

With the above, it may indirectly answer another question we see a lot. “When does the Test kick in?” and to
which the research shows your levels will rise very quick to supraphysiological levels. You will build upon this
with each shot. You probably will start noticing some increased recovery and some mild weight gain
(depending on diet) around week 3-4. You probably won’t notice much outside of greater recovery unless
you had low(er) T to begin with.

Estradiol Rise
With this testosterone peak, Estradiol (E2) has been found to correlate directly.[5] This is no surprise as
aromatization will occur, causing Estradiol to peak shortly after as well. See below:
• One study found that after a 200mg Test E injection, E2 values rose significantly in just 6hrs post injection in
eugonadal men and that peaked at 2 days after injection (base serum E2 was 23 ± 4 pg/ml, peaked at day 2
 (45 ± 4 pg/ml). Alternatively, hypogonadal men were also studied and found to increase significantly in just
6hrs as well and peaking the day after the injection, but bringing them to a more optimal range (base serum
E2 was 7.2 ± 2 pg/ml, peaked at day 1 to 29 ± 4 pg/ml).[2] Another study supports this level of change in
Hypogonadal men.[4]
• Another study found that after a 200mg Test C injection, E2 values rose significantly from a mean of 26.2 ±
14.9 pg/ml to 76.9 ± 26.3 pg/ml on days 4 to 5.[3]
The above two studies are strange showing that despite them being similar, Test E seems to peak E2 much
faster than Test C (side note: Test C is shown peaking Test levels much slower than seen in other studies as
well.[1] I believe it’s important to remember how much variance we can have as individuals). It’s important to
note that these peaks shown above are just that, the peaks — the levels begin to drop off after them, but
with each new injection you will reach a new peak, until finally around the time saturation levels are reached.
Note that you should reach close to ~94% saturation by the beginning of the 4th week and with that by week
5 you should know if your AI dosing is working for you or not, but week 5 or 6 get blood work done to
confirm.

One factor that you’ll notice from the first bullet point is the difference between raise in Estradiol in
eugonadal vs hypogonadal. For most individuals starting their first cycle it can be assumed you are eugonadal
unless you have been properly diagnosed as hypogonadal, thus your Estradiol can spike close to the upper
range after your first shot of Test. If you are doing the "Your First Cycle" outlined on this wiki page then your
first shot will be 250mg — 50mg over that of the study.

Another point of thought is your age. It was shown in individuals ~65 y/o that the aromatization is far greater
than that of someone in their 20s. This was even the case when controlling percentage fat mass as that can
increase aromatase.[5][6] So if your Gramps is wanting to do his first cycle, you may want to start his AI sooner.
Likewise If you are entering your 40s-50s, you may want to dose slightly early, if not I think you will be fine
with the below.

Study Disclaimer
The problem with these studies for us as anabolic steroid users are we’re not just injecting once. We are
injecting weekly, and with that we don’t have cold hard data for right at the beginning of the cycle—how E2
is affected injection by injection. The best we have is a table showing 300 mg and 600 mg injected weekly for
5 months, but the table with the data is just the average over the 5 months, this doesn’t show us each point
of data that they took. It would be interesting to see the first few weeks of the study.

Putting It All Together.

Since we are focusing on dosing preventatively and:

• Assuming you are a healthy eugonadal male

• Assuming you’re using Test E or C
• Assuming you are of decent BF% (ideal close to 10%)
• Assuming that you are a young guy (in your 20s-30s).
• Assuming your pre-cycle blood work did not show that you have borderline out-of-range high estradiol to
begin with.
You would start dosing on your 3rd injection.
For Example:
You are injecting on Mondays and Thursdays:
• You do your first injection on Monday
• You would start your AI on or after the following Monday injection
Dosing Disclaimer
We are all different. You may need to dose sooner than the above (sometime between your 1st and 3rd
injection), or you may feel symptoms of low E2 and skip a dose, but if possible, wait for sides before lowering
your E2. As a highly anabolic, cardioprotective and neuroprotective compound, estrogen provides multiple
advantages that enhance the effectiveness of your cycle.
Get regular blood work if you are unsure of anything.

References
1. Behre HM, Nieschlag E. 1998 Comparative pharmacokinetics of testosterone esters. In: Nieschlag E, Behre
HM, eds. Testosterone: Action, Deficiency, Substitution, ed 2. Berlin: Springer-Verlag; 329–348.
2. Sokol R, Palacios A, Campfield A, Saul C, Swerdloff R. 1982 Comparison of the kinetics of injectable
testosterone in eugonadal and hypogonadal men. In: Fertility and Sterility, 425-430
3. Nankin H. 1987 Hormone kinetics after intramuscular testosterone cypionate. In: Fertility and Sterility, 1004-
1009
4. Nakazawa R, Baba K, Nakano M, Katabami T, Saito N. Hormone Profiles after Intramuscular Injection of
Testosterone Enanthate in Patients with Hypogonadism. In: Endocrine Journal 2006, 53 (3), 305-310
5. Kishore M. Lakshman, Beth Kaplan, Thomas G. Travison, Shehzad Basaria, Philip E. Knapp, Atam B. Singh,
Michael P. LaValley, Norman A. Mazer, Shalender Bhasin; The Effects of Injected Testosterone Dose and Age
on the Conversion of Testosterone to Estradiol and Dihydrotestosterone in Young and Older Men, The
Journal of Clinical Endocrinology & Metabolism, Volume 95, Issue 8, 1 August 2010, Pages 3955–3964
6. Cohan P.G.; Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and
aging connection. In: Medical Hypotheses, Volume 56, Issue 6, June 2001, Pages 702-708

SERM On Cycle?

I thought SERMs were just for PCT, why do I need Raloxifene or Nolvadex for on cycle?
Raloxifene and Nolvadex will both bind to the Estrogen receptor at the breast site and be your first plan of
attack against uncontrollable gyno sides. If your Estrogen is wildly out of control and you are developing
puffy, sore, or itchy nipples, UP your AI dose and start taking your SERM (Rolax - 60mg ED) (Nolva - 20mg ED).
It usually will subside after a 7-12 days. Continue the SERM for 3 days after the symptoms have subsided
before you drop the SERM.
Note: If you choose Arimidex as your AI, just be aware the blood levels of Arimidex can drop a bit when used
alongside Nolvadex. To avoid this, you may choose Raloxifene.
This isn't required, but it is definitely RECOMMENDED. It's always better to have it and not need it rather
than need it and not have it.

Injecting Your Gear

The injection process itself is relatively straight forward. Perhaps nothing causes more anxiety for AAS users
than their 1st injection. This fear is far more psychological than physical, as the act of performing an injection,
especially when utilizing proper technique and the correct pin size, can be relatively painless. Some muscle
groups are more prone to causing discomfort than others and the possibility of hitting a nerve, scar tissue, or
a sore spot is a reality, but in general, an injection should not be considered a “painful” experience.

To Learn Step-By-Step On How To Inject Safely, Click Here

For a first cycle, the easiest not to mess up is Glutes, a nice big muscle with decent circulation and low risk of
hitting any nerve clusters. The twisting and turning can be a problem for some in which case shooting Ventro
Glutes is another option. If that is too hard to find for you, try Quads, but there is a slightly larger margin for
error in regard to hitting nerve clusters and puncturing large veins. But you should aim to have as many
injection sites as possible to avoid building scar tissue.
Visit our injection page to learn all about Safe Injection Technique.

Post Injection Pain

To Learn All About Potential Post Injection Pain, Click Here

Frontloading Test?

Frontloading simply means to take a calculated, especially high dose on the first day (or week) for injectable
AAS. This allows blood levels of the compound to reach a stable level faster. The problem is taking a large
amount of Test can be hard to control estrogen.

Should I Frontload My Test?

No, this is your first cycle and we want to keep things as simple as possible, that includes managing sides; the
optional oral is already pushing things.

OPTIONAL: What Oral Steroid Should I Use?

Again, an oral steroid is completely optional. Oral steroids can add greater complexity to cycles if we start
throwing in more compounds.
 It's suggested either to use dry orals or, to use aromatizing ones such as dianabol only if you can commit to
properly managing the added complexity in managing your estrogen levels.
If one has preexisting pubertal gyno, or if you are prone to massive aromatization, there's better choices.
Aromatizing orals might be better as finishers once you've already learned E2 management. But if you can
keep your estrogen under control, and aren't afraid of the added complexity, they can certainly be fun to run
in the beginning.
Dry orals such as anavar or turinabol can be added to your first cycle without the extra E2 concerns.

If you use a wet oral such as Dianabol, you'll find AI dosing starts to become more complicated. Not only do
you need to find your dosing for Dianabol and Testosterone, but then you also need to readjust once you
come off the Dianabol. Regardless, it's a timeless classic that has been used for first cycles for a long time.

Other options include Anadrol or Superdrol, both of which do not aromatize, but have been known to cause
Gyno by some other mechanism. If you choose to use Anadrol or Superdrol, it is recommended to have
Raloxifene on hand in case of a Gyno Flair-Up.
In the end, the choice is personal in nature.

Suggested Orals
• Dianabol (Dbol) is a very "wet" compound, which means that it converts to estrogen and at a high rate at
that. It is highly recommended to use an AI from day one of this cycle in order to prevent heavy water
retention, gynecomastia, and other high estrogen side effects. (Sides). Don't use Dianabol unless you know
how to manage E2, or you can afford the extra time and attention to properly dial it in. For this reason it's
oft-best left mid-cycle, or as a finisher when you have your E2 under control, unless you can commit to the
added estrogen management from the start.
• Anadrol (Adrol) is considered a "dry" compound, which means that it doesn't convert to estrogen. Despite
this, individuals using this compound will often report pronounced estrogen related side effects such
as gynecomastia and water retention, among others. (Sides.)
• Superdrol (Sdrol) is considered a "dry" compound, which means that it doesn't convert to estrogen. Despite
this, some individuals using this compound still report gynecomastia symptoms. There are theories on why
this may happen, but nothing has ever been proven. Sdrol is also known to cause lethargy in some. It is a DHT
derivative, so hair loss can be a concern. (Sides.)
• Turinabol (Tbol) is considered a "dry" compound, which means that it doesn't convert to estrogen. It also
doesn't convert to DHT. It is also one of the most "side-effect free" compounds, but it is also not known for
putting on as much potential mass as Dbol or Adrol. You should still review the compounds side effect profile.
It does still affect lipids negatively, but most oral steroids do.
• Anavar (Var) is considered a dry compound, which means that it doesn't convert to estrogen. It also doesn't
convert to DHT. Strength increases are common and mixed with less than dramatic weight gains. The
compound is very beneficial to athletes participating in sports that have weight divisions, or where extra
weight can be a hindrance.
Note: These are just some of the suggested orals based on their properties. You may also use any of the orals
in The Basic Cut. Anecdotally, some have reported just as good (if not better) size gains from the orals listed
in The Basic Cut as Turinabol (Tbol).

When Should I Take It?

There are two trains of thought when it comes to this, and a third if you mix the two. Whatever you decide, if
you experience gastrointestinal discomfort, you can avoid this by taking your oral steroids with meals when
possible.

Half-Life Method

Oral steroids have a short half-life of just a few hours. One classic method says that they should be split
throughout the day. So you'd start dosing as soon as you wake up and then every 4 hours or so (as much as
you can split it up) throughout the day.

Off Days: Same as above.

Pre-Workout Method

One recent trend which has become quite popular lately is the pre-workout method, in which the individual
administers the entire day’s dose of oral AAS immediately before training; usually around ~1.5 hours pre-
workout.

Off Days: Either all upon waking or the Half-Life Method.

Hybrid Method

A third option is to mix the two above methods. What you would do is take a small dose throughout the day,
but pre-workout (~1.5 hours pre-workout) you will take a slightly higher dose.

Off Days: Use the Half-Life Method.

How Often Should I Pin (Inject)?

It is suggested on /r/steroids that you should at least inject every three days (E3D) or every 3.5 days (E3.5D)
to keep blood levels as stable as possible for Testosterone Enanthate or Cypionate. This will minimize side
effects and make controlling estrogen easier. You may do once a week, but it is not optimal.
Here is an example of blood levels with 500mg of Test Enanthate injected once a week (E7D). This was
plotted with SteroidPlotter.
Here is an example of 250mg Test Enanthate injected every 3.5 days, also plotted with SteroidPlotter. As you
can see the release rate, in which Testosterone is released into your blood, is more stable.
Post Cycle Therapy (PCT)

After you did your 12-15 week cycle, you have to begin your Post Cycle Therapy (PCT). The first two weeks
after your last injection you do not take any drugs, as the endogenous testosterone is still disrupting your
natural endocrine system.

Then, you will either do a /r/steroids Recomended PCT

Human Chorionic Gonadotrophin (HCG)

Why Should I Use HCG?
Running a small dose of HCG will help to keep the testes full and will aid with recovery once you come to the
end of your cycle and need to PCT. It’s not 100% necessary, but if you have access to some and don’t mind
spending a small amount of money to speed up your recovery then it is probably worth looking at. Learn
more on the PCT wiki page.
How Do I Mix And Run My HCG?
An easy ratio for mixing is 1ml of bacteriostatic water per 5000iu of HCG which results in 10 units (5 small
lines on a 1 mL insulin syringe or 10 small lines on a 1/2 mL insulin syringe) being 500iu of HCG.
Note: To find out dosing for HCG use this HCG calculator.

Blood Work

Regular blood work is STRONGLY encouraged. It is recommend getting blood work before starting your cycle
(to assess your baseline Testosterone levels and general health), during your cycle (to confirm that your
Testosterone is legitimate and properly dosed), and after your cycle (to assess how well you have
recovered). The wiki page regarding blood work can be found here and some help in how to understand your
results can be found here.
When Should I Get Bloodwork?

The standard recommendation for Test E/C injections is to get bloodwork drawn 36-48 hours after your last
injection, in order to try to get a representative picture of your PEAK testosterone levels. Actual
pharmacokinetic calculations speculate the peak plasma levels of testosterone will happen at about 35-40
hours post last injection, but you must remember that everyone responds slightly differently to gear and that
injection site (ie glute or delt) may make a small difference.

Nutrition

It is recommended to eat about TDEE + 30%. Go find multiple TDEE calculators and calculate your TDEE on
each. /r/steroids highly recommend the 3-Suns Adaptive TDEE Spreadsheet. It gets more accurate the longer
you use it, but by week 3 or 4 it should be really close and closer than any online calculator. Just remember
it's better to over eat than under gain.
 Dosing

Note: For this example we are using the time frame for the 15 weeks. If you wish to end it sooner, obviously
all your ending weeks will change and the week you start PCT will as well.
• Weeks 1-15: Testosterone E or C, 250 mg every 3 or 3.5 days (E3D or E3.5D) for a total of 500 mg per week.
• Weeks 16-17: Nothing (This allows the exogenous testosterone to clear your body to a reasonable amount).
• Weeks 18-Til: Whatever PCT protocol you choose.
• Throughout Cycle (or at least on hand): An AI like Arimidex or Aromasin. Again, dosing is user dependent and
you should get blood work to dial in your dose, but MOST users will find .5 mg of Arimidex or 12.5
mg Aromasin E3D or E3.5D to be a good starting dose. Some may need more frequent (EOD) dosing or some
may even need less than E3.5D; this is really something that varies person-to-person too much. Watch out
for signs of low or high estrogen - especially high estrogen, like excessive bloating or itchy nipples.
Oral Steroid Options / Additives:
Test E & C takes about six weeks to fully saturate the blood (i.e., kick in). If you don't want to wait that long
and you want to aid in your bulk, a popular thing to do is start the oral from day 1 (kickstarting). Another
popular thing to do is to run your oral at the very end of your cycle, leading up to PCT (finisher). You can run
your oral anytime during the cycle though. You may pick one of the following:
• For 6 Weeks: Dianabol (Dbol), 30–60 mg, ED or
• For 6 Weeks: Anadrol (Adrol), 50–100 mg, ED or
• For 4 Weeks: Superdrol (Sdrol), 10–20 mg, ED or
• For 6 Weeks: Turinabol (Tbol), 40–80 mg, ED or
• For 6 Weeks: Anavar (Var), 30–50 mg, ED
Note: These are just some of the suggested orals based on their properties. You may also use any of the orals
in The Basic Cut. Anecdotally, some have reported just as good (if not better) size gains from the orals listed
in The Basic Cut as Turinabol (Tbol).

Why 500mg?
We answer this question ten times a day.

500 mg is recommended for your first cycle.

Contra what you may have been led to believe, this number was not just haphazardly chanced upon. There's
actually a great deal of critical thinking and rationale that went into arriving at this figure.

500 mg is a low dose.

Gains are linear up to 600 mg and beyond:

Testosterone dose-response relationships in healthy young men

Lean body mass:
 125mg = +3.4 kg.

300mg = +5.2 kg.

600mg = +7.9 kg

If you're going with 300 mg you're still shutting yourself down, and you're leaving gains on the table for
nothing.

There's no difference in sides between 300 and 500.

There's no difference in shutdown between 300 and 500.

500 mg is a low dose in that you can take ten times that without any Ill effects. Someone who is a low
aromatizer—not all that rare—can take 1000 mg Test with no AI and no sides, no problem.

500 mg is a low dose in that bodybuilders usually start from there and work up. 500 is low. 750 is medium.
1000+ is advanced.

At 300 mg, you're putting yourself in the no-man's land just between TRT and a full-on blast where it's
difficult to dial in your aromatase inhibitor (AI). Managing your estrogen with an AI is one of the most
important things you can learn from your first cycle.

The r/steroids wiki incorporates thousands of clinical studies and case reports to come to its numbers. Test is
a very benign compound. Unlike some of the synthetics, your body immediately recognizes it and knows just
what to do.

Taking a higher dose than it's naturally accustomed to simply results in adaptation to temporarily produce
relatively higher levels of aromatase to accommodate for the influx of hormone and attain equilibrium.

The immediate byproduct of that adaptive response—17β-Oestradiol (E2) is highly anabolic, cardioprotective,
neuroprotective, and essential for normal physiological functioning. No acute toxicity or organ stressors
manifest themselves, even at doses hundreds of times that of normal.

Your body knows how to handle testosterone. It's been synthesizing it since well before birth. It's essential
for normal physiological functioning. The Wiki recommends 500 mg on your first cycle for good reason.

Don't try to reinvent the wheel.

8 EXAMPLE CYCLES
• Use SteroidCalc To Plot Out Cycles
 Beginner Cycles

Your First Cycle

So, you got interested in steroids and are now trying to figure out where to start.

Beginners have one rule: KISS. That stands for "Keep It Simple, Stupid." The more chemicals you toss in at
once, the bigger your chances of going down in a flaming fireball. A big, bloated, gyno-y fireball.

The Basic Bulk

• See Your First Cycle

The Basic Cut

The Basic Cut differs very slightly from The Basic Bulk, mainly in dosing. The standard rule of thumb is to not
cut while off cycle as some hard earned muscle mass could be lost. Most users anecdotally notice less bloat
with Testosterone Propionate, so it's often used for cuts, but overall you can use Test E or C just fine as well.
Dosing:
• Weeks 1-12: Testosterone Propionate, 30-50 mg (ED) OR
• Weeks 1-12: Testosterone Enanthate or Cypionate, 100-200 mg (E3D or E3.5D). PCT differs from propionate
protocol below.
• Weeks 13: Nothing the first 2-3 days (This allows the exogenous testosterone to clear your body). PCT should
start day 3 or day 4 due to test propionate's active life of ~0.8 days.
• Weeks 13-til: Starting day 3 or 4. Whatever PCT protocol you choose.
• Throughout Cycle (or at least on hand): An AI like Arimidex or Aromasin. Dosing is user dependent and you
should get bloodwork to dial in your dose. Watch for signs of low or high estrogen—especially high estrogen,
such as excessive bloating or itchy nipples.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.
Note: You can extend up to 20 weeks. If you wish to extend it, all your ending weeks will change and the
week you start PCT will as well.
Alternatives/Additives:

ECA Stack

Another thing to consider is using a ECA (ephedrine, caffeine, aspirin) or EC (ephedrine, caffeine) stack. This
will function as an appetite suppressant and accelerate your metabolism and hence aid tremendously on a
cut:
• Last 8 Weeks: ECA or EC Stack, Up To 3xED
 Salbutamol Stack

Even more effective than an ECA stack is Salbutamol with caffeine. This stack is more effective than
ephedrine while being far safer than clenbuterol.
• Last 8 Weeks: Salbutamol/Caffeine, 4mg/200mg, up to 3xED
If you use Test E & C, it takes about six weeks to fully saturate the blood (i.e. kick in). If you don't want to wait
that long and you want to aid in your cut, a popular thing to do is start the oral from day 1 (kickstarting).
Another popular thing to do is to run your oral at the very end of your cycle, leading up to PCT (finisher). You
can run your oral anytime during the cycle though. You may pick one of the following:
• For 6 Weeks: Winstrol (Winny), 40-80 mg, ED or
• For 6 Weeks: Epistane (Epi), 40-80 mg, ED or
• For 6 Weeks: Anavar (Var), 40-80 mg, ED
WARNINGS:
• Winstrol (Winny) is considered a "dry" compound, which means that it doesn't convert to estrogen. It is a
DHT derivative, so hair loss can be a concern. (Sides)
• Epistane (Epi) is considered a "dry" compound, which means that it doesn't convert to estrogen. It is a DHT
derivative, so hair loss can be a concern. (Sides)
• Anavar (Var) is considered a "dry" compound, which means that it doesn't convert to estrogen. It also doesn't
convert to DHT. It is one of the most side-effect free compounds, but does affect lipids negatively, as most
oral steroids do. You should still review the compound side effects. (Sides)
Nutrition:

It is recommended to keep your caloric intake at no less than 80% TDEE.

Intermediate Cycles

Intermediate Bulk Cycle

By now, you have probably put on a fair bit of mass, and want to see how how much you are capable of. This
is a solid second cycle, perfect for putting on mass quickly with minimal side effects. Nandrolone also
provides excellent joint support, allowing you to push your body a bit harder. At this point you have a bit of a
feel for how your body responds to testosterone. You can extend the cycle a bit.
WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly suppressive for up to six months or more. No one
should take nandrolone or other 19-nor compounds unless they're on blast and cruise, because full
recovery from PCT will be rendered largely ineffective for as long as half a year—so long as to be impractical.
• Weeks 1-12: Testosterone Enanthate or Cypionate, 500–600 mg/week split E3.5D.
• Weeks 1-10: Nandrolone Phenylpropionate (NPP), 500–600 mg/week split every day or every other day EOD.
• Weeks 13-14: Nothing (This allows the extraneous testosterone to clear your body).
• Throughout Cycle (or at least on hand): An AI like Arimidex or Aromasin. Dosing is user dependent and you
should get bloodwork to dial in your dose. Watch out for signs of low or high estrogen, especially high
estrogen, like excessive bloating or itchy nipples.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.

You can extend it up to 20 weeks. If you wish to extend it, obviously all your ending weeks will change and
the week you start PCT will as well.

Cut/Recomp Cycles

Silver Standard
The following cycle is considered to be a very solid cutting cycle that maintains lean body mass while burning
fat. Keep your caloric intake at no less than 80% TDEE.

• WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly suppressive for up to six months or more.
Nobody should be taking nandrolone or other 19-nor compounds unless they're on blast and cruise,
because full recovery from PCT will be rendered largely ineffective for as long as half a year—so long as to be
impractical.
• Weeks 1-12: Trenbolone Acetate, 50-100 mg, every day (ED) to your tolerance level
• Weeks 1-12: Testosterone Propionate (or Testosterone Enanthate), 50 mg ED
• Weeks 1-12: Arimidex, .5mg E3D, watch for E2 crash, adjust accordingly.
• Weeks 13-14: Nothing (This allows the extraneous testosterone to clear your body).
• On Hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur.
• On Hand Throughout Cycle: A Dopamine Agonist like Caber or Prami to stop prolactin production.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on-
hand.
Q: What should my protein/carb/fat percentages be during this cut?
A: It depends on your goals.
• You're planning to eat below your TDEE for a true cut.

Get in your standard bulk protein and balanced nutrients. The rest does not matter. In a caloric deficit, your
body will not attempt to convert incoming food to fat. Trenbolone is highly anabolic and will tell your body to
not burn muscle for fuel (catabolism).
 People have regularly ran caloric deficits of 1,500 calories below TDEE without losing strength. You'll notice a
loss in energy, but not strength.

• You're planning to eat above your TDEE in an attempt to gain muscle while losing fat.
Trenbolone has the capability to stop the creation of new fat (de novo lipogenesis) from carbohydrates. This
only happens when blood plasma levels of estrogen are low. Regularly dose your AI's to control estrogen. It
will not stop storage of fat from intake in a caloric surplus. Therefore, above your TDEE, you want to consume
extra carbohydrates to avoid fat storage.
When excess carbs are eaten, Trenbolone will push them into the mitochondria of your cells, generating heat
and producing sweat. If your sweating is excessive, you are eating too many carbs. Adjust your carb intake so
as to only have a small amount of Tren sweats. It is recommend to not eat carbs at night and only light carbs
(vegetables) for dinner. The requirement for low estrogen for Tren to do it's magic is
why /r/steroids recommends high Tren/low Test cycles for cuts and recomps.
• WARNING: Trenbolone has been shown to be neurotoxic. Running low test with high tren for cutting may
lead to long-term neurophysiological damage. Running tren with high test allows estrogen to act in
a neuroprotective capacity: 17β-trenbolone, an anabolic–androgenic steroid as well as an environmental
hormone, contributes to neurodegeneration

Gold Standard
Works best when body fat is below or at 12%.

Add in the following to the Silver Standard Cut / Recomp Cycle:

• Weeks 1-12: Masteron Propionate, same mg as Testosterone Propionate

Contra Costa Contest Prep

Taken from this video (video taken down) by Michael Pacini. The weeks column is for the number of weeks
away from your contest.
• WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly suppressive for up to six months or more.
Nobody should be taking nandrolone or other 19-nor compounds unless they're on blast and cruise,
because full recovery from PCT will be rendered largely ineffective for as long as half a year—so long as to be
impractical.
Weeks Compound Amount Frequency

Weeks 14-8 Test C 500mg EW

Weeks 14-8 NPP 600mg EW

Weeks 14-8 1-Test C (DHB) 500mg EW

Weeks 8-5 Test C 250mg EW

 Weeks Compound Amount Frequency

Weeks 8-5 NPP 300mg EW

Weeks 8-5 1-Test C (DHB) 250mg EW

Weeks 14-0 Anavar 10mg 7xED

Weeks 14-0 Proviron 25mg 2xED

Weeks 14-0 Adex 0.5mg ED

Weeks 14-0 Nolva 10mg ED

Weeks 5-0 Salbutamol 4mg 3xED

Weeks 5-0 Oral Primo 25mg 2xED

Weeks 5-0 Winstrol 25mg 2xED

Weeks 14-1 GH 2IU 3xED

Equipoise (Boldenone) Cycles
Equipoise (EQ) is a fantastic compound that can be utilized in any cycle for almost any purpose. EQ tends to
give users a very healthy-looking reddish-brown hue to their skin tone, almost like a very light base tan.
Equipoise tends to visibly increase vascularity in those who are less than 15% body fat, and will grow the
delts and traps in a way that makes them look volumized and very full. Some forums have put EQ into their
Top 5 list of most important bodybuilding hormones. EQ is equally used in powerlifting circles for the
increased rate of recovery and dense dry gains that don't pack on 15+ lbs of water during a cycle.
Some users report an increase in cardiovascular endurance, along with a significant increase in appetite. One
of the reported negative side effects of EQ is that some users experience mild anxiety that will increase with
the dose. This is due to the aromatase-inhibiting effects of EQ metabolites ADD, ADT and 1-AD. Have
something on-hand to bring estrogen levels back up in case of crashed E2: test no ester (TNE or short-ester
test, Dianabol, HCG or Trestolone will all do the trick.
For EQ to really shine, it needs to be run longer and at higher doses than any other steroid, but it is incredibly
mild in terms of side effects and shouldn't be considered in the same class of “mega-dosing,” as with other
steroids. 1–1.5 grams is a good dose for the positive properties of EQ to really come into their own. Even a
cycle with 2–3 grams of EQ would still be mild.
EQ is best run as an accessory compound in a bulk cycle for those looking for that extra pop in their delts.
EQ can be run as an accessory to tren on a cut cycle to help mitigate the reduction in cardiovascular capacity
that comes along with tren use, while keeping muscle fullness, and helping to avoid looking flat.
EQ really shines as the main compound in a recomposition cycle, where it allows you to keep your muscle
fullness and vascularity while building a few pounds of muscle and dropping a few percent body fat.
 Bulk Cycles

Beginner EQ Bulk
For those with minimal AAS experience this cycle will add around 10–15 lbs of dry lean gains and you won't
lose much (if any) during PCT.

• Weeks 1-16: Equipoise, 300 mg, E3D

• Weeks 1-24: Testosterone Enthanate, 200 mg, E3D
• Run Testosterone for 8 weeks after dropping EQ to allow the Uncdeylenate ester to clear.
• On-hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur. Also
have something to bring estrogen levels back up in case of Crashed E2: test no ester (TNE) or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.

Intermediate EQ Bulk
Keep an AI on hand but you shouldn't need it.

• Weeks 1-16: Equipoise, 450 mg (E3D)

• Weeks 1-24: Testosterone Enthanate, 300 mg every three days (E3D)
• Run Testosterone for 8 weeks after dropping EQ to allow the Uncdeylenate ester to clear.
• On-hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur. Also
have something to bring estrogen levels back up in case of crashed E2: test no ester (TNE or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.

Advanced EQ Bulk
This cycle ups the dose a bit on the test and EQ and adds in some masteron to help keep the estrogen down
and the water off. Recommend running Aromasin proactively to hold down E2

• Weeks 1-20: Equipoise, 600 mg (E3D)

• Weeks 1-28: Testosterone Enthanate, 450 mg every three days (E3D)
• Weeks 1-20: Masteron Enanthate, 250 mg every three days (E3D)
• Weeks 1-20: Deca-Durabolin, 200 mg (E3D)
• Weeks 1-20: Aromasin, 12.5 mg, E3D — Adjust as needed
• On Hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur. Also
have something to bring estrogen levels back up in case of crashed E2: test no ester (TNE or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
• Run Testosterone for 8 weeks after dropping EQ to allow the Uncdeylenate ester to clear.
• WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly suppressive for up to six months or more.
Nobody should be taking nandrolone or other 19-nor compounds unless they're on blast and cruise,
because full recovery from PCT will be rendered largely ineffective for as long as half a year—so long as to be
impractical.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.

Cut Cycles

If you aren't subject to the increase in appetite that sometimes comes along with EQ use, EQ alone can be a
very viable compound to cut on. You end up seeing your results faster as you tend to stay a bit drier. This is
actually the same as the beginner bulk, calories just have to be adjusted. The effect of slimming down at the
waist and broadening your shoulders can be quite pronounced.

Beginner EQ Cut
Surprisingly, the same doseages as the Beginner Bulk, however, adjust your calories to be in a caloric deficit
no more than 80% of your TDEE.

• Weeks 1-16: Equipoise, 300 mg (E3D)

• Weeks 1-24: Testosterone Enthanate, 200 mg, E3D
• On Hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur. Also
have something to bring estrogen levels back up in case of crashed E2: test no ester (TNE or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.
• RUN TESTOSTERONE FOR 8 MORE WEEKS after dropping EQ to allow the Uncdeylenate ester to clear.
 Intermediate EQ Cut
The effect of Tren and EQ on your physique during a cut is nothing short of freakish. Estrogen is kept low so
de novo lipogenesis is strongly inhibited, Tren leans you out while both Tren and EQ give that huge boulder
shoulder and traps look.

• Weeks 1-16: Equipoise, 450 mg, E3D

• Weeks 1-24: Testosterone Enthanate, 300 mg (E3D)
• Weeks 4-16: Trenbolone Acetate, 50-100 mg, every day (ED) to your tolerance level
• RUN TESTOSTERONE FOR 8 MORE WEEKS after dropping EQ to allow the Uncdeylenate ester to clear.
• WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly suppressive for up to six months or more.
Nobody should be taking nandrolone or other 19-nor compounds unless they're on blast and cruise,
because full recovery from PCT will be rendered largely ineffective for as long as half a year—so long as to be
impractical.
• On Hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur. Also
have something to bring estrogen levels back up in case of crashed E2: test no ester (TNE or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
• On Hand Throughout Cycle: An Dopamine Agonist like Caber or Prami to stop prolactin production and
eventual lactation.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.

Advanced EQ Cut
Ensure that you have run several cycles with these compounds before attempting.

• Weeks 1-20: Equipoise, 600 mg (E3D)

• Weeks 1-28: Testosterone Enthanate, 450 mg (E3D)
• Weeks 4-20: Trenbolone Acetate, 50-100 mg, ED to your tolerance level
• Weeks 1-20: Masteron Propionate, 200 mg (E3D)
• RUN TESTOSTERONE FOR 8 MORE WEEKS after dropping EQ to allow the Uncdeylenate ester to clear.
• WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly suppressive for up to six months or more.
Nobody should be taking nandrolone or other 19-nor compounds unless they're on blast and cruise,
because full recovery from PCT will be rendered largely ineffective for as long as half a year—so long as to be
impractical.
• Weeks 1-20: Aromasin, 12.5 mg, E3D -- Adjust as needed
• On Hand Throughout Cycle: An AI like Arimidex in case signs of excessive bloating or itchy nipples occur. Also
have something to bring estrogen levels back up in case of crashed E2: test no ester (TNE or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
• On Hand Throughout Cycle: An Dopamine Agonist like Caber or Prami to stop prolactin production.
• Take AI only when sides necessitate. Estrogen is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning. Low E2 is far worse than high E2, which should be
proportionally out of range just as test. Gyno takes weeks to develop and can be taken care of with the AI on
hand.

Power Lifting Cycle

• Excerpt from Brandon Lily's Cube Method.

Estrogen Suppression Cycle

• Effects of aromatase inhibition in hypogonadal older men: a randomized, double-blind, placebo-controlled

trial
• Estrogen suppression in males: metabolic effects
• Arimidex vs Femara (Letro)
• Aromatase inhibitors for male infertility
• Hormonal Approaches to Male contraception
• Hormonal approaches to male contraception: approaching reality
• Changes in hormonal profile and seminal parameters with use of aromatase inhibitors in management of
infertile men with low testosterone to estradiol ratios

Very Advanced Insulin Cycle

Read the Insulin Compound Description Page
WARNING: Insulin use is VERY DANGEROUS. You can, quite literally, DIE FROM IT if not done properly. This
guide is to serve as only an example of what some people do in order to start using it.

|------------ READ -------------------------------------------------------------------------|

1. Insulin can easily kill you if mis-used. Do not fuck around.

2. BUDDY SYSTEM ALWAYS! Have a knowledgeable buddy with you
3. DO NOT go to sleep for two hours after insulin use
4. Keep emergency glucose tablets on hand. If you feel like shit, you need more glucose.
5. You must have your eating plan tuned to near perfection

|------------ THIS -------------------------------------------------------------------------|

I’ll use the 5 day training split as an example here. That will give you 20 days “on” insulin.
Day 1: 5 IU insulin / 50g Dextrose
Day 2: 5 IU insulin / 50g Dextrose
Day 3: 5 IU insulin / 50g Dextrose

Congratulations!! You’ve survived thus far. I assume(hope) you’ve been monitoring your BG levels. You
probably have noticed that you are in the higher range using 50 g of dextrose PWO. Now it’s time to drop the
carbs slightly. Don’t fret. This should be more than ample amounts(of carbs) to get you through to your
PPWO meal.

Day 4: 5 IU insulin / 40g Dextrose

Day 5: 5 IU insulin / 40g Dextrose
At this point you should have a good idea of how you react with Insulin in terms of blood glucose (BG)
levels vs. carbohydrate intake .

Let’s up the dose …

Day 6: 6 IU insulin / 50g Dextrose

Day 7: 6 IU insulin / 50g Dextrose
By this point in time you should be feeling good (i.e. more confident) but still respectful to Insulin. Let’s test
the waters for three days to give you the feel of things. By that I mean we’ll drop the carb intake slightly so
you can find a comfortable ratio in regards to IU’s vs. carbs per gram.
Day 8: 6 IU insulin / 40g Dextrose
Day 9: 6 IU insulin / 40g Dextrose
Day 10: 6 IU insulin / 40g Dextrose

Now, the above ratios are safe and effective. You can stop right here and continue on for the next 10 days at
the above doses/ratios. Or you can move forward slightly.

Day 11: 7 IU insulin / 50g Dextrose

Day 12: 7 IU insulin/50 g Dextrose
Day 13: 7 IU insulin/50 g Dextrose
Day 14: 7 IU insulin/50 g Dextrose
Day 15: 7 IU insulin/50 g Dextrose
If you felt confident with the above protocol, you could experiment on days 14-15 and drop your dextrose to
40g. If you do so, please monitor your BG levels every 15 minutes or so. Have glucose tabs, or another source
of quick carbs handy (like orange juice) to stave off any possible signs of hypoglycemia. Should this happen,
don't panic, just drink a glass of orange juice, or similar, and in 10 minutes the symptoms will have subsided.

OK, on to your final week.

Day 16: 8 IU insulin / 60g Dextrose

Day 17: 8 IU insulin / 60g Dextrose
 Day 18: 8 IU insulin / 60g Dextrose
Day 19: 8 IU insulin / 60g Dextrose
Day 20: 8 IU insulin / 60g Dextrose
Congratulations! You just completed your first cycle/experience with Insulin in a safe an effective manner. I
stopped at 8 IU, being that is enough to get your feet wet with the drug. You can experiment later on. This
was simply a guide.

One last thing. Guys ask “Which way is better?” to take your Whey/Dextrose in one shake, or Dextrose first,
and whey 15 minutes later”? Bottom line, it’s just preference.

9 SAFE INJECTIONS
Injection Methods

• Intramuscular injection: An injection into muscle tissue.

• Subcutaneous injection: An injection into the region between the skin and the muscle, also known as a
“SubQ” injection.
AS far as performance enhancement is concerned, there are two primary injection methods. These are
the intramuscular injection method and the subcutaneous injection method. An intramuscular injection is
exactly as it sounds; it is an injection given directly into a muscle. A subcutaneous injection is an injection
which is placed between the skin and the muscle. Which method is utilized will depend on the drug being
administered and the goals & preferences of the user. The overwhelming majority of individuals choose to
administer their AAS by way of IM (intramuscular) injection, although they can be injected subcutaneously, if
desired, although it is not recommended to inject over ½ cc/mL of AAS. HGH, Insulin, HCG, and Peptides) are
typically administered subcutaneously.

The Injection

The injection process itself is relatively straightforward. Perhaps nothing causes more anxiety for AAS users
than their first injection. This fear is far more psychological than physical, as the act of performing an
injection, especially when utilizing proper technique and the correct pin size, can be relatively painless. Some
muscle groups are more prone to causing discomfort than others and the possibility of hitting a nerve, scar
tissue, or a sore spot is a reality, but in general, an injection should not be considered a “painful” experience.
With the information presented in this document, you have been presented with everything you need to
know in order to properly perform an injection. For an abbreviated step-by-step walk through, see Safe
Injection Technique.
 Types Of Syringes

For a beginner, the many different types of syringes and their associated terminology can be confusing. Let us
look at these differences which define the various types of syringes. Generally, syringes are defined by the
following 3 things: Gauge size, how many cc’s a syringe can hold, and needle length. By learning what these
things mean, you will have no problem selecting the appropriate syringe for your needs.

You may have heard of a syringe type known as an “insulin syringe” or "slin pin." Regardless of whether a
syringe is classified as an insulin syringe or not, ALL syringes, including insulin syringes, are categorized by the
3 variables listed above. Insulin syringes are named as such due to the original purpose for which they were
produced, which was to administer insulin to diabetics. Because diabetics will often need to perform multiple
daily injections into the SubQ region, a smaller & shorter needed was needed in order to increase patient
compliance through more tolerable, and relatively painless, injections.

The 3 Variables
• Gauge: The gauge of the syringe refers only to the thickness of the needle itself. The lower the gauge
number, the thicker the needle. The higher the gauge number, the thinner the needle.
• CC: A cc refers only to how much volume a syringe can hold. The average syringe will hold anywhere between
1-3 cc’s. The more cc’s a syringe holds, the larger the barrel will be.
• Needle Length: Needle length refers to just that…the length of the needle. This is not a measure of the entire
syringe, but only the needle itself. The average needle will measure between 5/16th’s of an inch and 1.5
inches in length.

Typically, the syringes normally used for injecting AAS (non-insulin syringes) come individually wrapped and
can be purchased as little as one at a time. Insulin syringes come in individually wrapped or a plastic bag, but
regardless they come in packs.

Selecting The Syringe Needed

Standard Syringe Specifications

Most common syringe specs for steroid injections:
• 18-22g for drawing and 23-27g for injecting
• 1/2" to 1.5 inch needle length
• 3 cc syringe
Note: If your syringes come with the needles already attached, order the drawing needle to come on them.
Otherwise, you'll have to switch needles, each time you want to draw from a vial.
Most common syringe specs for peptide injections:
• 28-31 gauge
• 5/16th" to ½ inch needle length
• ½-1 cc syringe
 Gauge Numbers
Most of the steroid products on the market are oil-based. As an “oil-based” steroid, the steroid molecule has
been suspended in oil, with the oil being used as a carrier. Since AAS are measured in mg amounts and are a
solid in their natural form, they require a carrier if they are to be effectively delivered into the body by
injection. Since oil is significantly more resistant to bacterial proliferation than water, and is also inexpensive,
it is a logical choice. However, oil also has a higher viscosity than water, which means it will resist flow under
applied force to a greater degree than water. The higher the viscosity of an injectable product, the thicker the
needle will need to be in order to be able push the fluid through the needle.

When talking about needle “thickness,” which one of the three previously mentioned variables am I referring
to? If you thought “gauge,” you thought correctly. The “gauge” of a syringe pertains solely to the thickness of
the needle. Choosing the correct gauge is the an important factor in needle selection, because if you choose
a gauge number which is too high, the oil will not fit through (or at least be very difficult to force through)
and if you choose a gauge number which is too low, you will be piercing your tissue with an unnecessarily
thick needle and cause more tissue damage, scarring, and trauma than necessary. The most basic rule to
follow when it comes to gauge selection for your injection needle is to choose the highest gauge number
possible, BUT which will still allow the oil to flow through the needle easily. This will make the injection
nominally invasive, while reducing discomfort and minimizing scar tissue buildup. There is no machismo in
using a needle which is thicker than necessary—only idiocy.

Today, almost all steroids will fit through a 25 gauge syringe, so this gauge size should be your automatic go-
to choice when the viscosity of a steroid is unknown. This gauge is relatively thin in comparison to the
syringes used back in the day. Not too long ago the viscosity of many oil-based steroids was much higher than
it is today, requiring the use of 21-22 g. needle for basically every injection—and in some cases, such as when
injecting crude forms of Testosterone suspension or injectable Winstrol, an 18 g. syringe would be required
just to be able to fit the steroid crystals through the needle without clogging it. For those of you who are
trying to mentally picture an 18 g. needle without a reference point, it is more like a small nail than a needle.
Today, things are much easier.

Needle Lengths For Injection Sites

The recommendations below are the “average” needle lengths used for each body part listed.

• Glutes: 1-1.5 inch (For one's first purchase, unless you are exceptionally lean, it's best to stay with 1.5"
needles for Glutes to make sure you inject deep enough into the muscle.)
• Ventro Glutes: 1 inch
• Delts: 1 inch (some individuals can get away with ½ inch)
• Quads: 1 inch (some individuals can use as small as a ½ inch needle when injecting into the quads, depending
on how lean they are).
• Chest: ½-1 inch
• Biceps: ½-1 inch
• Triceps: ½-1 inch
• Calves: ½ inch
• Traps: ½-1 inch
• Lats: 1 inch

CC & mL
The term “cc” stands for cubic centimeters and is a unit of measurement for determining injection volume. It
is important to note that the term “cc” and “mL” (milliliter) are identical and interchangeable with each
other. 1 cc = 1 mL.

While syringes will indicate measurement in cc’s, steroid products (vials/bottles/ampules) will almost always
use ml’s as their unit of measurement. So, if your steroid product says it contains 10 ml per bottle at 250
mg/mL, you know it also contains 10 cc’s per bottle at 250 mg/cc. Therefore, if you wanted to inject 500 mg
of that steroid, you would need to inject 2cc’s (2 mL’s) of that product.

Syringe Size
Most 23-27 g syringes hold 3 cc’s, although some will occasionally hold less, so you when ordering you should
always specify exactly what you want to purchase. Since 3 cc syringes are no more costly than their smaller
counterparts and being that many steroid users will often inject more than 1 cc at a time, it makes sense to
strictly purchase 3 cc syringes for steroid injections (with the exception for the rare occasion you need
larger).

Syringe, Needles, etc. Suppliers

• [Apollo Lab Supply](www.apollolabsupply.com)

• GPZ Med Lab
• Total Diabetes Supply
• Medical Laboratory Supply
• Androusa

Rotating Injection Sites

One issue which may eventually arise if the individual continues injecting AAS long enough is the issue of scar
tissue build-up. Scar tissue is a dense, fibrous, connective tissue which forms over a wound or cut, either
external or internal. In the case of injection, the scar tissue formed is internal. Scar tissue can impede
contraction (make the muscle weaker), impair local muscle growth, decrease flexibility, and increase the
possibility of re-injury.
 Some scar tissue formation is unavoidable, as every time an injection is administered, scar tissue is formed.
The bottom line is that excess & problematic scar tissue is not something you want to have to deal with at
any point. Fortunately, we can take steps to minimize the appearance of scar tissue through rotating injection
sites. Scar tissue is much more likely to form to a greater degree if you repeatedly and frequently use the
same injection site. For this reason, it is a good idea to start a “rotation”, in which injections sites are
routinely transferred from one site to the next in a systematic fashion. Typically, the individual will select at
least 3 body parts to include in this rotation, while also altering the sites within each bodypart, in order to
decrease the number of times the same area is injected into per rotation.

Injection Frequency

How often a particular steroid should be administered will depend on a few factors, with injection frequency
being governed primarily by the half-life of each steroid. Obviously, longer-acting AAS will require a less
frequent injection schedule, while the opposite holds true for shorter acting versions. With injectable
steroids, the length of time it will stay active in the body depends on the type of ester which has been
attached to the steroid. Esters are molecular modifications to a steroid hormone, which have been added
solely to extend the life of the drug within the body.

When attempting to determine the injection frequency of a particular steroid, examine the ester and you will
have your answer. While there is some dispute regarding the proper injection frequency required among the
various esters, the differences in opinion are minimal.

Below is a list of some common esters used, along with the most commonly recommended injection
frequencies for each one:

• Acetate: ED
• Propionate: ED
• Phenylpropionate: ED or EOD
• Caproate: E3D or E3.5D
• Isocaproate: E3D or E3.5D
• Enanthate: E3D or E3.5D
• Cypionate: E3D or E3.5D
• Decanoate: E3D or E3.5D
• Undecanoate: E3D or E3.5D
• Undecyclenate: E3D or E3.5D
Note: These are just suggestions. If you choose to do less frequent injections you may be more susceptible to
side effects due to fluctuations in blood levels. If you wish to inject more frequently, regardless of ester, then
it is perfectly fine; it will only help blood levels be more stable.
 Some injectable AAS have no ester, such as the various suspensions & bases, such as Injectable Anadrol,
Injectable Winstrol, Trenbolone No Ester (TrNE) or Testosterone No Ester (TNE). These compounds are
typically injected 30 to 90 minutes preworkout.

Sterilization

Sterilization is a critically important part of the injection process, as unsanitary injection practices pose the
greatest risk in terms of acquiring serious infections & abscesses. As described above, these are health
problems you want to avoid at all costs and investing a little extra time and consideration into this aspect of
your program can go a long way towards ensuring you remain problem free.

There are 3 key components you have control over and which need to remain sterile at all times. They are the
needle(s) being used, the injection site(s), and the rubber stopper(s) of each vial you will be drawing from. It
is your job to make sure these components do not come in contact with anything other than the intended
object. When it comes to ensuring sterility, alcohol is your weapon of choice. Alcohol kills more germs &
bacteria safely, than any other household product. Sterilizing an injection site or object is a simple process.
Prior to sterilization, clean the area of any debris so that it appears visually clean. Afterwards, grab a alcohol
pad or wet a cotton swab with alcohol and wipe the intended area. After the area/object has been sterilized,
it should not come in contact with any other unsterilized object.

Note: The World Health Organization (WHO) states in their latest advice that swabbing with
alcohol beforehand, like aspiration, is an unnecessary and outdated practice so long as the surface is visibly
clean.

According to the medical establishment, an injection site should be covered with an appropriate bandage
post-injection. While this will help further ensure that bacteria does not enter the injection site and cause
infection, this practice is rarely employed among AAS users, typically with little to no negative consequences.

WHO: Alcohol swab skin prep is unnecessary

The procedure is superfluous so long as you're in a relatively clean environment—not in an infectious

diseases wing or exposed high-risk patients in an ICU ward.

Multiple trials were conducted and there was no difference in the infection rate. Swabbing has gone the way
of aspirating your pins.
• Skin antisepsis does not reduce incidence of infection
• Routine skin prep with alcohol swab: Is it necessary? (No)
• Intramuscular injections: To swab or not to swab
• Effectiveness of Alcohol Swabs for Preventing Infections
Using A Draw Needle

In order to properly load your syringe correctly, it will require 2 different syringes or more specifically, two
different needles. One needle will be required for drawing the steroid into the barrel, while the other needle
head will be used to inject the steroid.

The primary reason for using two different needles is due to the delicacy of needles, in general. Pushing a
needle through a rubber stopper or into muscle tissue just a single time will dull the needle considerably. In
fact, when viewing enhanced images of needles which have already pierced human muscle tissue, the viewer
can clearly see that the tip of the needle has been bent. The act of injecting is already an invasive process and
in order to minimize both discomfort, as well as scar tissue build-up, a fresh needle head should be used
every time when doing an IM injection. Close up view of a needle after penetrations.

A secondary reason for using one needle to draw with and another to inject is that it can take a long time to
draw a few cc’s of oil through a 25g. syringe or smaller. By using a lower gauge number to draw with (usually
18-22g.), it cuts down on the amount of time required to draw the oil into the barrel. It's recommended using
no smaller than a 21-22g pin to draw with is because bigger pins can damage the rubber stopper after
repeated uses, potentially allowing little pieces of rubber to break away from the rubber stopper and fall into
the vial. A 21-22g pin is sufficient for quick drawing and will more thoroughly maintain the integrity of the
rubber stopper.

Insulin Needles & BackLoading

While performing a sub-q inject with a dull 39-30 g. insulin syringe is not going to be as unpleasant as
performing an I.M. injection with a dull 23 g. syringe, the user can still take steps to ensure that ever injection
is performed with a fresh, sharp needle. Due to insulin syringes being so much smaller and more fragile than
their 23-25 g. counterparts, they dull much more quickly. The act of pushing an insulin syringe through a
rubber stopper even one time will significantly dull the needle head.

However, since the needle head of an insulin syringe can not be removed, as they can be with larger pins, the
only way to inject with a fresh needle head is by back-loading. The practice of back-loading is self-
explanatory. You simply load the pin through the back end instead of loading the pin through the needle
head. This is easily accomplished by using one insulin syringe (or any other syringe) to draw with and a
second insulin pin for the injection.

In order to back-load, begin by getting out 2 insulin syringes and setting them in front of you. Select one as
your drawing syringe and one as the injecting syringe. Load your drawing syringe as you normally would and
then set it down on a table, etc. Pick up your injecting syringe and remove the back plunger. You then want
to carefully squirt the contents of the loaded syringe into the back of the injecting syringe without letting any
spill out the back. At that point, pick up the plunger, gently press it back into the barrel, but not fully
inserting. Then, you flip the needle and wait for ALL the liquid to go to the bottom. Once it does, you may
now fully insert the plunger and you are done.
Very Helpful Video On Back-Loading

Disposal Of Used Needles/Syringes

When disposing of used syringes, it is of primary importance that the original protective covering be placed
back on the syringe prior to discarding. This will prevent anyone from accidentally coming in contact with the
syringe and accidentally piercing their skin. No one wants to be pulling a used needle out of their hand,
because the user was negligent in his responsibilities.

In addition, most individuals will place their used syringes in a medical sharps storage container designated
only for syringes, in order to minimize the occurrence of someone coming into contact with a stray needle.
But there are people who are negligent and use empty protein containers, plastic milk containers, juice
containers, etc., for disposal of their used syringes. Regardless of which method you employ, find out how to
legally dispose of your pins.

Aspiration

Note: The World Health Organization (WHO) states in their latest advice that aspirating is unnecessary, and
frequently causes more harm than good.

The act as aspirating was traditionally performed as safety measure to prevent one from accidentally
injecting directly into a blood vessel. In order to perform this simple procedure, one must have fully inserted
the needle into the injection site. Once the needle has been fully inserted, but before depressing the plunger,
gently draw (pull) back on the plunger by a few millimeters. If no blood enters the barrel, you are safe to
proceed with the injection. If blood pours back into the barrel, you have entered a blood vessel and need to
relocate the syringe.

Seeing traces or specks of blood is not indicative that you have entered a blood vessel. Typically, when a vein
(blood vessel) has been threaded, blood will pour into the barrel when pulling back the plunger. If you do
thread a blood vessel, you do not necessarily have to completely remove the syringe and start over again.
First, try pulling the needle out 1/4-1/2 inch and then try aspirating again. If blood does not pour into the
barrel after this 2nd attempt, then you have exited the blood vessel and are safe to proceed. If blood does
continue to enter the barrel, you will have to remove the needle and find a new injection site.

Aspiration is no longer recommended by any of the major health organizations.

Is Aspirating Required?
Answer: Many AAS users do not aspirate when injecting. It is considered a bit of an outdated methodology.
 The reason aspiration is no longer taught is that the major injection sites lack nerves or significant surface
blood vessels. Furthermore, even a tiny shift in movement while pinning can make the difference between
hitting a blood vessel or missing, so even if you aspirate, you can still end up hitting a vessel.

The act of aspirating also involves significant movement which causes further trauma to the muscle. If by
chance you inject into a vein, it will nearly immediately collapse, and is entirely harmless. It's nearly
impossible to inject intravenously while injecting IM at a ninety degree angle.

According to the CDC:

Aspiration: “Aspiration is the process of pulling back on the plunger of the syringe prior to injection to ensure
that the medication is not injected into a blood vessel. Although this practice is advocated by some experts,
the procedure is not required because no large blood vessels exist at the recommended injection sites.”
STTI International Nursing Research Congress Vancouver, July 2009:
"Aspiration is not indicated for SC injections."
"Aspiration is not indicated for IM injections."
Organizations which state aspiration is not necessary:
• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)
References located at the bottom of the page.

Safe Injecting Technique

Single Vial
1. Use A Draw Needle: Without one, you will dull your pin needle to the point that it'll be very painful and
potentially give a pip.
Note: If your syringes come with the needles already attached, order the drawing needle to come on them.
Otherwise, you'll have to switch needles, more than necessary. Close up view of a needle after penetrations.
2. Clean The Vial: Wipe top of the vial with an alcohol pad/swab and let dry.
3. Draw Air: Uncap the needle and fill the syringe with as much air as you plan to withdraw in liquid. (i.e. If you
plan to inject 1.5 mL/cc of liquid, you will draw 1.5 mL/cc of air.)
4. Inject The Air Into The Vial: Inject the air into the vial to create positive pressure inside the vial. This will
assist and make drawing easier.
5. Draw The Liquid: Draw your required mL/cc of liquid while ensuring to keep the needle point in the liquid.
6. Change To Your Injection Needle: Cap the drawing needle and remove the drawing needle from the syringe.
Attach your injection needle to the syringe.
7. Clean The Area: Clean the area you want to inject with a new alcohol swab in an outward going circular
motion and let dry. Uncap your injection needle.
8. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert the needle. This serves to decrease the
chances of muscle spasms.
9. Insert The Needle: Insert needle in a fast and precise motion, push needle in until 2 mm or so is exposed.
10. Aspiration (OPTIONAL): Gently draw (pull) back on the plunger by a few millimeters. If no blood enters the
barrel, proceed. If blood pours into the barrel, see [Aspiration]( )
11. Push The Plunger: Push the plunger on the syringe, injecting the liquid into the muscle slowly and smoothly.
Note: As a general rule of thumb, always inject slowly; take 30 seconds per mL.
12. Pull The Needle Out: Pull the needle out and cap it, then swab the area with a alcohol pad/swab.
13. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.

Multiple Vials
1. Use A Draw Needle: Without one, you will dull your pin needle to the point that it'll be very painful and
potentially give a pip.
Note: If your syringes come with the needles already attached, order the drawing needle to come on them.
Otherwise, you'll have to switch needles, more than necessary. Close up view of a needle after penetrations.
2. Clean The Vials: Wipe all of the vial tops with alcohol pad/swab, and let them dry.
3. Draw Air & Inject Air: Uncap the draw needle and fill the syringe with as much air as you plan to withdraw in
liquid for the 1st vial. (i.e. If you plan to inject 1.5 mL/cc of liquid, you will draw 1.5 mL/cc of air.) Then, Inject
the air into the vial and pull out the needle. Repeat for each vial.
4. Draw The Liquid: Pick the "most important" compound to draw first. (i.e. the one that I want the dose to be
the most exact). Load the pin with that compound. Going down the line of "importance", in the rest.
Note: Pick the "most important" compound to inject air into last. This way you can immediately start drawing
after injecting the air.
5. Change To Your Injection Needle: Cap the drawing needle and remove the drawing needle from the syringe.
Attach your injection needle to the syringe.
6. Clean The Area: Clean the area you want to inject with a new alcohol swab in an outward going circular
motion and let dry. Uncap your injection needle.
7. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert the needle. This serves to decrease the
chances of muscle spasms.
8. Insert The Needle: Insert needle in a fast and precise motion, push needle in until 2 mm or so is exposed.
9. Push The Plunger: Push the plunger on the syringe, injecting the liquid into the muscle slowly and smoothly.
Note: As a general rule of thumb, always inject slowly; take 30 seconds per mL.
10. Pull The Needle Out: Pull the needle out and cap it, then swab the area with a alcohol pad/swab.
11. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.

Ampoules
This is a very helpful video.
1. Grasp The Ampule: Grasp the ampule between thumb and forefinger of one hand.
2. Move All Liquid To The Bottom: Move liquid from the neck to the body of the ampule by tapping (thumping)
the ampule sharply.
3. Break The Ampule: Using gauze pad (or similar), grasp stem (the part above the neck) with other hand. Break
stem away from you and discard safely. Note: Another option is to get an ampule opener.
4. Set Ampule Upright: Set ampule upright on a flat and sturdy surface.
5. If Necessary, Reconstitute: If your ampule came unconstituted, reconstitute the compound with
bacteriostatic water or whatever liquid you are using. Make sure ampule is fully reconstituted before
drawing. Note: To find out dosing for HCG use this HCG calculator.
6. USE A SPECIAL FILTER NEEDLE TO DRAW LIQUID
7. Insert Filter Needle Into Ampule: Remove filter needle cap and insert the filter needle into the liquid.
8. Draw The Liquid: If needle is sufficiently long, draw the liquid with the ampule in the upright position. If a
short needle is used invert the ampule and draw the liquid.
9. Set Ampule Aside: If you are drawing multiple times to different non-insulin syringes, set the ampule in an
upright position. If you are - see below, otherwise, discard safely.
10. Remove Filter Needle: Draw (pull) back the plunger slightly to remove any liquid from the filter needle. Place
the needle cap back on and remove the filter needle.
11. Change To Your Injection Needle: Cap the filter needle and remove the filter needle from the syringe. Attach
your injection needle to the syringe.
12. Clean The Area: Clean the area you want to inject with a new alcohol swab in an outward going circular
motion and let dry. Uncap your injection needle.
13. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert the needle. This serves to decrease the
chances of muscle spasms.
14. Insert The Needle: Insert needle in a fast and precise motion, push needle in until 2 mm or so is exposed.
15. Push The Plunger: Push the plunger on the syringe, injecting the liquid into the muscle slowly and smoothly.
Note: As a general rule of thumb, always inject slowly; take 30 seconds per mL.
16. Pull The Needle Out: Pull the needle out and cap it, then swab the area with a alcohol pad/swab.
17. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.

Ampules To Sterile Vial

1. Grasp The Ampule: Grasp the ampule between thumb and forefinger of one hand.
2. Move All Liquid To The Bottom: Move liquid from the neck to the body of the ampule by tapping (thumping)
the ampule sharply.
3. Break The Ampule: Using gauze pad (or similar), grasp stem (the part above the neck) with other hand. Break
stem away from you and discard safely. Note: Another option is to get an ampule opener.
4. Set Ampule Upright: Set ampule upright on a flat and sturdy surface.
5. If Necessary, Reconstitute: If your ampule came unconstituted, reconstitute the compound with
bacteriostatic water or whatever liquid you are using. Make sure ampule is fully reconstituted before
drawing. Note: To find out dosing for HCG use this HCG calculator.
6. USE A SPECIAL FILTER NEEDLE TO DRAW LIQUID.
7. Insert Filter Needle Into Ampule: Remove filter needle cap and insert the filter needle into the liquid.
8. Draw The Liquid: If needle is sufficiently long, draw the liquid with the ampule in the upright position. If a
short needle is used invert the ampule and draw the liquid.
9. Set Ampule Aside: If you are drawing multiple times to different non-insulin syringes, set the ampule in an
upright position. If you are - see below, otherwise, discard safely.
10. Remove Filter Needle: Draw (pull) back the plunger slightly to remove any liquid from the filter needle. Place
the needle cap back on and remove the filter needle. Attach any normal needle to the syringe.
11. Clean The Vial: Wipe the vial top of your STERILE vial with alcohol pad/swab, and let them dry. Note: Most
places that sell syringes/needles will also sell sterile vials.
12. Inject The Liquid Into The Sterile Vial And Store Properly Until Needed.
When Needed, Draw and Inject:
1. Clean The Vial: Wipe top of the vial with an alcohol pad/swab and let dry.
2. Draw The Liquid: Uncap the insulin syringe and insert the needle through the stopper of the vial. Draw your
required iu/mL of liquid while ensuring to keep the needle point in the liquid. Remove and replace the cap on
the insulin syringe.
3. Clean The Area: Clean the area you want to inject with a new alcohol swab in an outward going circular
motion and let dry. Uncap your insulin needle.
4. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert the needle. This serves to decrease the
chances of muscle spasms. Note: This is not necessary for subcutaneous injections
5. Insert The Needle: Insert needle in a fast and precise motion, push needle in until ~2 mm is exposed.
6. Push The Plunger: Push the plunger on the syringe, injecting the liquid slowly and smoothly.
7. Pull The Needle Out: Pull the needle out and cap it, then swab the area with a alcohol pad/swab.
8. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.

Ampules To Preloaded Insulin Syringes

Here's Is An Alternate Way Of Preloading Insulin Syringes vs. Using A Sterile Vial. Taken From This Thread
1. Grasp The Ampule: Grasp the ampule between thumb and forefinger of one hand.
2. Move All Liquid To The Bottom: Move liquid from the neck to the body of the ampule by tapping (thumping)
the ampule sharply.
3. Break The Ampule: Using gauze pad (or similar), grasp stem (the part above the neck) with other hand. Break
stem away from you and discard safely. Note: Another option is to get an ampule opener.
4. Set Ampule Upright: Set ampule upright on a flat and sturdy surface.
5. If Necessary, Reconstitute: If your ampule came unconstituted, reconstitute the compound with
bacteriostatic water or whatever liquid you are using. Make sure ampule is fully reconstituted before
drawing. Note: To find out dosing for HCG use this HCG calculator.
6. USE A SPECIAL FILTER NEEDLE TO DRAW LIQUID.
7. Insert Filter Needle Into Ampule: Remove filter needle cap and insert the filter needle into the liquid.
8. Draw The Liquid: If needle is sufficiently long, draw the liquid with the ampule in the upright position. If a
short needle is used invert the ampule and draw the liquid.
9. Set Ampule Aside: If you are drawing multiple times to different non-insulin syringes, set the ampule in an
upright position. If you are - see below, otherwise, discard safely.
10. Remove Filter Needle: Draw (pull) back the plunger slightly to remove any liquid from the filter needle. Place
the needle cap back on and remove the filter needle.
11. Insert Insulin Needle: Remove the cap on the insulin syringe. Put the insulin syringe into the top of the
syringe you used to draw the liquid with; where the needle would normally attach to the syringe.

12. Slowly, carefully, push the liquid up so that you can suck it out with the insulin needle. Cap the insulin needle
and repeat until done. Store properly until needed.

When Needed, Draw and Inject:

1. Clean The Area: Clean the area you want to inject with a new alcohol swab in an outward going circular
motion and let dry. Uncap your insulin needle.
2. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert the needle. This serves to decrease the
chances of muscle spasms. Note: This is not necessary for subcutaneous injections
3. Insert The Needle: Insert needle in a fast and precise motion, push needle in until ~2 mm is exposed.
4. Push The Plunger: Push the plunger on the syringe, injecting the liquid slowly and smoothly.
5. Pull The Needle Out: Pull the needle out and cap it, then swab the area with a alcohol pad/swab.
6. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.

Special Injection Techniques

The purpose of the below injection techniques is to seal the injected compound deep within the muscle, by
allowing no exit path back into the subcutaneous area and skin. While using these techniques is not essential
to performing a proper injection, they will allow the user to minimize oil loss due to seepage.

• Z-track Technique: A technique utilized to prevent leakage of the injected substance post-injection.
• Air Bubble Technique: A technique utilized to prevent leakage of the injected substance post-injection.

Z-track Technique
The Z-track method requires temporarily displacing the skin & subcutaneous tissue prior to injection and
immediately releasing the tissue post-injection. In order to perform the Z-track method, prepare your syringe
and be ready to inject. Once the syringe is in hand, use your free hand to pull the skin at the injection site ½-1
inch away from its original location. While continuing to hold the skin in this stretched position, administer
the injection into the original location. Immediately after removing the syringe from the injection site, release
the skin which was being held in place. The Z-track method works best at locations where there is a greater
amount of lose skin. Utilizing locations with taut skin will be more difficult.

Very Helpful Video To See Technique

Air Bubble Technique

The air bubble technique involves injecting a small amount of air at the end of an injection. In order to
perform this technique prepare your syringe and be ready to inject. When the syringe is in hand, pull ½ cc/mL
of air into the syringe. Just prior to and throughout the injection, make sure the needle is pointing down, so
that the air floats to the top of the barrel (near the plunger) and is the last thing to be injected into the
muscle, as it is this small air bubble which will help to seal off the opening and prevent leakage. This is also
used by some to make sure all of the liquid they are injecting is out of the needle.

PIP (Post Injection Pain)

What Causes (Non-Infectious) Injection Pain?

• The Shorter The Ester, The Higher The Melting Point
• The Concentration Of The Gear
• The Solvents Used
• Injecting Too Quickly
• Virgin Muscle
The Shorter The Ester, The Higher The Melting Point
One thing that can cause pain is when the oil/solvents are absorbed by the body and crystals are left behind.
Short esters (Propionate, Acetate, etc.) are harder, more painful crystals with melting points in the 100c
range. A hormone with a longer ester (excluding Cypionate - Cyp is a long ester, but also has a high melting
point) can have a melting point in the 20c-40c range; not far off from human body temp.
The Concentration Of The Gear
Pain can also be caused by concentration of your gear. Building off of point 1: Hypothetically, let's say it takes
the body 24 hours to absorb 1mL of a certain oil/solvent blend and 24 hours to absorb 50mg of Testosterone
Propionate. If 50mg (or less) of Testosterone Propionate is in 1mL of that oil, this injection should be painless.
 On the other hand, if 100mg of Testosterone Propionate is in that same 1mL of solution, then after 24 hours
the body will have absorbed 50mg and 1mL, leaving 50mg behind in the injection area, crystalized and
painful.

It's better to shoot 3mL of 150mg/mL Testosterone Propionate, than 1mL of 150mg/mL Testosterone
Propionate.

This is also why water based suspensions (Testosterone base/no ester, Winstrol, etc.) hurt the most; water is
very easily absorbed in the body.

The Solvents Used

The solvents used can cause pain in two ways. Benzyl alcohol (BA) is used at 1-2% as a preservative and
antiseptic. If the alcohol content is too high the gear will burn. Pain in the first 24 hours is usually caused by
heavy solvents, pain in the next few hours is usually cause by crystallization. Another way is a bad recipe. If
someone used 2% BA, and the rest of the solution oil, the mg/mL would have to be low due to oil's weak
ability to hold crystals. On the other hand, a recipe like 2% BA, 5% Guaiacol (super solvent), 10% Benzyl
Salicylate (liquid aspirin) with the filler split 50:50 between Ethyl Oleate (oil/solvent hybrid) and normal oil
should be far less painful.

Injecting Too Quickly

If you inject too quickly, it can potentially tear tissue.

Virgin Muscle

If your muscle is new to the hormone, it will absorb the hormone slowly, but absorb the oil/solvent quicker.
This will cause more crystallization and pain. As your muscles recognize the hormones, they will be absorbed
more quickly, thus less pain. The deeper you inject into the center of a muscle group, the better.

How do I prevent pain before I inject?

• Cutting The Oil With Sterile Oil
• Warming Up The Oil
• Inject Slowly
• What If None Of Those Help?
Cutting The Oil With Sterile Oil
Cut your shots 50:50 with sterile filtered oil. If you want to use 50mg of Testosterone Propionate and you
have 100mg/mL Testosterone Propionate - pull 0.5mL of your Test Prop and 0.5mL of sterile filtered oil to
shoot 1mL of 50mg/mL Testosterone Propionate. This is the #1 best way. Don't bother with B-12, as it’s water
based and absorbed so quickly it will have little to no impact.
Warming Up The Oil
Before you shoot, it can help to warm your gear (especially suspensions). Carefully making sure the vial
 stopper (top) doesn't touch the water, you can put the vial in the bathroom sink and let hot water run over
the vial for ~2 minutes and shake well. This will lower the oils viscosity also making it easier it pull into the
syringe. One way some will make sure the vial doesn't touch the water, is to put the vial inside a zip lock bag.
If you don't want to constantly be reheating the entire vial each time, alternatively you can do the same once
you've drawn the oil into the syringe. If you heat the syringe it is recommended to use a zip lock bag or the
likes to protect the syringe from being exposed to the water.
Injecting Slowly
Inject slowly; take 30 seconds per mL. Use a 25g pin to inject so it forces you to move slower.
What If None Of Those Help?

If none of these work, you could have dirty gear. It’s possible there could be particles (although
bacteriostatic) in the gear that made it through the filter and is causing infection, although mild.
Alternatively, if using higher concentration gear, your gear is just too high concentration to be tolerable for
you.

How do I deal with pain once I have it?

The worst thing you can do is ice it. Cold will help the crystals fall out of solution/suspension. It’s okay to take
some ibuprofen to decrease the swelling and help with pain. Also being in a hot tub, jacuzzi, or warm bubble
bath will help melt the crystals down. Using a heating pad can help as well.

Where Do I Inject?

Inevitably, one of the first questions many individuals will ask themselves shortly before their 1st injection is
“where do I inject?” While there is no right or wrong answer, the most commonly injected muscle among
first time users are the Glutes. It is a muscle group that's relatively painless (potentially), does not have any
major veins/arteries near the surface, and contains a lower density of nerves. The twisting and turning can be
a problem for some, in which case injecting Ventro Glutes is another option. If that is too hard to find for you,
try Quads, but there is a slightly larger margin for error in regard to hitting nerve clusters and puncturing
large veins. But you should aim to have as many injection sites as possible to avoid building scar tissue.

Basically, any muscle can be injected into, although larger, thicker muscles are typically superior to small,
shallow muscle groups. An example of a body part which falls into the latter category would be the forearms.
This body part is rarely ever injected into and is a poor choice all the way around, so avoid them. Never inject
into the hands, feet, or neck

Locations To Inject

Noteworthy Sites For Injection Descriptions:

• Spot Injections
• IPED Info
 Glutes (Dorsogluteal)
When people talk about injecting Glutes, they are referring to injecting into the Gluteus Maximus / Gluteus
Medius via dorsogluteal.

Diagram For Injection Area Glutes Injection Photos (Thanks to Spot Injections)
Helpful Dorsogluteal Injection Video
Another Helpful Glutes Video

Ventro Glutes
Ventro Glutes is the common term, but in actuality we are injecting into the Gluteus Medius via
ventrogluteal.

Start by finding three bony landmarks - the greater trochanter (at your hip joint), the iliac crest (top of your
pelvis), and the anterior superior iliac spine (front of your pelvis). Diagram for reference. Now that you've
found these markers it's time to find the injection spot. We'll be injecting the gluteus medius. Think of an
imaginary line between the iliac crest (IC) and the greater trochanter (GT); now imagine another line
intersecting that one from the anterior superior iliac spine (ASIS). Where those lines meet is your spot.
• A Picture For Reference
• Diagram For Reference
• Additional Diagram For Reference
• Additional Diagram For Reference
• Additional Diagram For Reference
• Penis Pic... Just To Be Sure.

This spot may feel hard, almost like bone; but as long as you stay in the prescribed spot you will be fine. Here
are some techniques to further clarify the injection spot.

• Lay on your side and put your hand on the prescribed area. Now raise your leg like so. You will feel a muscle
flex. That is your gluteus medius.
• Stand up and place your hand on the prescribed area. Now shift your weight from one foot to the other. You
will feel a muscle tense. This is your gluteus medius.

When you're confident you've found the correct spot begin your injection routine.

Excellent Video On The Process Of Finding Vento Glutes

Quads (Vastus Lateralis)

When injecting into the Quads it can be a bit trickier. Never inject into the inner-thighs…only inject into the
actual quadriceps muscles themselves, particularly the Vastus Lateralis. The Rectus Femoris can also be
injected, but most users will find it more painful and increases the risk of hitting a nerve (causing the muscle
to "twitch"). Lastly, the Vastus Medialis (teardrop) can be injected into as well, although it is not a preferred
area, especially for a beginner.

Quads Injection Photos (Thanks to Spot Injections)

Very Helpful Video Of Locating The Vastus Lateralis

Delts (Deltoid)
When injecting into the delts, all 3 heads are suitable, although the side & rear heads are a bit more
comfortable, on average.

Diagram For Injection Area

Delts Injection Photos (Thanks to Spot Injections)
Helpful Delt Injection Video

Chest (Pecs)
The diagram below shows the places on your Chest (Pec) where you can inject. In the Photos they just use
the upper options. In the video below he uses the lowest option. It is just a preference thing; try them all and
see what you like best.

Diagram For All Three Injection Areas

Chest Injection Photos (The Upper Options) (Thanks to Spot Injections)
Helpful Chest Injection Video (He Does The Lowest Option)

Lats (Latissimus)
Diagram For Injection Area
Lats Injection Photos (Thanks to Spot Injections)
Very Helpful Lats Injection Video

Traps (Trapezius)
Diagram For Injection Area
Traps Injection Photos (Thanks to Spot Injections)

Triceps
For Triceps, there are three heads you may inject in: The outer (horseshoe) tricep head, the lower rear tricep
head, and middle rear tricep head.

Diagram For Injection Area (Horseshoe)

Diagram For Injection Area (Lower Rear)
Diagram For Injection Area (Middle Rear)
Triceps Injection Photos (Horseshoe) (Thanks to Spot Injections)
Helpful Triceps Injection Video

Biceps
For Biceps, there are two heads you may inject in: The outer bicep head, and outer bicep head.

Diagram For Injection Area (Inner)

Diagram For Injection Area (Outer)
Biceps Injection Photos (Thanks to Spot Injections)

Calves
Diagram For Injection Area
Calves Injection Photos (Thanks to Spot Injections)

Subcutaneous (SubQ)
SubQ is excellent for TRT or cruising purposes. See Injection Tips in the TRT page.

Volume Each Site Can Hold

Site Volume

Glutes (Dorsogluteal) 3-5 mL/cc

Ventro Glutes 3-5 mL/cc

Quads (Vastus Lateralis) 3-5 mL/cc

Delts 2-3 mL/cc

Chest 2 mL/cc

Lats 2 mL/cc

Traps 2 mL/cc

Triceps 1.5 mL/cc

Biceps 1.5 mL/cc

Calves 1.5 mL/cc

Subcutaneous (SubQ) < .5 mL/cc

Frequently Asked Questions (FAQ)

Below are common questions and answers regarding injecting.

 My Injection Spot Is Red, Itchy, Or Sore?
Answer: Get to a doctor for some antibiotics if it is red, itchy, or hot. If it is simply sore and/or swollen it is
probably going to be okay see: Post Injection Pain (PIP). If in doubt, get some antibiotics; a common thing to
tell your doctor is that you injected B12.

Is It Normal To Bleed After An Injection?”

Answer: Yes, it is common to occasionally nick a vein close to the surface of the injection site, which will
cause blood to leak from the surface. The amount of blood which can seep from an injection site can be
anywhere from a drop or two, to a very light stream which slowly flows down that body part. Even in the
event a larger vein is hit when doing an injection, this type of bleeding is relatively easy to stop and will not
pose any harm to the individual.

Is Aspirating Required?
Answer: Many AAS users do not aspirate when injecting. It is considered a bit of an out-dated methodology,
but it never hurts to do it.
According to the CDC:
Aspiration - Aspiration is the process of pulling back on the plunger of the syringe prior to injection to ensure
that the medication is not injected into a blood vessel. Although this practice is advocated by some experts,
the procedure is not required because no large blood vessels exist at the recommended injection sites."
STTI International Nursing Research Congress Vancouver, July 2009:
"Aspiration is not indicated for SC injections."

"Aspiration is not indicated for IM injections."

Organizations which state aspiration is not necessary:
• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)
References located at the bottom of the page.

Does Injecting Build Up Scar Tissue?

Answer: Yes, repeated Intramuscular injections can cause the muscle to build up scar tissue. Generally there
is no inflammation or inclusion in the tissue. In an effort to minimize scar tissue build up, users will rotate
through many injection sites. If you're interested, here is a case study of a woman in an extreme case, it
includes stained muscle biopsies
How Do I Open Ampules?
Answer: Ampules can be aided in opening by scoring (some ampules come pre-scored). Scoring is a process in
which in a fine line is ground away around the neck of the ampule. Scoring makes it much easier to snap the
top of the ampule off without breaking the vial and spilling the oil. Normally, a scoring tool is used for this
process, although sometimes knives or other objects can be used.

An amp opener can be used, which is the fastest and the least time consuming methods.

If you don't have an ampule opener. Grasp the ampule between thumb and forefinger of one hand. Move
liquid from the neck to the body of the ampule by tapping (thumping) the ampule sharply. Using gauze pad
(or similar), grasp stem (the part above the neck) with other hand. Break stem away from you and discard
safely. This is a very helpful video that shows the process

Lastly, the tape-method can be employed, as well. The tape method involves taping the entire vial all the way
up to the neck line. Several layers of tape should surround the vial, so that it is properly secured. The point of
taping the vial is two-fold. One purpose is to prevent the contents of the ampule from spilling, should the
ampule break somewhere other than the neckline. The other purpose is to reinforce the ampule, so that it is
more likely to break at the neckline. One can combine both the tape method and the scoring, which is the
best way to ensure that the oil contained in the ampule will not be spilled.

Can I Re-Use Syringes?

Answer: Absolutely not. You should never take a needle which has entered the body and re-insert it back into
a steroid product, as this can result in bacteria build-up and cause potential future infections.

How Fast Should I Inject?

Answer: As a general rule, 30 seconds per mL/cc.

Is It Dangerous To Inject Small Air Bubbles?”

Answer: No, a small amount of air will do no harm. Air bubbles injected into muscle tissue is of no concern.
Even if the individual were to thread a vein and inject the entire contents of the syringe into the vein, the
small air bubbles contained within it would be the least of that person’s worries. In reality, several cc’s of air
would have to be injected directly into a vein all at once, in order to cause cardiac arrest. Even injecting 2-3
cc’s of air directly into a muscle would be largely inconsequential. Of course, such an action is not
recommended, but you get the point.

My Gear Crashed…How Do I Fix It?

Answer: Gear can crash due to storing the product in colder than recommended temperatures (or in
shipment)…or because the ratio of AAS to oil is out of balance (this can be either a manufacturer error or a
personal error if home brewing). This does not damage the steroid. In order to correct the problem, simply
 run the vial under warm water until the products reverts back to its normal state. Clean with alcohol swab
after drying off.

My Gear Has Particles Floating In It?

Answer: You can choose to either dispose of the product or you can re-filter it by using a Whatman filter.
While opinions will differ on this subject, the opinion of re-filtering is still available and a suitable solution in
many cases, assuming the product is not badly polluted. In cases where it is apparent that the product is very
poor quality and contains a large amount of foreign material, it would be wise to dispose of the product. This
should not occur with reputable UGL’s and will never occur with Pharm-grade versions, although an
occasional speck may occur with UGL products here and there and is usually not a big deal.

Related Posts

• How To Inject For Noobs.

• Aftermath Of An Abscess

References

Atkinson, W. L., Pickering, L. K., Schwartz, B., Weniger, B. G., Iskander, J. K., & Watson, J. C. (2002). General
Recommendations on Immunization: Recommendations of the Advisory Committee on Immunization Practices
(ACIP) and the American Academy of Family Physicians (AAFP). Morbidity and Mortality Weekly Report, 51,
RR2. 1-33.
Chiodini, J. (2001). Best practice in vaccine administration. Nursing Standard, 16(7), 35-38.
Diggle, L. (2007). Injection technique for immunization. Practice Nurse, 33(1), 34-37.
Gammel, J. A. (1927). Arterial embolism: an unusual complication following the intramuscular administration
of bismuth. Journal of the American Medical Association, 88, 998-1000.
Ipp, M., Taddio, A., Sam, J., Goldbach, M., & Parkin, P. C. (2007). Vaccine related pain: randomized controlled
trial of two injection technique Archives of Disease in Childhood,92,1105-1108.
Li, J.T., Lockey, R. F., Bernstein, I. L., Portnoy, J. M., & Nicklas, R. A. (2003). Allergen immunotherapy: A
practice parameter. Annuals of Allergy, Asthma, & Immunology, 1-40.
Livermore, P. (2003). Teaching home administration of sub-cutaneous methotrexate. Paediatric Nursing,
15(3), 28-32.
Middleton, D. B., Zimmerman, R. K., & Mitchell, K. B. (2003). Vaccine schedules and procedures, 2003. The
Journal of Family Practice, 52(1), S36-S46.
Nicoli, L. H., & Hesby, A. (2002). Intramuscular injection: An integrative research review and guidelines for
evidence-based practice. Applied Nursing Research,16(2), 149-162.
Ozel, A., Yavuz, H., & Erkul, I. (1995). Gangrene after penicillin injection: A case report. The Turkish Journal of
Pediatrics, 37(1), 567-71.
Peragallo-Dittko, V. (1995). Aspiration of the subcutaneous insulin injection: Clinical evaluation of needle size
and amount of subcutaneous fat. The Diabetes Educator, 21(4), 291-296.
Roger, M. A., & King, L. (2000). Drawing up and administering intramuscular injections: A review of the
literature. Journal of Advanced Nursing, 31(3), 574-582.
Talbert, J. L., Haslam, R. H. & Haller, J. A. (1967). Gangrene of the foot following intramuscular injection in the
lateral thigh: A case report with recommendations for prevention. The Journal of Pediatrics, 70(1), 110-114.
Workman, B. (1999). Safe injection techniques. Nursing Standard, 13 (39), 47-53.
World Health Organization (2004). Immunization in Practice, Module 6: Holding an immunization session.
Immunization in Practice: A practical resource guide for health workers –2004 update,1-29.
Center for Nursing History at Misericordia University: http://www.misericordia.edu17. Levels of Evidence,
Canadian Medical Association & Centre for Evidence-Based Medicine (2001). Available
at:http://www.cebm.net/index18. Melnyk, B. M., & Fineout-Overholt, E. (2005). Evidence-Based Practice in
Nursing & Healthcare: A Guide to Best Practice. Philadelphia: Lippincott, Williams & Wilkins.
Reference For A Lot Of Info Here
Reference For Volume

10 POST CYCLE THERAPY (PCT)

Post Cycle Therapy or PCT is a period of medication treatment that follows the use of anabolic steroids. Post
Cycle Therapy is also one of the most confusing topics for many steroid users; this is largely due to
misconceptions. When to start PCT, which meds to use, how long to use them and what you should expect,
these are all common questions and ones we’ll address here.

The Purpose of PCT

When we supplement with anabolic steroids we suppress our natural testosterone production. Testosterone,
the primary male hormone, is essential to our very well being. Most men who supplement with anabolic
steroids will always include at least a minimal amount of testosterone in their cycle due to this suppression
factor.

Following the use of exogenous anabolic steroids, the majority of users will experience what has been
dubbed a “hormonal crash” or “post cycle crash”, which is a bodily environment in which key hormones
essential to the retention of the newly created muscle mass has been suppressed or shut down. The key
hormones in question are LH (Luteinizing Hormone), FSH (Follicle Stimulating Hormone), and subsequently
(and most importantly), Testosterone. LH and FSH are known as gonadotropins, which are hormones that
signal the gonads (testes) to begin or increase the manufacture and secretion of Testosterone. Alongside low
levels of these hormones, the overall balance of total hormones will be essentially thrown off, whereby
Testosterone levels will be low, and most of the time (depending on many factors), Estrogen levels will be
higher, and levels of Cortisol (a steroid hormone that destroys muscle tissue) will be at normal levels. With
Testosterone levels low and Cortisol levels in the normal (or high) range, Cortisol now becomes a threat to
the newly created muscle that was created during the recent anabolic steroid cycle (Testosterone properly
suppresses and counteracts Cortisol’s catabolic effects on muscle tissue). SHBG (Sex Hormone Binding
Globulin) is also a concern here as well, which is a protein that binds to sex hormones (Testosterone) and
renders them inactive, essentially ‘handcuffing’ them and preventing them from exerting their effects. SHBG
will also normally be elevated during the post-cycle weeks as a result of the supraphysiological levels of
androgens from the recent anabolic steroid cycle.

The human body will normally restore this imbalance of hormones and recover its endogenous Testosterone
levels on its own over time with no assistance, but studies have demonstrated that without the intervention
of Testosterone stimulating agents, this will occur over the course of up to 4 months or so. This is quite
evidently enough time for the hormonal imbalance to wreak havoc on the body and result in any individual
losing most or all of the newly gained muscle during this time. Therefore, all anabolic steroid users should be
concerned with the fastest possible hormonal recovery, assisted and boosted with the use of Testosterone
stimulating compounds in the proper manner. Furthermore, the attempt to allow the body to recover on its
own will present a very high probability of long-term endocrine damage to the HPTA over time whereby the
individual will develop anabolic steroid induced hypogonadism (the inability to manufacture proper levels of
Testosterone for the rest of their life). It is therefore paramount that a proper post cycle therapy that
includes multiple recovery compounds be utilized so as to not only restore the HPTA function to normal
levels as quickly as possible, but to avoid any possible permanent damage, which takes priority over the
concern of maintaining the recently gained muscle mass.

The HPTA: How It Works

The HPTA is the Hypothalamic Pituitary Testicular Axis, which is an axis of interconnected endocrine glands in
the body that deal with and control Testosterone production.

Click here For HPTA Diagram

Outlined above is a diagram of the HPTA. The HPTA regulates how much Testosterone is manufactured and
circulating the body at any one given time. Every individual is essentially programmed by their genetics (DNA)
as to how much maximum Testosterone they will manufacture, and this is the prime determining factor.
There exist other factors that determine how much Testosterone an individual will produce as well, and these
include: age, diet, body composition, lifestyle habits, and physical activity. All of these factors play a role in
how much Testosterone an individual will generate overall.

The HPTA functions under what is known as the negative feedback loop, whereby the body will reduce its
manufacture and secretion of Testosterone if too much Testosterone is detected circulating in the body, and
will also adjust as such if insufficient amounts of Testosterone are detected. This detection and adjustment,
 known as the negative feedback loop, is controlled by the hypothalamus, which is essentially considered the
‘master’ gland for all endocrine and hormonal functions in the body. The negative feedback loop is ultimately
the body’s attempt to maintain hormonal homeostasis, which refers to the regulation of a system (in this
case, the internal systems of the body) in order to maintain stable and constant favorable conditions. All
endocrine glands operate by way of the negative feedback loop in one way or another, and to varying
degrees. In the case of post cycle therapy, the concern is primarily with the negative feedback loop of the
HPTA.

Within the HPTA, the concern during PCT is the restoration and regulation of the following 5 hormones to
homeostasis:

• GnRH (Gonadotropin Releasing Hormone)

• LH (Luteinizing Hormone)
• FSH (Follicle Stimulating Hormone)
• Testosterone

The HPTA begins with the first axis point, the hypothalamus, which will detect a need for the human body to
manufacture more Testosterone, and will release varying amounts of GnRH. GnRH is a hormone that signals
the next axis point, the pituitary gland, to begin the manufacture and release of two important
gonadotropins: LH and FSH. LH and FSH are two hormones that work to signal the third axis point, the testes,
to begin production and secretion of Testosterone. This is the final stage of Testosterone production in the
HPTA.

There are two primary hormonal factors that serve to inhibit, reduce, suppress, or shut down Testosterone
production in the HPTA:

• Excess Testosterone
• Excess Estrogen

Although there exist other hormones that serve to inhibit and suppress HPTA function (such as Progestins
and Prolactin), these are the two primary conditional hormones that are of concern. When the hypothalamus
detects excess levels of Testosterone and/or Estrogen in the body (either from the use of exogenous
androgens on an anabolic steroid cycle or otherwise), the hypothalamus will act to attempt to restore a
balance by essentially doing the opposite of what was previously described. The hypothalamus will reduce or
stop its production of GnRH, which halts production of LH and FSH, which ultimately reduces or halts
production of Testosterone. Until the hypothalamus’ ideal hormonal environment is restored, the production
of the various signaling hormones within the HPTA will not begin, and this will often require months of time
for the body to do this on its own without the intervention of any Testosterone stimulating agents. The
reason as to why the recovery of the HPTA naturally takes such a long time should be very clear due to the
described workings of the HPTA.
 This very basic understanding of the mechanisms of the HPTA and negative feedback loop described above is
essential to understanding how and why a proper PCT program must be developed and utilized following an
anabolic steroid cycle.

Determining Factors In Difficulty Recovering the HPTA

With anabolic steroid use, there are several different major determining factors in how much difficulty an
individual will experience in recovery of their HPTA and endogenous Testosterone function during PCT. They
are the following factors, in no particular order of importance:

1. Individual Response
2. Type of Anabolic Steroid(s) Used
3. Length of Cycle (Degree of Testicular Desensitization)

Individual Response

Every single individual will respond in a different manner to any chemical, compound, anabolic steroid, food
or drug in existence. While some individuals might experience absolutely no HPTA suppression or shutdown
at all, other individuals might experience severe HPTA suppression and shutdown to the extent where they
might require far longer periods of time to ensure full recovery than most. This, like anything else, is a
spectrum whereby there are the very ‘lucky’ individuals that recover very quickly and easily on one end of the
spectrum, and the ‘unlucky’ individuals that have extreme difficulty recovering during post cycle therapy. In
between the two extremes is the average. Once again, this is due to the individual’s genetic programming as
to how the HPTA will respond and attempt to maintain homeostasis.

Type of Anabolic Steroid(s) Used

All anabolic steroids exhibit suppression or shutdown of the HPTA through the mechanisms of the negative
feedback loop, and there are no exceptions to this. It’s often said that if you take any anabolic steroid you
now produce no testosterone, but this isn’t exactly true. Various anabolic steroids are known as being mildly
suppressive (something like Anavar), while others are known as being heavily suppressive (something like
Nandrolone Decanoate). In any case, no matter how mild or severe an anabolic steroid exerts HPTA
suppression, all anabolic steroids when utilized for typical cycle lengths of weeks at a time will eventually
cause the HPTA to shut down, or at the very least severely suppress its hormonal signal processes. Even if
suppression may not reach 100%, it will still be enough in every case for there to be a need for testosterone
supplementation during use due to putting your testosterone into a low level state.
• Important Note: the need for testosterone supplementation during anabolic steroid use does not apply to
women nor does the need for PCT. See the PCT For Women Section below.
 Length of Cycle

This is perhaps the most important and most influential factor. As the length of anabolic steroid use
continues, the majority of the Leydig cells of the testes remain dormant and inactive, and the longer these
interstitial cells remain dormant and inactive, the greater the difficulty in essentially getting these cells to
respond to the stimulus of LH and FSH once again. It has been discovered in studies that the issue of recovery
of the Leydig cells following anabolic steroid use is not due to a lack of LH, but due instead to the
desensitization of the Leydig cells to LH.\1]) In one study in which exogenous Testosterone was administered
to male test subjects for 21 weeks, LH levels were suppressed shortly after beginning administration.
However, at the end of the 21 week period, LH levels were observed to rise within 3 weeks once the
exogenous Testosterone administration stopped, but Testosterone levels did not rise until many weeks later
in most of the test subjects.

PCT Medications

The main testosterone stimulating agents for HPTA recovery during PCT are:

Primary
• SERMs (Selective Estrogen Receptor Modulators)
Secondary:
• HCG (Human Chorionic Gonadotropin)
• Aromatase Inhibitors
SERMs: Classes of drugs in the SERM category include: Nolvadex (Tamoxifen Citrate), Clomid (Clomiphene
Citrate), Raloxifene, and Torem (Toremifene Citrate). The nature of a SERM is that it exhibits mixed Estrogen
agonist and Estrogen antagonist effects on the body. This means that although a SERM might block the effect
of Estrogen at the cellular level in certain tissues, it can enhance Estrogenic effects in other areas of the body.
These can be positive effects as well as negative effects. In terms of the effect of SERMs on endogenous
Testosterone stimulation, they serve to act as an Estrogen antagonist at the pituitary gland, triggering the
release of LH and FSH as a result. Elevated levels of Estrogen in men can and does suppress the output of
endogenous Testosterone via the negative feedback loop, leading to hypogonadism.\2]) SERMs for this
purpose are an absolutely essential addition to any PCT protocol and are not to be excluded under any
circumstance.
HCG: Human Chorionic Gonadotropin is, for the most part, synthetic LH. It is a protein hormone
manufactured in high amounts by pregnant females that contains a protein subunit that is 100% identical to
LH, and therefore when administered to men, it will mimic the action of LH in target tissues, such as the
testes. What results is an increase in Testosterone production via stimulation of the Leydig cells by HCG. HCG
should never be utilized alone, as its nature as a gonadotropin will itself trigger a negative feedback loop
whereby once HCG is utilized, the pituitary gland will halt output of LH until HCG use has discontinued.
Therefore, HCG must be utilized prior to PCT or with a SERM and especially an aromatase inhibitor, as HCG
has demonstrated to increase aromatase activity in the testes, resulting in rising Estrogen levels.\3])
Aromatase inhibitors: These are compounds such as Aromasin (Exemestane), Arimidex (Anastrozole), and
Letrozole (Femara). Rather than block the activity of Estrogen at the cellular level in different tissues,
aromatase inhibitors (AIs) serve to lower total circulating Estrogen levels in the body by way of inhibiting the
aromatase enzyme, which is the enzyme responsible for the conversion of androgens into Estrogen. The
conversion of androgens into Estrogen results in excess Estrogen levels, which, as explained earlier on this
wiki page, will trigger the negative feedback loop leading to suppression of Testosterone production. By way
of lowering total circulating blood plasma Estrogen levels, AIs will engage the negative feedback loop in a
positive manner and result in the release of LH and FSH for the manufacture and secretion of more
Testosterone. This is essentially due to the hypothalamus realizing that circulating Estrogen levels are too
low, and will attempt to increase circulating levels of Testosterone in order for a portion of the Testosterone
secreted to be able to become aromatized into Estrogen in order to restore the hormonal balance. The main
importance of aromatase inhibitors is the ability to mitigate the Estrogenic effects of HCG, if HCG is utilized in
certain ways that will be expanded on later. It is important to note, however, that the majority of aromatase
inhibitors have known drug interactions with Nolvadex that will reduce blood levels of those AIs. Very specific
choices should be made in regards as to which AI is used during PCT with what SERM.

SERMs: Nolvadex, Clomid, Toremifene, & Raloxifene

The question is often asked among the anabolic steroid using community: Clomid or Nolvadex? Which one
for PCT? But there are also relatively newer SERMs as well. Toremifene (Torem) & Raloxifene (Ralox).

First of all, we will look at the two main SERMs people use for PCT -- Nolvadex & Clomid. Nolvadex on a mg
for mg basis is far more effective than Clomid in stimulating endogenous Testosterone production, as well as
being a more cost-effective choice than Clomid itself. Studies have demonstrated that 150mg of Clomid
(Clomiphene Citrate) administered daily raised endogenous Testosterone levels of 10 healthy males by
approximately 150%, while incidentally, 20 mg of Nolvadex (Tamoxifen Citrate) daily raised endogenous
Testosterone levels by the same amount.\11]) It is very evident here that Clomid is very effective for this
purpose, but Nolvadex seems to be a more cost-effective choice seeing as though it is more effective than
Clomid when compared mg for mg. In the same study, they directly examined the effects of Nolva and Clomid
on the pituitary. They infused the men with 100 mcg of GnRH and then measured LH output from the
pituitary. The men taking nolvadex at 20 mg/day had a significantly increased LH response to GnRH. In
contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers
stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen
(Nolva) seems the most probable explanation."\11]) Likewise, Clomid actually has been studied to exhibit
Estrogen agonist effects at the pituitary in vitro.\12]) What all this means is that Clomid potentially will work
in varying degrees as an Estrogen at the pituitary gland, triggering the negative feedback loop and reducing
the output of Testosterone stimulating gonadotropins (LH and FSH). This is a problem during post cycle
therapy, which is a period in which individuals are trying to recover their HPTA function rather than halt it
even further. Ideally, one would want a SERM that exhibits almost 100% Estrogen antagonistic effects on the
pituitary gland.
In addition to all this, vision sides are common Clomid and could may cause irreversible changes.\18])
Nolvadex may potentially cause some vision sides as well,\19]) but they are known to be more prominent in
Clomid than Nolvadex.\16]) More on Side Effects below.
Despite all of this, it should still be noted that the FDA actually recommends clomid for treatment of male
hypogonadism and that high doses are unnecessary to bring hypogonadal men into range.\14][17])
To touch lightly on Torem & Ralox, they have all been compared and studied alongside Nolva.\15]) The study
looked at the effects of each SERM in just under 300 infertile men with low sperm count and low
testosterone levels. The men were given 20 mg Nolvadex, 60 mg Toremiefene or 60 mg Raloxifene every day
for three months. See Figure 1 from the study here showing results month to month or see table below with
the medians and results after three months:
Normal
FSH Testosterone Sperm concentration
SERM LH (mIU/mL) sperm forms
(mIU/mL) (ng/dL) (x 106 / mL)
(%)

5.72 to 8.42 4.54 to 7.84 496.59 to 763.34 32.08 to 41.94 18.91 to

Nolvadex
(+47%) (+72%) (+53%) (+30%) 31.64 (+67%)

5.64 to 9.53 4.05 to 6.54 498.96 to 743.92 25.84 to 37.82 23.09 to

Torem
(+69%) (+61%) (+49%) (+46%) 31.73 (+37%)

6.39 to 6.87 4.18 to 4.75 583.55 to 604.35 27.01 to 32.64 14.72 to

Ralox
(+7%) (+13%) (+3%) (+20%) 21.86 (+48%)

As seen Nolvadex came out on top here in LH, Testosterone & Normal sperm forms. Torem topped Nolva in
FSH and Sperm concentration. Both are very suitable PCT options (as already known with Nolva, but this
shows Torem as a viable option as well). Ralox was unfavorable and is probably best used just for
gynecomastia treatment.

IMPORTANT NOTE: Also be sure to check out the Drug Interactions section, as it contains important
information for those using SSRIs and SERMs.

Dosing

Nolvadex
In all studies involving Nolvadex, for doses used to stimulate endogenous Testosterone production, only 20–
40 mg daily of Nolvadex was utilized, and it has in fact been shown that doubling the dose to 40 mg or higher
will not produce any significant difference in endogenous Testosterone secretion.
 The only reason why many elect to higher daily doses of Nolvadex for the first 1-2 weeks of a PCT is for the
purpose of achieving optimal peak blood plasma levels more quickly, so as to ensure more rapid HPTA
recovery.

This isn't necessary and just further increases your risk of potential sides.

Furthermore, the first week of PCT, there may be lingering suppressive AAS still in the bloodstream, simply
leading to greater oxidative stress on the body by taking more compounds.

Recent studies have found that even lower doses than traditionally-prescribed are equally as effective.

• A weekly low-dose tamoxifen vs raloxifene vs placebo in premenopausal women with estrogen receptor-
positive breast cancer
• Randomized dose trial of tamoxifen at low doses in hormone replacement therapy
• Randomized trial of low-dose tamoxifen on breast cancer proliferation and estrogen biomarkers

PCT dosing with Nolvadex has been updated (2020) as follows:

• 6–8 Weeks at 10 mg ED. Doses can be taken as low as 5 mg/day if sides are a concern.

Clomid
According to the study previously mentioned,\14]) and thus recommended by the FDA, clomid for
hypogonadism should be run at 25 mg EOD, 25 mg ED, or 50 mg EOD. Again, the side effects of clomid can be
quite bothersome and bad. Why risk vision changes or loss running +50-150 mg ED when you could just do
25mg ED or 50mg EOD and get fantastic results? Dosing of a PCT including Clomid is as follows:
• 6-8 Weeks: 25mg ED or 50mg EOD

Torem
In the study above comparing Nolva, Torem, & Ralox, 60mg was the dosage used and found to be very
sufficient for PCT purposes. 60mg ED is the FDA recommended dosage and they found no benefit upon
doubling the dose in women with breast cancer. Again, doubling the dose for the purpose of achieving
optimal peak blood plasma levels quicker isn't necessary and just further increases your risk of potential
sides. Dosing of a PCT including Torem is as follows:

• 6-8 Weeks: 60mg ED

SERM Dosing Note

Note: As you've noticed above, /r/seroids recommends 6-8 weeks of SERMs. It is common for a lot of PCT
options to only be 4 weeks. These protocols usually used double the dose for the first week or two. The only
reason why many elect to utilize doubling the dose for the first 1-2 weeks of a PCT program is for the purpose
of achieving optimal peak blood plasma levels quicker so as to ensure HPTA recovery quicker. This isn't
necessary and just further increases your risk of potential sides. It has been studied that the longer you are
on SERMs, the better your results of stimulating Testosterone.\15]) So to prevent unwanted sides as well as
potentially achieve better results, we choose to suggest lower dosing over a longer period than 4 weeks.

HCG

The majority of anabolic steroid users from the 1960s – mid 1980s did not even utilize any compounds for the
purpose of hormonal recovery, and the term PCT did not even exist at that time. When the use of HCG
became increasingly popular (circa 1980), it was the only compound utilized. Since then, the medical and
scientific understanding of such things has increased exponentially and there should be no reason for any
informed and properly educated individual to utilize HCG on its own for PCT. When utilized in conjunction
with one of the other two categories of compounds (an AI and a SERM), the dynamics change considerably.

HCG mimics LH and therefore actually keeps the testicles producing testosterone even when anabolic
steroids are present. However, it does not induce the production of actual LH. The use of HCG on cycle, this is
primarily done so that post cycle recovery is easier. HCG is also used on cycle to prevent or at least minimize
testicular atrophy that occurs due to the use of anabolic steroids. The testicular atrophy that occurs is not
permanent but will reverse once steroid use is discontinued and natural testosterone production begins
again.

It has been mentioned already that much of the difficulty in recovering the HPTA following an anabolic
steroid cycle is the result of Leydig cell desensitization. HCG is essentially an analogue of LH, and the testes
after a prolonged anabolic steroid cycle would be as equally desensitized to HCG as they are to LH. The
human body, however, produces LH amounts on its own that are far too inefficient for proper and rapid
Testosterone production. The body’s natural increase of LH and FSH following an anabolic steroid cycle is also
not a rapid peak, but a very slow and steady incline, as evidenced by the study referenced earlier in which it
was not until 3 weeks when LH levels only began to reach the normal physiological measurements following
the cessation of exogenous Testosterone. Therefore, the body’s own natural LH production does not provide
a high enough dose for stimulation, nor an immediate stimulation to the testes required for the initial
increase in Testosterone needed during the post cycle therapy weeks. Now in our PCT will will be utilizing a
SERM which will stimulate FSH/LH, but most will find recovery being a smother transition when HCG is
utilized. Studies have in fact demonstrated the incredible effectiveness of HCG for this purpose, and it is even
suggested clinically that HCG be utilized for the purpose of treating anabolic steroid induced
hypogonadism.\4])
If you choose to include HCG in your PCT protocol, the best possible SERM for the PCT protocol is Nolvadex,
as studies have demonstrated that HCG and Nolvadex utilized together have exhibited a remarkable
synergistic effect in terms of stimulating endogenous Testosterone production, and that Nolvadex will
actually work to block the desensitization effect on the Leydig cells of the testes caused by high doses of
HCG.\10]) This is very important, because just as too little LH secretion for extended periods can cause
 desensitization to gonadotropins, too much gonadotropin stimulation (in the form of HCG or otherwise) may
likewise cause a desensitization effect.

Dosing

HCG is ran a couple different ways:

1. Over The Entire Cycle

2. Weeks Leading Up To PCT
3. 1-2 Weeks Before PCT
4. First 1-2 Weeks Of PCT

1. Over The Entire Cycle

This is the preferred option, as it keeps the Leydig cells active, reducing atrophy and the reactive oxygen
species (ROS) free radical damage incurred by prolonged shutdown. HCG can be ran over the entire length of
the cycle to make PCT easy and efficient, if desired:
• Over Entire Length Of Cycle: 250 IU EOD
• Stop HCG use before starting PCT (SERM)
Important Note: 250 IU 2x/week is used by some, but there have been studies on maintaining intratesticular
testosterone in healthy men with gonadotropin suppression. This study found 125 iu EOD (437.5 iu/week)
was 25% less than baseline. Alternatively, 250 iu EOD (875 iu/week) was found to only be 7% below
baseline.\13]) For this reason, it is recommended to use at least 250 iu EOD. If desiring to be as close to
baseline as possible, you would need more than 875 iu/week (7% less than baseline) and less than 1750
iu/week (26% above baseline). This is where the 500 iu 2x/week come in, but without a study comparing, we
are only speculating and you could need more. Alternatively, if money is a factor, it is best to use some HCG
rather than no HCGand you may do less than the recommended: 500-750 iu/week.

2. Weeks Leading Up To PCT

This is the preferred method after Option 1, especially for those that are coming off a long cycle or blast and
cruise.

Starting 6 weeks before PCT:

• Weeks 6-4: 500-1000 iu 3x/week

• Weeks 3-1: 500-1000 iu 2x/week
• Week 0: Start PCT (SERM)
 3. 1-2 Weeks Before PCT
Typically this will be run in the ~2 weeks leading up to PCT after your last injection, while you are waiting for
your AAS esters to clear (assuming long esters -- Ex: Test E or C). If using short esters (Prop and/or Ace),
nothing changes. You just start the HCG while on cycle (1-2 weeks before PCT).

If you chose to utilize HCG in this fashion (unless using short esters (Prop and/or Ace), there is one remaining
issues to be addressed:

• The fact that HCG causes increased production of aromatase, leading to increased Estrogen levels. See Below

This is where the AI is to be utilized as a supportive compound for HCG use in this 1–2 week period, and after
HCG is discontinued early on in PCT, only the SERM to be used in order to carry along the hormonal recovery
process. HCG utilized in this fashion will be ran:

• 1-2 Weeks Before PCT: 1000-1500 iu EOD

• 1-2 Weeks Before PCT: AI will be used only as long as HCG

4. First 1-2 Weeks Of PCT

Some will say HCG shouldn't be ran into PCT as it's suppressive, but as noted above in the study with
Nolvadex, it has shown to be effective and fine when ran simultaneously with Nolvadex.\10])

If you chose to utilize HCG in this fashion, there is one remaining issues to be addressed:

• The fact that HCG causes increased production of aromatase, leading to increased Estrogen levels. See Below

This is where the AI is to be utilized as a supportive compound for HCG use in this 1–2 week period, and after
HCG is discontinued early on in PCT, only the SERM to be used in order to carry along the hormonal recovery
process. HCG utilized in this fashion will be ran:

• First 1-2 Weeks Of PCT: 1000-1500 iu EOD

• First 1-2 Weeks Of PCT: AI will be used only as long as HCG

Aromatase Inhibitors: Aromasin (Exemestane) Above All Else

This Section Is Optional, UNLESS Utilizing HCG dosing 3 or 4.

As noted above in HCG dosing 3 & 4, one issue that needs to be addressed will be the fact that HCG will
trigger increases in testicular aromatase expression, and result in Estrogen increases in the body. If you are
on cycle, as you would be with HCG dosing 1 & 2, you will already be taking an AI and be taking care of this. It
should also be noted that HCG will also cause an increase in testicular progesterone levels. Estrogen rising is
of course undesirable during PCT, as it has already been explained that Estrogen will trigger suppression of
endogenous Testosterone production, and there is no doubt that any individual wishes to encounter
Estrogenic side effects during PCT either.
Therefore, the option here is to include an aromatase inhibitor. However, there exists a problem in regards to
the other two of the three major aromatase inhibitors (Arimidex and Letrozole). The issue is the fact that in a
PCT program that includes the use of Nolvadex, Arimidex and Letrozole have direct negative interactions with
Nolvadex. The potential problem here is that Arimidex & Letrozole both have decreased blood plasma
concentrations when used alongside a Nolvadex.\5][20][21]) Aromasin completely circumvents this problem,
as it has been demonstrated to have no interactions what so ever with Nolvadex, unlike the other two
aforementioned aromatase inhibitors. In one study, Aromasin displayed no such reduced effectiveness or any
reduced blood plasma levels when utilized with Nolvadex.\6]) The conclusion here is that the use of Arimidex
or Letrozole would be last resort options for controling Estrogen during HCG dosing 3 & 4 use.
The other benefit of selecting Aromasin over all other AIs is the fact that Aromasin has demonstrated in
several studies to impact cholesterol profiles in a negative manner far less than other aromatase inhibitors
have, where in one particular study on cancer patients, 24 weeks of Aromasin (Exemestane) administration
held no impact on cholesterol profiles.\7]) Some other studies have also demonstrated a nil effect on
cholesterol profiles from the use of Aromasin.\8]) Although there have also been some studies that have
demonstrated a negative effect on cholesterol profiles resultant from Aromasin use, it is evident that there is
not as a significant or as a negatively impacting effect from Aromasin on cholesterol as other aromatase
inhibitors.\9])
Finally, in addition to these benefits from Aromasin, it is very clear that Aromasin holds the ability to increase
Testosterone levels in males as demonstrated by studies. For example, one particularly notable study
selected 12 healthy young male test subjects, and were administered random Aromasin doses of 25mg and
50mg for a 10 day period, and not only was Estrogen suppressed by a significant amount (38%), but
Testosterone levels in the test subjects were observed to have increased by an incredible 60%.\8])

Dosing

Note: This is a lot of Aromasin, but has clinically be shown to be effective. You may end up experiencing low
E2 sides. Most common include the possibility of stiff joints and lethargy. If you wish to avoid this, consider
skipping the need for this and utilizing HCG dosing 1 or 2
Following these details, Aromasin would be the best possible aromatase inhibitor of choice in order to
combat the increased aromatase activity caused by HCG. Therefore, Aromasin would then be utilized up to a
full 25mg ED, and only while HCG is utilized in HCG dosing 3 or 4. Once HCG is discontinued, Aromasin too
should be halted.
This section is optional, UNLESS utilizing HCG dosing 3 or 4.

Drug Interactions

As with all drugs you use, you should always check for Drug Interactions. One known issue during PCT is with
people taking SSRIs. Nolvadex and Toremifene have both been shown to have major interactions with one
another.
Most notably, SSRIs have been shown to reduce effectiveness of Nolvadex and SSRIs when taken with
Toremifene have been shown to cause irregular heart rhythm that may be serious and potentially life-
threatening, although it is a relatively rare side effect. In any case, if you're on a SSRI, it is best to use Clomid.

Side Effects

Common post-cycle complaints include depressive mood alterations, fatigue, lethargy, insomnia, and
decreased libido.\22]) As stated earlier, vision sides are common for both Clomid & Nolva, more so with
Clomid. Hot Flashes, Nausea are two common side effects of Clomid, Nolva, & Torem. Depression is known to
affect many in PCT and is an actual listed side effect of Nolva. Please make sure you are aware of this and in
a good place mentally before ever starting a cycle as you will be faced with the potential of depression in
PCT.

What to Expect from PCT

As stated above in the Side Effects section above, common post-cycle complaints include depressive mood
alterations, fatigue, lethargy, insomnia, and decreased libido.\22]) You should be fully prepared to go through
these symptoms if you chose to run a cycle.

The biggest problem with most PCT plans is the individual having unrealistic explanations. Most PCT plans will
last 4-8 weeks and many men expect everything to be back to normal once this 4-8 week period is complete.
PCT does not work this way. Many men also expect for all their gains be they weight or strength gains to be
maintained post-PCT if the PCT plan was proper and appropriate. Again, PCT does not work this way.

A good PCT plan will help you protect and maintain some of the progress you made, but if the high influx of
hormones is no longer there (the high influx of hormones that helped you make your gains), without that
support system you will lose some of your gains. A good way to look at is as we look at food – the nutrients
you eat help you buildup your body. The nutrients you eat become the support system. Take away the
nutrients and the support system goes away with it and the “building” begins to collapse. For this reason it’s
not uncommon for some men to begin consuming extra calories during PCT in order to protect their gains –
in simplistic terms they’re substituting in nutrients for the hormones that have been taken away. This can
help maintain weight but it’s not always a good idea. Weight is just weight and if it’s not weight that’s muscle
tissue it’s rather useless. It’s not uncommon for some men to put on a good bit of body fat during this phase
due to their desperation to hang onto gains.

As stated, the primary purpose of PCT is to stimulate natural testosterone production. Some gains may be
lost during this period, but it’s not the end of the world. For the steroid user he will be on cycle again one
day. For the present period he should focus on his hormone recovery, continue to train and eat properly
protecting the gains he can without putting on excess body fat.
When NOT to Run PCT

If you’re a steroid user that is on cycle more than you’re off, running a PCT can be counter productive. For
example, a man completes a cycle, implements PCT and then jumps back on cycle right after or soon after
PCT. This is a very harsh practice and terrible for your body. You are shutting down your natural testosterone
production, stimulating it through PCT and then shutting it right back down. You’ve put yourself on a never
ending rollercoaster with your hormone levels that’s going to wreak havoc on your body. For such an
individual he would be better off running a low dose of testosterone, therapeutic levels, during his time
between cycles. This is not an approach most men should take. Most men who use steroids need to come off
and stay off after PCT is complete for a time if long-term health is important to them.

Another time not to run PCT is if you are prescribed Testosterone Replacement Therapy (TRT). A low
testosterone patient has been found by a medical professional to no longer have the natural ability to
produce enough testosterone on his own, which is why he needs testosterone supplementation. If he
happens to implement a cycle at some point during his treatment, once the cycle is over he should simply
continue on with his previous Testosterone Replacement Therapy (TRT). If you implement a PCT plan, you’re
attempting to stimulate your natural ability that medical professional has deemed to not be enough, and it
will serve no purpose.

When to Start PCT

Timing is a very important factor when it comes to PCT. You want to start PCT around the time the compound
will be exiting your body and no longer a major factor in causing suppression. In the medical field, after 4
half-lives the amount of drug (6.25%) is considered to be negligible regarding its therapeutic effects. The
chart below is based on known terminal half-lives of AAS esters, as well as some theoretical half-lives (as
some haven't been studied). You will choose the ester that will require the most amount of time before
starting PCT (SERM).
IMPORTANT NOTE: This is just the time the compound itself will be low enough to start PCT. This does not
take into account for metabolites that have been found to have a correlation to LH & FSH recovery in
nandrolone.\23]) This could very well happen in other compounds as well. Be sure to get post PCT blood work
to ensure recovery. See Below
Ester Time To Wait After Last Pin Before Starting PCT (SERM)

Acetate 3-4 day

Propionate 3-4 days

Phenylpropionate 5-6 days

Isocaproate 14-16 days

Enanthate 14-18 days

 Ester Time To Wait After Last Pin Before Starting PCT (SERM)

Cypionate 14-20 days

Decanoate 26-30 days

Undecylenate 52-56 days

Undecanoate 80-84 days

As you can see, if using a compound like Nandrolone Decanoate (Deca), Sustanon (Testosterone Decanoate is
its longest ester), Boldenone Undecylenate (EQ), or Testosterone Undecanote, there is a very long waiting
period before starting PCT.

Very Long Ester AAS & PCT Transition

If using Nandrolone Decanoate or Boldenone Undecylenate, most will opt to continue running Testosterone
up until the point the half-lives will both be considered negligible at the same time.

*For Example: *In a Testosterone Cypionate and Boldenone Undecylenate cycle you will continue to run the
Testosterone Cypionate for 8 weeks AFTER your last Boldenone Undecylenate injection.

On cycle, you can are taking supraphysiological doses of Testosterone. When you are doing this transition
into PCT you may either choose to continue with your supraphysiological doses or drop your Testosterone
down to TRT doses (80-200 mg/week).

Very Long Ester Testosterone & PCT Transition

If you are using Sustanon or Testosterone Undecanote, you may want to transition into a shorter ester to
make the waiting period for the Decanoate or Undecanoate ester to clear. Otherwise, due to the ester, it will
get rid of the exogenous Testosterone much slower and with that it will be releasing VERY small minuscule
amounts that will get very low at the end and will not be optimal. Due to this using a Testosterone Enanthate
or Propionate could be very beneficial to you, your well being, and allowing the most successful PCT possible
(you wouldn't want to start early wile the compound is still aiding in suppression).

Important Metabolites Note

The table above is just the time the compound itself will be low enough to start PCT. This does not take into
account for metabolites that have been found to have a correlation to LH & FSH recovery—particularly, in
one study involving Nandrolone Decanoate.\23])

In the study researchers found that even after six months LH and FSH were both still repressed. The recovery
of LH and FSH was correlated to the urinary level of the nandrolone metabolite 19-norandrosterone (19-NA).
19-NA was detectable for several months after the last nandrolone administration, and there was a large
inter-individual variation in the excretion rate. Some individuals still tested positive (>2 ng/mL) even one year
after their last nandrolone dose and still sustained suppression of LH and FSH during that time. Limitations
are that this study did not state a post cycle therapy was used by any of the steroid users. We do not know
much a proper PCT would have sped up recovery.

This could very well happen in other compounds as well. Be sure to get post PCT blood work to ensure
recovery.

When to Start Your Next Cycle

For optimal health the general rule to follow is time on + PCT, equals time off. If your cycle last 12 weeks, you
wait 2 weeks to start PCT, and your PCT plan lasts 6 weeks, then you will wait 20 weeks before starting a new
cycle. A mistake many men make is saying testosterone levels have recovered shortly after PCT and it is now
okay to start a new cycle. If you do this you have not allowed your body time to normalize. True recovery
means your levels can hold without any type of supplementation, if not then full recovery has not been
reached.

Blood Work

It’s always a good idea to get blood work done after PCT to see where your body is at; however, this won’t be
the full story. When we run a PCT we are artificially stimulating natural testosterone production -- the
stimulation would not exist without the implementation of SERMs. The true tale of the tape is where your
numbers are good after a bit of time has passed since cessation of the SERM; say several months. The earliest
time to check blood work would be a minimum of one month after cessation of SERM's. You will be looking
for LH/FSH returning to fairly normal, as well as total and free testosterone levels alongside estradiol. How do
you know what normal i for you? If your cycle was run properly, you should have gotten pre-cycle natural
blood work. What were you levels on that blood work? That will be your base point you are attempting to get
back to with PCT.

The Danger

If you’re going to supplement with anabolic steroids there is one single truth you need to understand: risks
exist. One of these risks is permanently lowering your natural testosterone production and forever being in
need of TRT. Even with the best PCT plan this risk exists. The point of PCT is to help and minimize this risk; it
does not completely remove it. If this is something you cannot accept then anabolic steroid use is not for you.
PCT for Women

Michael Scally (former) M.D.'s Thoughts:

In the case of pre-menopausal females, tapering the anabolic-androgenic steroids (AAS) would be the best
treatment. Anabolic steroid administration, like males, causes the HPGA to shutdown. However, stopping the
AAS will produce menopausal like symptoms, therefore tapering until menses returns is best. The labs follicle
stimulating hormone (FSH), luteneizing hormone (LH), progesterone (P) and estradiol (E2) will be the best
indicator. They will show if the HPGA is affected adversely. In marked contrast to a man, the period typically
returns within 1-2 months and will occur while tapering.

I would NOT suggest “selective estrogen receptor modulators” (SERMs) or aromatase inhibitors (AIs) for a
woman! NEVER! It is the equivalency of forcing them into menopausal symptoms. The HPGA/HPTA are very
different. In fact, SERM/AI (such as Nolvadex and Arimidex) are used in Breast Cancer, which includes a
significant number of adverse effects. Decreasing E2 in a man is far different from doing the same in a
female. E2 and P are the main female hormones. Just imagine how a man feels that receives Androgen
Deprivation Therapy (ADT) for Prostate Cancer.

References

[1] Mauss J, Börsch G, Bormacher K, Richter E, Leyendecker G, Nocke W. Effect of long-term testosterone
enanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone
and seminal fluid analysis in normal men. Acta Endocrinol (Copenh). 1975 Feb;78(2):373-84. Link
[2] Faloon, W. “Dangers of Excess Estrogen In the Aging Male”. Life Extension Magazine, November
2008. Link.
[3] Valladares LE, Payne AH. Acute stimulation of aromatization in Leydig cells by human chorionic
gonadotropin in vitro. Proc Natl Acad Sci USA 76:4460-3/1979. Link.
[4] Gill GV. Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin. Postgrad
Med J. 1998 Jan;74(867):45-6. Link.
[5] Boeddinghaus IM, Dowsett M. Comparative clinical pharmacology and pharmacokinetic interactions of
aromatase inhibitors. J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):85-91. Link.
[6] Zaccheo T, Giudici D, Di Salle E. Inhibitory effect of combined treatment with the aromatase inhibitor
exemestane and tamoxifen on DMBA-induced mammary tumors in rats. J Steroid Biochem Mol Biol. 1993
Mar;44(4-6):677-80. Link.
[7] Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C, Cufer T, Lobelle JP, Mattiaci MR,
Piccart M, Paridaens R. The effect of exemestane on serum lipid profile in postmenopausal women with
metastatic breast cancer: a companion study to EORTC Trial 10951, 'Randomized phase II study in first line
hormonal treatment for metastatic breast cancer with exemestane or tamoxifen in postmenopausal
patients'. Ann Oncol. 2004 Feb;15(2):211-7. Link.
[8] Mauras N, Lima J, Patel D, Rini A, di Salle E, Kwok A, Lippe B. Pharmacokinetics and dose finding of a
potent aromatase inhibitor, aromasin (exemestane), in young males. J Clin Endocrinol Metab. 2003
Dec;88(12):5951-6. Link.
[9] Engan T., Krane J., Johannessen D. C., Kvinnsland S. Plasma changes in breast cancer patients during
endocrine therapy — lipid measurements and nuclear magnetic resonance (NMR) spectroscopy. Breast
Cancer Res. Treat., 36: 287-297, 1995. Link.
[10] Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg PW. Tamoxifen suppresses
gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men. J Clin Endocrinol Metab.
1980 Nov;51(5):1026-9. Link.
[11] Vermeulen A, Comhaire F. Hormonal Effects Of An Antiestrogen, Tamoxifen, In Normal And Oligospermic
men. Fertil Steril. 1978 Mar;29(3):320-7. Link.43160-2/pdf)
[12] Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Disparate effect of clomiphene and tamoxifen on pituitary
gonadotropin release in vitro. Am J Physiol. 1981 Feb;240(2):E125-30. Link.
[13] Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK, Anawalt BD, Sutton PR, Wright WW,
Brown TR, Yan X, Zirkin BR, Jarow JP. Low-dose human chorionic gonadotropin maintains intratesticular
testosterone in normal men with testosterone-induced gonadotropin suppression. J Clin Endocrinol Metab.
2005 May;90(5):2595-602. Epub 2005 Feb 15. Link.
[14] Katz DJ1, Nabulsi O, Tal R, Mulhall JP. Outcomes of clomiphene citrate treatment in young hypogonadal
men. BJU Int. 2012 Aug; 110(4):573-8 Link.
[15] Tsourdi, E., Kourtis, A., Farmakiotis, D., Katsikis, I., Salmas, M., & Panidis, D. (2009). The effect of
selective estrogen receptor modulator administration on the hypothalamic-pituitary-testicular axis in men
with idiopathic oligozoospermia. Fertility and Sterility, 91(4), 1427–1430. Link.01280-6/pdf)
[16] Dobbs M. R. (2009). Clinical Neurotoxicology: Syndromes, Substances, Environments. pg 106. Link.
[17] Teodósio Da Ros C. Twenty-five Milligrams Of Clomiphene Citrate Presents Positive Effect On Treatment
Of Male Testosterone Deficiency - A Prospective Study. Vol. 38 (4): 512-518, July - August, 2012. Link.
[18] Purvin VA. Visual Disturbance Secondary to Clomiphene Citrate. 1995;113(4):482-484. Link.
[19] Alfred R. Ashford MD Irina Donev MD Ram P. Tiwari MD T. J. Garrett MD, FRCP(C), FACP. Reversible
ocular toxicity related to tamoxifen therapy. 1988. Link.
[20] The ATAC Trialists’ Group. Pharmacokinetics of anastrozole and tamoxifen alone, and in combination,
during adjuvant endocrine therapy for early breast cancer in postmenopausal women: a sub-protocol of the
‘Arimidex™ and Tamoxifen Alone or in Combination’ (ATAC) trial. British Journal of Cancer (2001) 85(3), 317–
324. Link.
[21] Dowsett M. Drug and hormone interactions of aromatase inhibitors. Endocrine-Related Cancer (1999) 6
181-185.
[22] Cyrus D. Rahnema, B.S., Larry I. Lipshultz, M.D., Lindsey E. Crosnoe, B.S., Jason R. Kovac, M.D., Ph.D., and
Edward D. Kim, M.D. Anabolic steroid–induced hypogonadism: diagnosis and treatment
 [23] Gårevik, N., Strahm, E., Garle, M., Lundmark, J., Ståhle, L., Ekström, L., & Rane, A. (2011). Long term
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Official /r/steroids PCT Protocols

These are the official /r/steroids recomended PCT Protocols. In general, the longer that you have been on
cycle and not producing your own natural Test, the greater precaution you should take in your PCT.

When something is written as "X/X/Y/Y", think of it as Week 1 daily dose/Week 2 daily dose/Week 3 daily
dose/Week 4 daily dose/etc., etc..

SERM Dosing Note

Note: As you've noticed in our SERMs Dosing section, as well as below, /r/steroids recommends 6-8 weeks of
SERMs. It is common for a lot of PCT options to only be 4 weeks. These protocols usually used double the
dose for the first week or two. The only reason why many elect to utilize doubling the dose for the first 1-2
weeks of a PCT program is for the purpose of achieving optimal peak blood plasma levels quicker so as to
ensure HPTA recovery quicker. This isn't necessary and just further increases your risk of potential sides. It
has been studied that the longer you are on SERMs, the better your results of stimulating Testosterone.\15])
So to prevent unwanted sides as well as potentially achieve better results, we choose to suggest lower dosing
over a longer period than 4 weeks.

Optimal/Primary PCT Options

This is the PCT plans you should use if you want PCT to be as as effective as possible. This is highly
recommended to those that have been on cycle a long time or that are coming off a Blast & Cruise.

Nolvadex

Option 1
Starting at the beginning of the cycle.

• Over Entire Length Of Cycle: 250 iu EOD or 500 iu 2x/week

• Stop HCG Before Starting SERM
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Option 2
Starting 6 weeks before PCT (SERM).

• Weeks 6-4: 500-1000 iu 3x/week

• Weeks 3-1: 500-1000 iu 2x/week
• Week 0: Stop HCG & Starting SERM
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Clomid

Option 1
Starting at the beginning of the cycle.

• Over Entire Length Of Cycle: 250 iu EOD or 500 iu 2x/week

• Stop HCG Before Starting SERM
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

Option 2
Starting 6 weeks before PCT (SERM).

• Weeks 6-4: 500-1000 iu 3x/week

• Weeks 3-1: 500-1000 iu 2x/week
• Week 0: Stop HCG & Starting SERM
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

Torem

Option 1
Starting at the beginning of the cycle.

• Over Entire Length Of Cycle: 250 iu EOD or 500 iu 2x/week

• Stop HCG Before Starting SERM
• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Option 2
Starting 6 weeks before PCT (SERM).

• Weeks 6-4: 500-1000 iu 3x/week

• Weeks 3-1: 500-1000 iu 2x/week
• Week 0: Stop HCG & Starting SERM
• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Secondary PCT Options

This is the PCT plans you should use if you were in a position where HCG wasn't an option until something
changed and you now have access to it at the VERY end of your cycle.
 Note: Aromasin is added in to combat the E2 sides from HCG. Previously HCG was utilized on cycle and you'd
just adjust AI as necessary. Since you are no longer on cycle, we will use Aromasin. This is a lot of Aromasin,
but has clinically be shown to be effective in aiding to stimulate testicular function. You may end up
experiencing low E2 sides. Most common include the possibility of stiff joints and lethargy. If you wish to
avoid this, consider skipping the need for this and utilizing the Optimal/Primary PCT Options

Nolvadex

Option 1
Taking HCG right before PCT.

• 1-2 Weeks BEFORE PCT: HCG 1000-1500 iu EOD

• 1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See Section)
• Stop HCG Before Starting SERM
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Option 2
Taking HCG and SERM together.

• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

• First 1-2 Weeks Of PCT: HCG 1000-1500 iu EOD
• First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See Section)

Clomid

Option 1
Taking HCG right before PCT.

• 1-2 Weeks BEFORE PCT: HCG 1000-1500 iu EOD

• 1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See Section)
• Stop HCG Before Starting SERM
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

Option 2
Taking HCG and SERM together.

• 6-8 Weeks: Clomid 25mg ED or 50mg EOD = 25/25/25/25/25/25 (/25/25)

• First 1-2 Weeks Of PCT: HCG 1000-1500 iu EOD
• First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See Section)
 Torem

Option 1
Taking HCG right before PCT.

• 1-2 Weeks BEFORE PCT: HCG 1000-1500 iu EOD

• 1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See Section)
• Stop HCG Before Starting SERM
• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Option 2
Taking HCG and SERM together.

• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

• First 1-2 Weeks Of PCT: HCG 1000-1500 iu EOD
• First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See Section)

Minimalist PCT Options

This is the PCT plans you should use if you were in a position where HCG isn't an option. It may not
be as effective as the other plans, but it is sufficient and will aid tremendously.

Nolvadex

• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)

Clomid

• 6-8 Weeks: Clomid 25 mg ED or 50 mg EOD = 25/25/25/25/25/25 (/25/25)

Torem

• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)

Post Blast & Cruise Recovery Not Endorsed By /r/steroids
These are PCT protocols listed are NOT endorsed by /r/steroids and should be used for information purposes
only. They have proven effective for some, but optimally you will use a PCT protocol listed above

ASRM Guidlines For Physicians To Prescribe

Based on this 2014 paper by the American Society for Reproductive Medicine this is what they recommend
physicians prescribe for anabolic steroid–induced hypogonadism (ASIH):
• Before Starting: Initial blood work will be taken and will include: hormonal panel (LH, FSH, E2, T, freeT, SHBG,
and PRL), complete blood cell count, lipid profile, prostate-specific antigen, and a comprehensive metabolic
profile.
• Week 1-4: For the severely symptomatic patients, a 4-week tapered course of transdermal or injectable
TRT may provide immediate symptom improvement (i.e. those that have been off for a while and have not
recovered or are experiencing Low T symptoms). Simultaneous administration of a SERM (such as clomiphene
citrate, 25 mg every other day) will interact at the hypothalamus causing stimulation of LH and ultimately
increase intratesticular T. For patients with ASIH-induced gynecomastia, 10–20 mg tamoxifen daily will block
the breast estrogen receptors and stimulate HPG axis recovery.
• Week 5-8: After 4 weeks of treatment with TRT and/or a SERM, repeated hormone panels should be
obtained. If the patient has had either a poor gonadotropin response or a poor T response, the authors
commence a 4-week course of hCG (1,000–3,000 IU, 3 times per week) while continuing daily treatment with
a SERM at the initial starting dose. If a patient develops gynecomastia while on hCG, Tamoxifen aka Nolvadex
10 mg b.i.d. (twice a day) or Anastrazole (Arimidex) may be commenced.
• After Week 8: After 8 weeks of hCG and adjunctive treatment, you should get blood work again and hormone
levels should once again be assessed.
• If the total serum T remains low and the patient continues to be symptomatic: primary testicular failure is
likely. These patients will require a longer duration of TRT to avoid permanent ASIH.
• If appropriately increased serum T and gonadotropin levels are observed: the SERM may be reduced to 50%
of its starting dose at 10 weeks of treatment and continued through weeks 12–16 or until target serum T
level is achieved. Recovery of hormonal function may be limited in men with testicular failure, and close
monitoring is recommended.

Original PoWeR PCT

by Michael Scally (former) M.D.

• HCG - 2500 IU EOD – first 16 days
• Clomid - 100 mg ED - split the dose ½ in the AM, ½ in the PM for the first 30 days
• Nolvadex - 10 mg ED – entire 45 days
NOTE: Clomid and HCG dosing are extremely high, 50 mg clomid should be the upper limit as you should
never need more. Blasting high doses of HCG could lead to desensitization of receptors.
The above is a documented and approved PCT plan by former Dr. Scally. This can be found in Anabolics 10th
Edition by William Llewellyn.

New PoWeR PCT

by Michael Scally (former) M.D.

• HCG - 2000 IU EOD – (first 20 days)
• Clomid - 100 mg ED - split the dose ½ in the AM, ½ in the PM (first 30 days)
• Nolvadex - 10 mg ED – (entire 45 days)
NOTE: Clomid and HCG dosing are extremely high, 50 mg clomid should be the upper limit as you should
never need more. Blasting high doses of HCG could lead to desensitization of receptors.

The above is a documented and approved PCT plan by former Dr. Scally.

You Can See Both The Original And New PoWeR Protocols: Here

Controversy

Aside from the high Clomid and HCG dosages, it should be noted that there is some controversy on whether
using two SERMs at once is beneficial or not.

This is one of the explanations that Dr. Scally has given:

Clomid acts as an estrogen, rather than an anti-estrogen, by sensitizing pituitary cells to the action of GnRH.
Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has
little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The
estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen
may be devoid of estrogenic activity at the pituitary level.

Some strongly disagree with Dr. Scally's reasoning behind the use of clomid. What he is describing here is
believed to be "estrogen priming," the concept that estrogen makes the pituitary more sensitive to GnRH
from the hypothalamus, so that more LH is released for a given GnRH stimulus. This is well known to occur in
females leading up to ovulation. Unlike females, however, men don't have a preovulatory period or spikes in
LH. The research is fairly clear that estrogen priming does not occur in males. For starters, take a look at an
authoritative reference work like Grossman's Clinical Endocrinology, which states (pg. 99):

Progesterone, acting synergistically with oestrogens, exerts negative feedback on the hypothalamus during
the luteal phase, thus limiting GnRH pulsatility and slowing LH pulse frequency. The mechanism of positive
oestrogen feedback at the time of the LH surge has been much debated. There is now evidence that
enhancement of both hypothalamic GnRH pulse generator activity and pituitary responsiveness to GnRH are
involved. All species so far studied have shown an increased 'self-priming' effect of GnRH on the pituitary
during the preovulatory period... In males, the situation is more straightforward. Since LH surges do not
occur, only negative feedback effects are relevant. testosterone (and its active metabolite
dihydrotestosterone, DHT) exerts major suppressive effects on both LH and FSH secretion, largely by
inhibiting the GnRH pulse frequency generator, but possibly also by direct pituitary actions. Oestrogens in the
male reduce pituitary responsiveness to GnRH.

That states clearly that there is no priming in males, only negative feedback. The last emboldened sentence in
this quote directly contradicts Dr. Scally's quote above. If clomid were to produce estrogenic action in the
pituitary, it would only serve to inhibit LH secretion.
 Grossman's statement is corroborated by the more recent research on the specific effects of androgens and
estrogen on the pituitary and hypothalamus of healthy men. Here, it was shown that estrogenic action at the
pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to
GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated
in its conclusion that: "These data confirm previous work from our group which ... showed [estrogen] has
both hypothalamic and pituitary sites of negative feedback in the male." In fact, "negative feedback at the
pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.
This older paper had a very interesting finding:
The positive estrogen feedback was found to be a relatively sex-specific reaction of the hypothalamo-
hypophyseal system in rats as well as in human beings. It is dependent--most of all--on the estrogen
convertible androgen level during sexual brain differentiation, but also on an estrogen priming effect in
adulthood. The lower the estrogen convertible androgen or primary estrogen level during brain
differentiation, the higher is the evocability of a positive estrogen action on LH secretion in later life. In
clinical studies, we were able to induce a positive estrogen feedback on LH secretion in most intact
homosexual men in clear-cut contrast to intact hetero- or bisexual men. These findings were strongly
confirmed by Gladue and associates.

In other words, estrogen levels during brain development are responsible for the sex-specific differences in
gonadotrophin secretion and estrogen feedback at the pituitary. The important point of this research is that
males (with the exception of homosexuals) were not found to have any positive feedback from estrogen.
Those results that were "strongly confirmed."

Finally, there's this research (that was referenced above), which couldn't have been any more relevant. It
directly examined the effects of nolva and clomid on the pituitary of human males. They infused the men
with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking Nolvadex at 20
mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced
LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic
activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."

Jcaesar369 Recommended PCT Protocol

Please Read The Original Post Here

TL;DR:

Last 6 Weeks of Your Cycle / Blast & Cruise:(including the time needed to allow all compounds to clear)

We will count down the last 6 weeks (plus 3 days - 45 days total). You will start the SERM's after day 0.

• T-minus 45 to 24 Days: 500–1000 IU HCG 3x weekly (IM) for 3 weeks

• T-minus 23 to 2 Days: 500–1000 IU HCG 2x weekly (IM) for 3 weeks OR 250 to 500 iu HCG 3x weekly (injected
IM) for 3 weeks
• T-minus 2 to 0 Days: Wait 3 days before starting SERM's
Starting The SERMs
SERMs should be run for a much longer time period, depending on the time of your Cycle or Blast and Cruise
(i.e., total time on steroids). Use your head and think about this one. If a standard 12–16 week cycle uses 4
weeks of SERM's, how long should a 3-year BnC PCT be? There is no right answer, but you will probably want
to err on the side of caution and run at least 8–12 weeks of SERMs.
• 10 mg Nolvadex (Tamoxifen) everyday OR 60 mg Toremifene everyday
AND
• 25 mg Clomid (Clomiphene) everyday

Controversy

It should be noted that there is some controversy on whether using two SERMs at once is beneficial or not,
with consensus leaning towards the latter.
How long to wait to check blood work to see if you've recovered?
Answer: ONE MONTH after cessation of SERM's. You will be looking for LH/FSH returning to fairly normal, as
well as total and free testosterone levels. How do you know what normal is? What your levels were that you
got with your pre-cycle natural self blood work.
Disclaimer: All of these RECOMMENDATIONS (not mandatory) are to be used as advice. All of the
suggestions by Jcaesar369 are based off of clinical FDA trials and studies, found in the original post for
reference.

Triptorelin PCT

• Triptorelin 50–100 mcg injected intramuscular ONCE

Pick one:

• Nolvadex 10/10/10/10
• Toremifine 30/30/15/15

The reason for the Nolvadex or Toremifine is to prevent the estrogen rebound that is common with
Triptorelin, one may also use an AI such as Armidex or Aromasin.

A Doctor's Recommended PCT (TRT Clinic)

/u/DeludedOldMan's TRT doctor recommend this plan when coming off a 9-month cruise:
Weeks 1-2 (last 2 weeks of injecting test)
• Test C/E (normal TRT dose)
• 400 iu HCG E3D
• 20 mg Clomid EOD
Weeks 3-4
• 400 iu HCG E3D
• 20 mg Clomid EOD
Weeks 5 - 6
• 20 mg Clomid EOD
Week 7-8
• 20 mg Clomid E3D

Miscellaneous Findings

Triptorelin/GnRH

A newer approach receiving recent attention is Triptorelin, the GnRH agonist. This is used in a continuous
manner to chemically castrate a man, but in a one off dose, has been reported to kick start the PTA in a
hypogonadic BB. Triptorelin is a synthetic analogue of GnRH. It causes constant stimulation of the pituitary
gland and by acting as such, it stimulates the pituitary gland to pump out LH and FSH. The dose needed to
cause chemical castration is much greater than the dose one would use to restart HPTA. The way Triptorelin
hinders gonadotropin release is similar to how HCG will hinder test production in the testes. A small amount
of HCG will stimulate the Leydig cells to produce testosterone, but too much will desensitize the Leydig cells.
This is what GnRH does, but with the pituitary gland. Triptorelin has been studied to restore full HPTA
function in a steroid user who cycled for 13 years. Due to it's nature it is advised that Triptorelin only be used
if coming off long-term blasting and cruising or if one plans to cease AAS forever.

Anecdotal evidence claims that Triptorelin is capable of restoring HPTA function to those diagnosed with
hypogonadism.

• Anabolic steroids purchased on the Internet as a cause of prolonged hypogonadotropic hypogonadism

• Pituitary gonadotropin-releasing hormone receptors. Effects of castration, steroid replacement, and the role
of gonadotropin-releasing hormone in modulating receptors in the rat
• Effects of castration on luteinizing hormone and follicle-stimulating hormone secretion by pituitary cells from
male rats

Misc.

Mechanism by which Nolvadex works:

• While the literature is scant in this field, a recent paper has shed some light on this mechanism: Short-Term
Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and
Testosterone Secretion in Older Men
• How clomid affects the eyes: Effect of clomiphene on [Ca2+]i rises and cell viability in rabbit corneal
epithelial cells
• Explains the possible cause behind vision effects: Oxidative stress plays an important role in the
pathogenesis of drug-induced retinopathy

11 THE ESTROGEN HANDBOOK

Gynecomastia Mechanics

First of all there are three different types of Gynecomastia (Gyno): Estrogen induced, Progesterone induced
and Prolactin induced. Of course, you can avoid all three types of Gyno by keeping Estrogen (E2) within the
normal range (unless using a 19-nor). The precursor to any type of Gyno is almost always Estrogen! Once you
let Estrogen build up you signal to your brain that you have conceived, it doesn’t matter if you are a man or
woman, your body at this point will have to go through certain processes to prepare you for lactation. Firstly
your body will rush to use that Estrogen and build up breast tissue (which will form a lump) which is
mandatory for the lactation process. Once this stage has been completed and you have let Estrogen still high
your Progesterone will increase (Estrogen can still remain high) which is an attempt from your body to make
the tissue larger and also make your aerolas bigger (puffy and enlarged nipples) again to get them ready for
lactation. Last stage of Gyno is Prolactin lactation, all previous stages were preparing the body for this
moment at this point your Progesterone and Estrogen will drop and your Prolactin will spike, this is when
someone starts lactating.

Estrogen (E2)

Estrogen is commonly referred to as “E2”. Estrogens are made up of Estrone (E1), Estradiol (E2), and Estriol
(E3) (though the one we’re concerned with is E2 specifically). It is fine to simply refer to these as Estrogen,
but it’s more important that you know how to control your own and have a basic understanding of the topic.

The mechanisms through which E2 interacts with sexual reproductive organs and other hormones in the male
body is actually much more complex than in a woman’s body. This is mainly because we have so little E2
compared to our female counterparts. The same can be said of Testosterone in women; a slight change in
levels can trigger huge changes. A lot of people know the term “aromatase” or “aromatization”, but do
people know exactly what it is?

The most challenging hormone for the steroid user is Estrogen by far. It is the cause of any changes in your
nipple/pecs (gyno), mood, libido, hardness, bloat, skin, prostate, appetite – you name it, when you feel off
90% of the time is due to low/high Estrogen levels.
 When you hit your sweet spot you will know, you can’t miss it. You will feel happy, content, you will sex like a
champ, eat like a champ and train like a champ and to top it off everybody around you will be happy as well.

Here is an indicators of low/high Estrogen levels:

Low Estrogen Sides

• Dry skin/lips
• Feeling of dehydration
• Loss of libido
• Erectile Dysfunction
• Loss of sensitivity
• Dry glans (penis)
• White glans
• Loss of girth
• Irritability/Mood swings
• Crying for no reason
• DHT rage (aggression you take out on others)
• Dull orgasm
• Hesitation just before urinating
• Night sweats
• Loss of appetite
• Constant fatigue
• Lethargy
• Constipation (due to dehydration)
• Diuretic effect (pissing more water than you are consuming)
• Itchy scalp
• Obsessive thoughts

Low and high Estrogen sides are very alike, the more experienced you get the easier it is to differentiate
between them, but it will always be tricky. The best way to tell is always to get your Estradiol (E2) checked
though blood work.

High Estrogen Sides

• Acne
• Loss of libido
• Water retention (Bloat)
• Moon face
• Small testicles
• Scrotum hanging too high
• Soft testicles
• Extreme oiliness all over
• Moodiness (Aggression, depression, increased irritability)
• Lethargy
• Insomnia
• Soft erections
• Extreme cravings for sugar/chocolate
• High BP
• BP spikes
• Enlarged prostate
• Pressure in lower abdomen when urinating
• Thin stream when urinating
• Constipation (from water retention)
• Itchy nipples
• Gynecomastia

When you get one side effect, it is just an indication use this list to potentially make a full picture. Never go
by one side only, being bloated only means nothing, having dry skin only means nothing again. Again, the
best way to tell is always to get your Estradiol (E2) checked though blood work.

Aromatase

Aromatase is an enzyme that converts testosterone to estradiol and androstenedione to estrone. Similarly,
17-ketosteroid reductase is an enzyme that is capable of converting androstenedione to testosterone and
estrone to estradiol. Aromatase is named based upon the fact that it removes a methyl group on the 19th
carbon and rearranges ring A into an aromatic ring, hence it aromatizes the testosterone molecule.

Aromatase is found in many different cells in the body, however it is primarily found in adipose tissue. The
liver, skin, and testes are also primary sites of aromatization. In the testes, you have two different cells that
respond to the gondaotropic hormones (LH and FSH). Leydig/interstitial cells respond to LH and initiate the
synthesis of testosterone. Sertoli/sustentacular cells respond to FSH and initiate and support
spermatogenesis. Sertoli cells do not produce testosterone but they contain FSH-dependent aromatase. The
estradiol produced in Sertoli cells binds to E2 receptors in Leydig cells and the estradiol will suppress the
Leydig cell’s response to LH stimulation. Aromatase activity in other cells are not FSH-dependent. Much of
the brain contains aromatase, except the pituitary gland.

Aromatase Regulation

Aromatase is decreased endogenously by prolactin and anti-Mullerian hormone, although AMH is irrelevant
and concentrations are almost non-existent in adult males. It is also decreased exogenously by aromatase
inhibitors, nicotine, zinc, vitamin E, and resveratrol. The enzyme is increased endogenously by gonadotropins,
insulin, testosterone, and androstenedione. Increased adipose tissue increases quantity of aromatase in
body.

Aromatase Inhibitors (AIs)

Keep in mind Estrogen is good for you in many ways (libido, mood, skin quality, hair, nails etc). But, most
importantly, Estrogen is good for your lipids. I am sure you have heard how Arimidex and Letrozole are bad
for your lipid values while Aromasin is ‘better’, in reality all AI’s are as bad as each other for your liver values.
The more you lower Estrogen, the worse your liver values will get – it doesn’t matter which AI you use, all
that matters is how much you are lowering your Estrogen. If you lower your Estrogen by 10 pg/mL you won’t
notice much difference. If you crash your Estrogen down to single digits I guarantee you that your HDL/LDL
will be completely out of whack no matter which AI you used.

Suicidal AI vs. Non-Suicidal/Binding AI

Arimidex and Letrozole are non-suicidal AI’s, all they do is bind any Estrogen you convert directly on your
aromatase enzyme. Each AI binds a different percentage of Estrogen, Letrozole binds more than Arimidex of
course. The problem with binding AI’s is that once you cease use, all of the Estrogen that had accumulated
when you were using that AI suddenly gets released – this process is called "Estrogen rebound" and I am sure
you know it can be far worse than Estrogen while on a cycle since normally when you drop your AI you either
cruise with a low dose of Test or PCT. In both cases you have far less Test in you and once all that Estrogen is
released you got a much higher chance of getting Gyno and of course you are going to be bloated and feel
soft for weeks till your Estrogen comes down to normal levels.

Aromasin is the new generation of AI and it is suicidal, the difference between Aromasin and the other AI’s is
Aromasin will actually destroy/kill a certain percentage of your aromatase enzyme so by doing so it also 'kills'
any estrogen that was attached to that enzyme. This means when you stop using Aromasin you won’t
rebound at all like you would with the binding AI’s. If anything, you will have to wait for a while for your body
to start producing more aromatase (very bad if you crashed your Estrogen comparing to using the other AI’s).
Each person is different in the rate they create new aromatase; it can take one to three weeks.

Arimidex (Anastrozole)
Arimidex (Adex) will lower your Estrogen by about 50-60%. Of course, if you keep taking it that percentage
accumulates so you lower 50% by another 50% and so on, you can easily end up with your Estradiol in the
singles if you take it for long enough at a high enough dose and you aren’t converting much Estrogen from
aromatizing gear (using low dose of Test and high dose AI). Arimidex is a good for new steroid users as if they
overestimate their dosing for AI and get symptoms of low E2, they will bounce back back up fairly quickly and
adjust as needed.
Dosage on cycle: dosing is user dependent and you should get blood work to dial in your dose,
but MOST users will find .5 mg of Arimidex E3D or E3.5D to be a good starting dose for 500-600 mg
 Testosterone (just for a reference). Some may need more frequent (EOD) dosing or some may even need less
than E3.5D; this is really something that varies person-to-person too much and without blood work there is
no way to know for sure what dosage you need.

Aromasin (Exemestane)
Aromasin (Asin) is an orally available suicidal aromatase inhibitor. Because Aromasin is steroidal this gives it a
favorable Estrogen suppression profile and confers a few really awesome benefits over other anti-estrogens
both on paper and in real experience. Steroidal anti-estrogens have the benefit of being lipid-friendly and
they all lower SHBG which increases the ratio of free to bound Testosterone, which as many experienced
bodybuilders know can have a relatively profound, positive impact on gains.

It is important to understand how drugs work in order to properly dose them, Aromasin is a suicidal
aromatase inhibitor, this means that it binds with aromatase enzymes and as it does so permanently disables
the enzyme and destroys it. Hence the “suicidal” this compound. Just beware, if you crash your estrogen on
Aromasin, it can take a long time waiting for your E2 to rise again (compared to the non-suicidal AIs), which
will have a negative impact on lipid profile, joint integrity, mental health, libido and overall gains.

Aromasin’s half life in the male body is actually very short (~9 hours) and it is quickly eliminated, however,
since as soon as it enters your bloodstream it quickly destroys the aromatase enzymes present in your body,
it is effective in maintaining significant reductions in estrogen for up to +72 hours after a single 25mg dose.
Estrogen levels only begin to rise again after your body has begun to make new aromatase enzymes to
replace the ones destroyed by Aromasin.

There is a great study on the pharmacokinetics of Aromasin in men which found the following:
• 24 hours after one 25mg dose estrogen levels are reduced by 58 ± 21%
• 3-6 days after initial dose estrogen levels return to baseline (without rebounding)

This means that you can find the timing and dosage that works for you; this flexibility is what makes
Aromasin such a versatile Anti-E.

BUT WAIT, there’s more. In males, Aromasin was found to increase total testosterone by ~60% after 10 days
@ 25mg/day, however the same study found that while it increased total testosterone by 60%, free
testosterone was increased by over 100 percent! that’s right, it DOUBLES bio-available testosterone (in
naturals of course). With all this said, it is an option to be ran into PCT like the study, when utilizing HCG right
before or the first couple week of PCT. See the PCT wiki page for more info.
The Good:
• Lowers SHBG, increasing free test & makes all other anabolic steroids more bio-available (i.e. more gains)
• Increases IGF-1
• No adverse changes in lipid profiles for men (unless you crash estrogen - studies were also not on cycle and
may be different)
• Is not liver toxic
• No Estrogen rebound
The Bad:
• Typical aromatase inhibitor issues here, include stiff joints and possibly lethargy if E2 gets too low
• If you crash your E2 levels, it will remained crashed until your body makes more aromatase at it's own rate.
• Typically more expensive than Arimidex or Letrozole
• Alopecia. The other two AI’s have hair loss/hair thinning as a side effect, but not full blown Alopecia.
Dosage on cycle: dosing is user dependent and you should get blood work to dial in your dose,
but MOST users will find 12.5 mg of Aromasin E3D or E3.5D to be a good starting dose for 500-600 mg
Testosterone (just for a reference). Some may need more frequent (EOD) dosing or some may even need less
than E3.5D; this is really something that varies person-to-person too much.

Letrozole
Letrozole is by far the harshest of all AI’s, not necessarily because your Estrogen will be too low but because
Letrozole as a compound/active ingredient is really harsh. The main applications for Letrozole is for Contest
Prep or apart of Gyno Reversal (along with a SERM) as this is the nuclear option. Whenever used, always be
sure to taper off to avoid rebound.

On cycle dosage: This AI is very easy to crash your estrogen with. It is not typically recommended as your
main AI

Selective Estrogen Receptor Modulators (SERMs)

After your cycle is complete and the steroid esters start to clear the system, a post cycle therapy (PCT) is
done to help get the pituitary glands running again. SERM's work by blocking estrogen going into the pituitary
glands, which cause a rise in LH/FSH and testosterone levels, temporarily. This helps give a boost after cycle,
and it helps maintain gains.

Keep in mind all 3 SERMs will work in favor of your liver (Agonists) since they are mild Estrogens, like stated
earlier Estrogen is good for your liver so adding a SERM will always improve your HDL/LDL. All SERMs don’t
lower Estrogen, in fact they will increase your total Estrogen. They also block your Estrogen in the nipple
area.

Nolvadex (Tamoxifen)
Agonist: Liver, Uterus (female)
Antagonist: Breast/Nipple
Nolvadex is more suited for PCT purposes rather than Gyno Flair-Ups or Gyno Reversal, as it increases natural
Test levels by 60%, but will decrease IGF-1 levels +25%.
Dosage on cycle: 20-40mg ED
Dosage for PCT: See PCT

Raloxifene (Evista)
Agonist: Liver, bone (increases bone density and is a recognized treatment for osteoporosis)
Antagonist: Breast/nipple

Raloxifene doesn’t affect IGF-1 levels whatsoever, also it increases bone density. It is the ideal SERM for Gyno
Flair-Ups or Gyno Reversal since its an agonist for your bones, doesn’t affect IGF-1 levels, and is perfectly safe
to run with a 19-Nor. Raloxifene shouldn’t be used in PCT since it raises natural test levels by 40% only, 20%
less than Nolvadex.

Dosage on cycle: 60mg-120mg ED

Nolvadex vs. Raloxifene for HGH/IGF-1

Taken from this study
Conclusions: Tamoxifen, but not Raloxifene, reduces IGF-I levels. Both SERMs stimulate the gonadal axis, with
tamoxifen imparting a greater effect. We conclude that in therapeutic doses, Raloxifene perturbs the GH and
gonadal axes to a lesser degree than Tamoxifen.

Nolvadex vs. Raloxifene for Gyno

Taken from this study
Conclusion: Inhibition of estrogen receptor action in the breast appears to be safe and effective in reducing
persistent pubertal gynecomastia, with a better response to Raloxifene than to tamoxifen. Further study is
required to determine that this is truly a treatment effect.
Gyno Flare-Up Protocol
If your Estrogen is wildly out of control and you are developing puffy, sore, or itchy nipples, UP your AI dose
and start taking your SERM.
Note: If you choose Arimidex as your AI, just be aware the blood levels of Arimidex can drop a bit when used
alongside
Nolvadex.](/r/steroids/wiki/faq/list#wikiq.3A_can_nolvadex.28tamoxifene.29and_arimidex.28anastrozole.29
_be_used_together.3F) To avoid this, you may choose Raloxifene.
Dosing: Pharmaceutical Raloxifene 60mg ED or Pharmaceutical Nolvadex 20mg ED. It usually will subside
after a 7-12 days. Continue the SERM for 3 days after the symptoms have subsided before you drop the
SERM. It is suggested to use Raloxofine over Nolvadex when possible, due to Nolvadex decreasing IGF-1 as
seen above.
Gyno Reversal Protocol

If your Gyno is pubertal, as seen above, this potentially could help, but most likely surgery is your best option.
If your Gyno is from AAS use, this has worked for multiple users on our board:
 Dosing: Pharmaceutical Raloxifene 120mg ED - split the dose ½ in the AM, ½ in the PM for a month, then
60mg ED - split the dose ½ in the AM, ½ in the PM until you've seen sufficient reduction in size.

Toremifene (Fareston)
[Under Construction]

Clomid
Agonist: Liver
Antagonist: Breast/nipple
Clomiphene is a harsh drug, if you get the visual sides/blurry vision from clomid they stay for life. They are
rare, but do happen.

Clomiphene is a mixed agonist/antagonist. This is due to the fact that Clomiphene is composed of two
isomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene). Enclomiphene is an Estradiol
receptor antagonist. Zuclomiphene is an estradiol receptor agonist. In all likelihood, the net antagonist effect
might be due to the composition being 70% trans (enclomiphene) and 30% cis (zuclomiphene).
Nolvadex/Raloxifene is more of a strict anti-estrogen, decreases the effect of estrogen in the body, and
potentiates the action of clomiphene. This combination came about after 100s of clinical experience.

So Nolvadex/Raloxifene is more of an antagonist, than Clomid is. They are better at blocking the ER than
Clomid is. Clomid also seems to exert agonistic effects in parts of the brain that control emotion. That would
explain why some turn into women on periods during there experiences with Clomid.

Tamoxifen is also made of slightly more isomers, the cis isomer of tamoxifen (inactive one) trans-tamoxifen
and trans-4-OHT isomer.

All you really need to know about clomid can be learned here: Product Information: Clomid(R), Clomiphene
citrate. Aventis Pharmaceuticals, Kansas City, MO, 96.
Here is the clomiphene drug monograph

• If you want to learn about any drug, the manufacturer PRODUCT INFORMATION and DRUG MONOGRAPH are
excellent and probably the best way to learn about any drug, especially these PCT medications, as these
sources are FDA approved and studied in large clinical trials.

• The FDA recommended dosage for clomid for male hypogonadism (what we are trying to beat with PCT) is 25
mg EOD or every day, titrated up to 50 mg EOD MAXIMUM for HPTA restart.
Dosage for PCT: See PCT

Prolactin Support

Of all the potential side effects connected to AAS use, decreased libido and sexual dysfunction are regarded
as two of the most undesirable and for good reason. Not only do they interfere with one of man’s most
prized activities. Although excess estrogen and testosterone deficiency are often responsible for these side
effects, elevated prolactin, which has begun to afflict steroid users with increasing frequency, also deserves
its share of the blame. When it comes to the latter, we can fairly point the finger at 19-Nors like Trenbolone
and Nandrolone - two mainstays in the world of AAS.

Although steroids are the primary culprit when it comes to prolactin-induced side effects, certain Growth
Hormone (GH) peptides also have the potential to increase prolactin levels, although to a much smaller
extent than the aforementioned AAS. Generally speaking, the increase in prolactin witnessed with this class
of supplementation is inconsequential, as levels do not rise high enough to cause problems. In fact, this effect
is so mild that levels usually remain within a normal physiological range. However, when combined with
other prolactin elevating drugs, they may add further fuel to the fire, giving cause for consideration. Lest
anyone decide to shy away from GH peptides for this reason, when used alone - and often even when used
with other prolactin elevating drugs - the benefits far outweigh the risks. It is only when one’s prolactin levels
are already high that they increase the potential for side effects. Of the different GH peptides on the market
today, only GHRP-6, GHRP-2, and Hexarelin are capable of increasing prolactin levels.

What Is Prolactin?
Most commonly referred to as the lactation hormone, prolactin is responsible for the production of breast
milk in nursing mothers and also plays a critical role in the growth & development of the mammary glands.
Despite its connotation with pregnancy, it is a diverse hormone, having influence over a large number of
functions and being implicated in over 300 separate actions. When it comes to steroid users, most are
interested in circumventing just two of these—the development of glandular tissue in the breast (gyno) and
lactation.

However, prolactin also encourages bodyfat storage by directly increasing the production of a specific protein
called lipoprotein lipase (LPL). Lipoprotein lipase plays an important role in fuel metabolism by hydrolyzing
triglycerides from circulating plasma chylomicrons (chylomicrons are fat globules which transport dietary
triglycerides from the small intestine into circulation) and other low-density lipoproteins, providing free fatty
acids to adipose tissue for storage. The higher one’s LPL levels, the more likely one is to accumulate bodyfat.
Prolactin has also been shown to increase estrogen receptor concentration within breast tissue, increasing
one’s sensitivity to circulating estrogen and making the individual more susceptible to gynecomastia and
other estrogenic side effects.

When reviewing the effects of elevated prolactin on the male body, it becomes readily apparent that it is in
one’s best interest to keep this hormone under control. While some of the side effects associated with
increased prolactin are readily recognizable, others, such as increased bodyfat and estrogen receptor
proliferation, are frequently attributed to other causes or not recognized at all. Regardless of one’s
awareness, excess prolactin will wreak hormonal havoc on the body, directly working against our
 bodybuilding goals while simultaneously initiating the development of female secondary sex characteristics.
All bad—all preventable.

Choosing Your Medicine

Until recently, alleviating hyperprolactinemia (excess prolactin) involved the routine administration of one of
various side effect-laden pharmaceutical preparations. In many cases, the accompanying side effects were
worse than the primary condition one was trying to treat, negating the drug’s beneficial effects and leaving
the you between a rock and a hard place. For years Bromocriptine was the go-to of defense when it came to
lowering prolactin for dopamine agonists. It was effective, readily available, and reasonably priced, but many
found the resultant side effects just too much to handle. But today, most will either use Cabergoline
(Dostinex) or Pramipexole (Mirapex)

First Line Of Defense

When you're wanting to preventatively take action against prolactin, a Dopamine Agonist may not be the
best choice to start with as they come with many unwanted sides and can be harsh drugs. You should always
have a Dopamine Agonist on hand if you wish to take a 19-Nor, but if you wish to run something
preventatively, you should start with some supplements.

Supplements To Help Control Prolactin:

PLEASE READ: Prolactin-Inhibiting Supplements Wiki Page
• Vitamin B6 (Pyridoxine Hydrochloride & P-5-P) - To lower prolactin levels it's recommend you take 50-
200mg of P-5-P a day, in divided doses. If you want to take regular B6, which can sometimes cause minor side
effects, take 300-1000 mg per day in divided doses.
Read the label before you buy B6 (if you choose not to get P-5-P), because the Pyridoxine Hydrochloride
type of B6 (in most supplements) has been shown to be a prolactin inhibitor, but Pyridoxal Hydrochloride
has been shown to be ineffective at lowering prolactin – make sure you buy the right type!
• Vitamin B6 - Examine Page
• Vitamin E - When using Vitamin E as a prolactin inhibitor, it's recommended that you take 300-400 IU per day
of natural Vitamin E – this can be raised up to dosages such as 1000 IU for greater prolactin control, but be
aware of the possible side effects outline here
Natural Vitamin E is labelled D-Alpha Tocopherol whereas synthetic is labeled DL-Alpha Tocopherol – the
natural form works best. D-Alpha Tocopherol with mixed natural tocopherols or D-Alpha Tocopherol with
mixed natural tocotrienols are the absolute best forms to take.
• Vitamin E - Examine Page
• SAM-e - Take 400-1200 mg a day of SAM-e along with Vitamin B6 and Vitamin E. An added bonus is SAM-E's
ability to detoxify the liver.
• SAM-e - Examine Page
• Other Effective Prolactin-Inhibiting Supplements
Remember, only use your Dopamine Agonist if blood work shows elevated levels or if your nipple(s) leak ON
THEIR OWN. Do NOT squeeze your nips and force liquid out, even natural guys can do this, by doing this you
will stimulate and cause an increase in prolactin.
DO NOT TOUCH YOUR NIPS.

The Dopamine Connection

Anti-prolactin drugs work by mimicking the activity of a substance in the brain called dopamine, thereby
classifying them as dopamine agonists. Dopamine itself is a neurotransmitter; a chemical messenger between
nerve cells in the brain. When levels of this neurotransmitter are normal the body functions properly, but if
levels become imbalanced serious problems can develop, such as Parkinson’s or Restless Leg Syndrome.

However, in order for dopamine to have an effect it must first attach to dopamine receptor sites, which are
found on the surface of the cell. Once attached, the receptor receives, recognizes, and responds to this
chemical signal. Dopamine Agonists works by stimulating these same receptor sites, thereby producing the
same effects as dopamine, but you may be wondering, how is this relevant to prolactin?

As one of the predominant regulators of prolactin, dopamine has a direct impact on its production. More
specifically, dopamine works to reduce prolactin levels by attaching to D3 receptors, which inhibit the
production of prolactin by lactotrophs (lactotrophs are prolactin producing cells located in the pituitary).
Acting as a dopamine substitute, dopamine agonists works through the same mechanism, fooling the body
into thinking that dopamine levels are high. This shuts down, or reduces the production prolactin, depending
on the dosage administered.
Exactly how the steroids trenbolone and nandrolone increase prolactin levels, we can’t be sure, but one thing
we do know is that many who use these drugs have experienced dramatic elevations of this hormone—
sometimes far above normal levels. This can and often does lead to one or more of the aforementioned side
effects. Dopamine agonists works to address the issue directly, shutting down prolactin production at its
root.

Cabergoline (Dostinex)
Cabergoline (Caber) will lower both progesterone and will inhibit prolactin/lactation. It’s a dopamine agonist
means it wont allow your body to lactate since it will occupy your dopamine receptors which are responsible
for lactation. Caber is the best prolactin support when running any 19-Nor since the side effects are minimal
– no drowsiness, doesn’t affect sleeping patterns, and in general as far as dosing goes is far more flexible
than Pramipexole or Bromo. Also there is no withdrawal when ceasing use of Caber like with Prami.

Caber is a recognized ED med, it reduces downtime (not to be confused with multiple orgasm) so if you need
24 hour recovery between sessions two weeks after taking Caber you will see a significant decrease in
downtime you will need 12-16 hours to be ready for the next session, if you need 2 hours you will need 1
hour with Caber.
Also its known for its potential multiple orgasm effect - when you ejaculate you will feel as if you are
releasing two or three loads at the same time. This needs some input for the user though its not instant, the
more you hold it in the more orgasms you will potentially have in the end.

Common Dose On Cycle: 0.25-.5mg E3D or E3.5D

Common Does To Stop Lactation: 1-1.5mg E3-5D

Pramipexole (Mirapex)
Pramipexole (Prami), like Caber, will decrease progesterone and will inhibit prolactin/lactation. It’s a
dopamine agonist, like Caber, so it will occupy dopamine receptors which are responsible for lactation.

Pramipexole (Prami) is a very peculiar drug! You need to taper up really slowly to get to the desired dose and
also taper down slowly to avoid the mild withdrawal effect it will cause. Prami is an addictive substance
and /r/steroids is hesitant recommending it, as the more you use it the harder it will be to come off it, also
you will find you will want to increase the dose to maintain the ed effect. Prami’s ED effect is not as good as
Caber. It does reduce downtime like Caber does but that’s about it there is not potential enhancement in
your orgasm or your libido contrary to caber. Only advantage of Prami over caber is that if taken at the right
time (2-3 hours) before bedtime it can work as good as a Benzo to knock you out to sleep. Which when
running Tren is a bonus. If, however, you dose it wrong (unwillingly of course) say 30 minutes – 1 hour before
bed time you will find that after 2-3h of sleep you will be wide awake and probably sweating since the
dopamine you suppressed 4 hours ago rebounds and you feel as if you just had a hit of coke in your sleep, not
a good feeling. Also every time you up the dose it takes some adjusting even if you are used to the substance.

Sleep sides like vivid dreams and waking up mid night can be avoided by taking Prami at the right time so you
got to experiment with this (the earlier you take it the better). Make sure you never take Prami in the
morning or too early in the evening you are going to feel drained, dizzy, nauseous and like a zombie all you
will think its when the time comes to go to sleep.

The worst part with Prami starts when you quit, for the first few days after you quit, you will wake up in your
sleep many times as if you were quitting cigarettes or weed even, then you will have the lightest sleep ever
as if you were sleeping with your eyes open and the dreams will be negative and intense. Basically you get all
the Prami sides you had earlier only they cant be avoided since you don’t take Prami anymore. This will
subside completely after 5 – 7 days.

Common Dose On Cycle: taper up from 0.125mg to 0.25mg-0.50mg (the high dose only if you are stacking
two 19-Nors or high dose of tren). After you are done with your cycle taper down even slower from 0.50mg
to 0.125mg and stay one week on each increment then quit. No matter what you do expect some discomfort
the first 3-5 days after you quit.
Dose To Stop Lactation: You would probably need 1-2mg per day to stop lactation, but wouldn’t recommend
it, it would take ages to rump up to that dose, if you are already lactating, use Caber worse thing that could
happen when jumping to a high dose of caber would be to get a flush face that lasts 12-14h (annoying but
much better than puking your guts of for hours).

12 NUTRITION
There are many schools of thought on nutrition, especially when it comes to strength and power athletes.
Unfortunately there are no human studies on nutrition involving supraphyisiological doses of AAS making
most "bodybuilding" and "powerlifting" diet advice anecdotal.

If you've never considered nutrition or diet, /r/fitness has a very good breakdown for you
To paraphrase however, specific food choices are less important, in terms of muscular gains/fat loss, than
overall calories and macronutrient ratios

As a reminder- 1g Carbohydrate -> 4kCal

1g Protein -> 4kCal

1g Fat -> 9kCal

1g Alcohol -> ~7kCal

All successful diet programs are based around one thing, whether or not they agree on macronutrient ratios,
or timing, is another issue entirely. This single goal is consuming a surplus of calories in order to gain muscle
mass or eating at a caloric deficit in order to lose fat.

Common thought among users is that during cycles it is possible to diet at a very high caloric deficit without
losing much if any muscle mass. On the flip side, with high doses of AAS it is possible to eat at a higher caloric
surplus than a natural athlete without gaining as much fat, because the nutrients will be partitioned more
favorably for glycogen storage and muscle growth/repair.

Macronutrients

A macronutrient is an essential nutrient required in relatively large amounts, such as carbohydrates, fats,
proteins, or water. Some minerals are sometimes included as well.

Protein
Protein is necessary for muscle repair/growth, as well as normal function and is sometimes used as an energy
source. Protein is not "stored" in humans like fat (in adipose) or carbohydrates (glycogen).

Due to this increased efficiency in nutrient partitioning there have developed two trains of thoughts when it
comes to protein intake
The first is that, because consuming 1g protein/lb (2.2g/kg) of bodyweight is more than enough for natural
athletes, consuming more than that amount of protein for AAS users is seen as a waste of calores/money.
The increased nutrient partitioning will allow the body to build more muscle off of less of this macronutrient.

The second is that due to the increased efficiency it makes sense to increase protein intake because the body
will be able to utilize more of the macronutrient than it could normally.

I urge you to try out both methods and decide for yourself what works best or you like the most

(Needs work on aminos, complete sources, sources-complimentary)

Varied Protein Types.

From this article:

Protein intake that exceeds the recommended daily allowance is widely accepted for both endurance and
power athletes. However, considering the variety of proteins that are available much less is known
concerning the benefits of consuming one protein versus another. The purpose of this paper is to identify and
analyze key factors in order to make responsible recommendations to both the general and athletic
populations. Evaluation of a protein is fundamental in determining its appropriateness in the human diet.
Proteins that are of inferior content and digestibility are important to recognize and restrict or limit in the
diet. Similarly, such knowledge will provide an ability to identify proteins that provide the greatest benefit
and should be consumed. The various techniques utilized to rate protein will be discussed. Traditionally,
sources of dietary protein are seen as either being of animal or vegetable origin. Animal sources provide a
complete source of protein (i.e. containing all essential amino acids), whereas vegetable sources generally
lack one or more of the essential amino acids. Animal sources of dietary protein, despite providing a
complete protein and numerous vitamins and minerals, have some health professionals concerned about the
amount of saturated fat common in these foods compared to vegetable sources. The advent of processing
techniques has shifted some of this attention and ignited the sports supplement marketplace with derivative
products such as whey, casein and soy. Individually, these products vary in quality and applicability to certain
populations. The benefits that these particular proteins possess are discussed. In addition, the impact that
elevated protein consumption has on health and safety issues (i.e. bone health, renal function) are also
reviewed.

TL;DR Vary your protein intake types for best results.

Bio-availability of Protein

From this article:

Protein Type Bio-Availability Index

Whey Protein Isolate Blends 100-159

Whey Concentrate 104

 Protein Type Bio-Availability Index

Whole Egg 100

Cow's Milk 91

Egg White 88

Fish 83

Beef 80

Chicken 79

Casein 77

Rice 74

Soy 59

Wheat 54

Beans 40

Peanuts 43

Max usable protein

It is often claimed that "anything over 30g of protein in one hour is unusable by the body." This is untrue.

http://examine.com/faq/how-much-protein-can-i-eat-in-one-sitting.html
There really is no literature to indicate this number as a 'holy grail' of protein absorption.

It may have arisen from looking at the rate of amino acid transporters, assuming 10g/hour as a standard, and
applying that to the typical mini-meal approach to bodybuilder nutrition (with a meal every three hours).

and

Research done on Intermittent Fasting supports the theory that your body can cope with far more protein
than most people think, with two studies showing that the consumption of an average of 80-100g of protein
in 4 hours yielded no differences in lean mass

Carbohydrates
Carbohydrates are the body's main source of energy. The muscles, and liver, store carbohydrates in the form
of glycogen, a branched polysaccharide. AAS increase the amount of glycogen that will be stored in the
muscle giving it a larger appearance and more energy from which to draw during workouts. Carbohydrates
are also muscle/protein sparing. Glucose, Insulin and Glucagon after a high carb meal.
During mass gaining phases carbohydrates are generally exaggerated in AAS users due to the increase in
gylcogen storage capabilities. In fat loss phases carbohydrates are generally the first macronutrient to be
manipulated to decrease overall calorie intake.

When lowering one's carbohydrates significantly it is worth noting that during high fat/low carb (ketogenic-
type) diets, T3, the active thyroid hormone (or essentially one's metabolic rate) is lowered more than when
compared to high protein/low carb.1 The average minimum carbohydrate intake recommended is 130 grams
per day, with less promoting ketosis,
Carbohydrates can be broken into two basic groups. Fast-acting (mono- & disaccharides) and slow-acting
(polysaccharides). The biggest difference is how long the carbohydrate takes to get broken down by the
body. Fast-acting carbohydrates (sugars) illicit a more pronounced glycemic response by the body, requiring
higher levels of insulin, providing the body with energy in the short term. (Refined sugars can also increase
cholesterol, LDL, and risk of cardiovascular disease).5 Traditionally "fast" carbs are placed before, during, and
after a workout in order to supply the muscles with energy as well as promote nutrient uptake following a
workout. "Slow" carbohydrates (some sources include brown rice, sweet potato, and oats) are then
traditionally placed everywhere else in one's diet, including before a workout, especially if the workout in
question will take more than an hour. These carbohydrates illicit a smaller, and more long-term insulin
response, keeping the body at more stable blood-glucose levels.

Fiber

Fiber contains a different bond between saccharides than other polysaccharides like glycogen or starches
(beta vs. alpha). The body has trouble breaking down these beta-glycosidic bonds and this creates the idea of
"Net Carbohydrates". Some people consider "net carbs" while others do not. Net carbohydrates are
determined by taking the total carbohydrate intake and subtracting it by the amount of fiber ingested. The
resulting carbohydrate is the "net" and that number is used to calculate calories as opposed to the total
carbohydrate intake.

Fiber can be broken into two types, insoluble and soluble. Insoluble fiber (sources are hole grains) are not
fermented by bacteria in the colon and add bulk to the stool. Soluble fiber (sources are psyllium, rice, beans,
fruit, oats, bran, soy) CAN be fermented and thus can count towards total calorie intake (though some still
choose not to, or assign it 2kCal/g). Soluble fiber holds water and binds to cholesterol, it has positive effects
in cholesterol ratios.

The recommended amounts of fiber are 25g for women and 38 for men. Too much fiber (>60g) will require
extra fluid intake, bind to certain minerals, impairing absorption, and cause excess bloating.

Dietary fiber slows glucose absorption, decreasing the risk for type 2 diabetes by modulating blood glucose
and decreases hypertension. This should be a concern for AAS users since high blood pressure is a common
side effect of anabolic steroids.
High Fructose Corn Syrup

High fructose corn syrup (HFCS) is a major sweetener in the US. It is composed of 55% fructose and 45%
glucose and is sweeter than sucrose. HFCS is thought to contribute to obesity for a few proposed reasons.

1) In the liver, fructose is more easily converted to glycerol/fatty acids which form triglycerides, which are
transported in the blood and stored in adipose tissue.

2) Fructose does not stimulate insulin release in the way glucose does, which in turn will reduce leptin
production and does not suppress ghrelin, a peptide hormone that contributes to feelings of hunger.

No/Low Cal Sweetners

Sugar Alcohols: Each sweetener (sorbitol, xylitol, mannitol) is somewhere between 1.5-3 kCal/g. They are
absorbed and metabolized at a reduced rate when compared to sucrose and large amounts can cause
diarrhea, and bloating.

Saccharin (Sweet N Low): A 0 Calorie sweetener derived from coal tar and is 150-300x sweeter than sucrose,
with a bitter aftertaste.

Aspartame (NutraSweet or Equal): 180-200x sweeter than sucrose and 4 kCal/g. Only very small amounts are
needed to sweeten however. As a component is Phenylalanine it is not recommended for those with PKU.
Many people seem to believe that Aspartame is incredibly toxic. Although a small amount are sensitive to
aspartame (causing nausea, headaches, dizziness etc...) there is no need to be concerned if one does not
have PKU. Methanol, (methyl ester of phenylalanie) gets converted by the liver into formeldahyde which is
itself a toxic by product, however when compared to diet sodas, fresh fruit/juice such as tomatoes and
bananas have between 1-2x more methanol.

Sucralose: More than 600x sweeter than sucrose, chemically it is sucrose with chlorine as opposed to
hydroxyl groups, this allows it to mostly by-pass metabolism. Sucralose has about 2kCal per teaspoon.

Truvia (Stevia): 200x sweeter than sucrose, stevia doesn't issue any glycemic response.

Fats
Fat is another one of they body's energy sources, certain lipids, and consumption amounts are also important
for hormone production, maintenance of organs, and keeping joints healthy.

Excess in calories are converted and stored as fat in adipose tissue, the body's fat stores.

According to the USDA, in order to properly maintain one's organs, joints, and hormones fat consumption
should be between 20-35% percent of the overall caloric intake.
Because users create and manipulate major hormones on their own it is common for users to lower fats to
below 20%. In order to stay healthy it is not advised to dip fats too drastically for long periods of time. It is
always better, for health and safety, to err on the side of caution.

Saturated Fatty Acids

Saturated fatty acids are characterized by having all carbons between the omega (terminal, methyl) end and
the alpha (beginning, carboxyl) end "saturated" with hydrogens. Saturated fats are generally solid at room
temperature (lard, butter, coconut oil etc...). Saturated fats are not necessarily bad to include in one's diet.
There seems to still be some controversy over whether or not saturated fats are unhealthy. One one hand
saturated fats can increase LDL2,3 but on the other, diets with reduced saturated fats have a higher amount of
LDL receptors in a complementary concentration to the amount the saturated fat was reduced by.4 One's
target for saturated fats should be no more than 10% of total fats because unsaturated fats in fact do have
healthier properties.

Unsaturated Fatty Acids

Unsaturated Fats have one (mono) or more (poly) double bonds between carbons, this creates a "kink" in the
otherwise linear structure. Unsaturated fats are generally liquid at room temperature (olive oil, canola oil,
fish-oils etc...). When a diet that was once high in saturated fats has much of the saturated fats replaced by
mon- and poly-unsaturated fats LDL, cholesterol, and risk of cardiovascular disease decreases.5
Here is a chart of various oils and their fat makeup

Essential Fatty Acids

These are polyunsaturated fatty acids and are necessary because the body can only create a double bond at
the 9th carbon from the omega end (hence omega 9). The number (3,6) refers to the location of double
bonds. In the omega 9 fatty acid there is one double bond at the 9th carbon from the omega end. In the
omega 6 there are double bonds at the 6th and at the 9. In the omega 3 there are double bonds at the 3rd,
6th, and 9th carbons.

Essential fatty acids are necessary for immune function, vision, cell membranes, brain growth, and
production of hormones.

Omega 3 and omega 6 fatty acids work in opposition in certain respects. Omega 3s decrease blood clotting,
reduce heart attack, and decrease inflammation. Omega 6s increase blood clotting and increase
inflammatory responses. Due to this the target ratio for 6s/3s should be <4g/1g. Common sources for omega
3 fatty acids include: fish, flax, and hemp oils. Common sources for omega 6 fatty acids include: nuts,
walnuts, peanuts, poultry, corn, and soybean oils.
Trans Fats

For all intents and purposes all that should be noted about trans fats are two things: The double creates a
"trans" relationship between two hydrogens, thus maintaining the linear fatty acid structure while still having
a double bond. The "more important" aspect of trans fats are that ingesting 1 or more grams of trans fats per
day increases LDL, decreases, HDL, increases cholesterol, decreases insulin sensitivity, and increases risk for
heart disease.6 If a food contains <0.5g of trans fats it legally does not need to report trans fats. Look for
"trans fat free" and steer clear of "partially hydrogenated" oils in ingredients.

Water

Notable Macronutrient Minerals

(Na, K, Ca)

Micronutrients

Water Soluble Vitamins

Fat Soluble Vitamins

Minerals

Eating "Healthy"

Common Dieting Strategies

Videos

Fat Head - A Documentary that debunks much of the conventional wisdom about health and examines the
reality of Morgan Spurlock’s work Super Size Me Gary Taubes Lecture - Why We Get Fat and historical
references to the truth Doctor's Discussion of Keto - Andreas Eenfeldt, M.D. discusses the parameters of
Ketogenic Diets Sugar: The Bitter Truth - Robert H. Lustig, M.D. discusses the issues and dangers with sugar
Robb Wolf on Paleo - Robb Wolf answers community questions on the benefits of low-carb/paleo The Paleo
Solution - Robb Wolf discusses ancestral nutrition and “Western” diseases Your Leaky Gut and Grain - Loren
Cordain discusses auto-immunity and Western diet How Bad Science and Big Business Created the Obesity
Epidemic - David Diamond explains how industrial influences have shaped our diet and health care
infrastructure King Corn - A documentary following the effects of the corn industry on rural America and her
inhabitants Dr. Mary Vernon Lecture - A video playlist of great information and resources.
 Web Resources

My Fitness Pal - An online and smartphone application to track macronutrients and calories. The TDEE
calculator in this is not very good.
Low Carb Recipes - One redditor’s excellent collection of meal recipes

References

1. Ullrich IH, Peters PJ, Albrink MJ. Effect of low-carbohydrate diets high in either fat or protein on thyroid
function, plasma insulin, glucose, and triglycerides in healthy young adults. J Am Coll Nutr. 1985;4(4):451-9.

2.Faghihnia N, Mangravite LM, Chiu S, Bergeron N, Krauss RM. Effects of dietary saturated fat on LDL
subclasses and apolipoprotein CIII in men. Eur J Clin Nutr. 2012;66(11):1229-33.

3.Dreon DM, Fernstrom HA, Campos H, Blanche P, Williams PT, Krauss RM. Change in dietary saturated fat
intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am J Clin Nutr.
1998;67(5):828-36.

4.Mustad VA, Etherton TD, Cooper AD, et al. Reducing saturated fat intake is associated with increased levels
of LDL receptors on mononuclear cells in healthy men and women. J Lipid Res. 1997;38(3):459-68.

5.Siri-tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin
Nutr. 2010;91(3):502-9.

6.Trumbo PR, Shimakawa T. Tolerable upper intake levels for trans fat, saturated fat, and cholesterol. Nutr
Rev. 2011;69(5):270-8.

Reading

Title Author ISBN

Burn the Fat, Feed the Muscle Venuto, Tom 978-0804137843

The New Atkins for a New You Westman, Phinney, Volek 978-0091935573

Wheat Belly William David 978-1609611545

Why We Get Fat Gary Taubes 978-0307272706

Good Calories, Bad Calories Gary Taubes 978-1400033461

The Paleo Diet Loren Cordain 978-0470913024

The Paleo Solution Robb Wolf 978-0982565841

The Primal Blueprint Mark Sisson 978-0982207703

 Title Author ISBN

The Ketogenic Diet Lyle McDonald 978-0967145600

Ultimate Keto Food List Arcita, Joseph http://document.li/S01S

Nutrition Crowdsource

13 WOMEN & PEDS

DISCLAIMER

This is an overview of all the various supplements and hormones that women have been known to use
towards “fitness goals”. This wiki is in the interest of giving you a starting place to do the basic research so
you can make your own informed decisions instead of relying on some guy you know (guys have different
body chemistry than women) – regardless of how experienced they are with their own cycling and
supplementation, it doesn’t necessarily translate into anything useful for you as a female. It is beyond critical
for YOU to own your own decisions – your goals, your results, your sides. This is not a case where because
you know someone who "you trust and would never hurt you”, it is YOUR decision and YOUR responsibility.
No one else is going to experience the results AND the sides. No one can guarantee what will or won’t
happen – you are literally your very own petri-dish. YOU need to educate yourself so you can make informed
choices. There are no quick fixes or magic pills. None of this stuff matters if you don’t already have a solid
and performing diet, training, cardio & recovery program. And even in having this information available, just
because it’s there or you have access to it, doesn’t mean it is the appropriate path to your goals. You need to
have reasonable expectations. The body simply can’t support changes that are forced on it faster than it can
accommodate. “Drugs aren’t always the answer.”
Always remember that steroids are NOT particularly fat burners (even if some may have fat burning
properties). If you aren’t already lean or your diet isn’t optimized already, you may find yourself “thick” when
everyone else told you [fill in the steroid] would lean you out & tone you up. You’re screwing with your
hormone profile. Women’s hormone balance is much more complex than men’s, and doesn’t work the same.
Additionally women’s bodies can be much more complex in their response to something as simple as just the
diet. All sorts of metabolic fun can result from any sort of extreme. Going into desperation mode and
throwing more drugs on to force a result you want, but your body isn’t ready to produce yet, is just going to
aggravate the situation.

OTC Fat Burners

Ephedrine
If you want to go back to basics, you can build your own ECA or EC stack.
 To Build Your Own Stack

• EC Stack: Typical is 20-30mg Ephedrine + 200mg Caffeine

• ECA Stack: Adding in Aspirin is typically used to help prevent clotting, but the other two compounds share
the same anti-clotting mechanisms. Overall the difference to the stack is negligible without the Aspirin.
Recommendations for Aspirin are typically baby aspirin (81mg).

Another variation is Ephedrine / Caffeine / Yohimbine HCl (ECY). Yohimbine is great as an appetite
suppressant, but too much of it can leave you feeling sick to your stomach.

• ECY: 20-30 mg ephedrine + 200 mg caffeine + 5 mg Yohimbine.

You can take any of these combinations at 2-3 times ED, but it is generally recommended to not take
anything after 3pm, or determine how late into the day the last dose affects you, and make that the latest
time of your last dose so you can sleep. Anything that affects your sleep will reduce your quality recovery
time and can begin to negate any progress you make from the compound you’re taking.

Non-OTC Fat Burners

Women are often more interested in ‘fat loss’ before they are interested in muscle growth, particularly for
competition prep. The following compounds are explicitly not steroids, but they are generally controlled
substances or by prescription only. These are some of the other supplements that women start to “lose fat”
or “lean up”.

Clenbuterol (Clen)
Clenbuterol is prescribed as a bronchodilator for asthma, but also has the additional effect of increasing
metabolism. The claim is a 10% increase in metabolism over ECA, which claims a 3% increase in metabolism.
(This often quoted, but never found an original study to back this up.) Clenbuterol has a 36-39 hour half-life –
meaning if you take it, or worse, too much, you have to ride it out for about a day and a half. Some people
panic if they take too much, and head to the Emergency Room, where the doctors will still just tell you that
you need to ride it out until it wears off. There is nothing you can take to “make it stop” before then.

Clenbuterol has also been called “anti-catabolic” – meaning it does not promote muscle loss as part of the
increase in metabolism to reduce bodyfat. Here are a couple studies that imply that clenbuterol, interestingly
on a restricted diet, does promote some amount of muscle growth (or preservation) in research animals:

Some additional considerations when using clenbuterol:

• Supplement with (3-5g ED) L-Taurine – Clenbuterol tends to inhibit L-Taurine in your system, producing
cramps

• Using Ketotifen with Clenbuterol (2-3mg ED) - Ketotifen is an antihistamine that inhibits down regulation of
beta receptors, but you should do more outside research before using.
 Common Clenbuterol Cycles

• 2 weeks ‘on’ / 2 weeks ‘off’ for 8-12 weeks – Starting at 20mcg, increasing by 20mcg units as you can handle,
until what you can handle or a maximum of 100mcg per day, and then stay at that amount for the duration of
the two weeks. Then stop and go off for 2 weeks, substituting your favorite OTC thermo, and then repeating
the 2 weeks ‘on’, again starting at 20mcg.
• Continued ‘on’ for 8-12 weeks, include ketiotifen – Starting at 20mcg for a week, increase by 20mcg per
week until what you can handle or a maximum of 100mcg per day, and then stay at that amount for the
duration of the cycle

Thyroid Medication: T3 and T4

The thyroid hormones thyroxine (T4) and triiodothyronine (T3), are tyrosine-based hormones produced by
the thyroid gland primarily responsible for regulation of metabolism. T4 converts to T3, with T3 being 3-4
times stronger than T4. Synthetic T4 is often prescribed for people diagnosed with hypothyroidism (“sluggish
thyroid”).

On a side note, thyroid disease is not uncommon in women. I would hesitate to blame “can’t lose weight” on
the thyroid, as people often look for pills-based solutions or some excuse before they’ll spend the time
revisiting their diet & training programs. But that said, if you feel there is an issue, by all means, talk to your
doctor about it and get a thyroid panel done.

T3 is frequently suggested as part of a fat-loss protocol. It is important to be conservative with use of T3 if

you choose to go that route. You are manipulating your thyroid via self-medication. Too much and you will
immediately feel lethargic. General guidance also suggests to be slow in your dosing – taper off when you are
coming off instead of just dropping it cold. The body generally can adapt to small changes, but tends to
rebound with large, sudden changes.

Another very important consideration with T3 is that bumps up metabolism… but that means metabolism of
everything – both lean muscle mass and bodyfat. Women tend to be so focused on “fat loss” that they forget
about the importance of muscle mass. Building and preserving muscle mass has nothing to do with “looking
like a man” or “getting huge”, but rather about the keeping the body component that helps you burn bodyfat
more efficiently, and it also goes into what makes up a bodyfat percentage. “What’s your bodyfat?” means
what is the ratio of lean muscle mass to bodyfat in your body? It is great to drop bodyfat, but if you are
sacrificing muscle mass, your overall bodyfat percentage will not drop the way you want it to. The lack of
muscle mass can contribute to a higher bodyfat percentage (what we often call “skinny-fat”) just as higher
bodyfat percentage.

To this end it is not generally recommended to cycle T3 without an anabolic support. Either an AAS or, a very
common stack is with clenbuterol, which has been shown to be anabolic, or at least anti-catabolic.
 Typical Cycle

It is not recommended to run T3 by itself. Combine the following with an AAS cycle.

• 12.5-50mcg per day, for the duration of your cycle

• Start at 12.5mcg for a week. You can either keep it here or increase. Increases shouldn't be more than
12.5mcg per week until a maximum of 75mcg (high dose - advanced users only). At the end, taper back down
by 12.5mcg every 3 days.

Anti-Estrogens

There are two classes of estrogen manipulators that often fall under the term “anti-estrogens”. The first are
Selective Estrogen Receptor Manipulators (SERMs). The only current example out there is Tamoxifen Citrate
(Nolvadex). This operates specifically on the ovarian-driven estrogen process. The second category that falls
under “anti-estrogens” are Aromatase Inhibitors (AI’s) that operate not on ovary-originating estrogen, but
rather that resulting from aromatization (or conversion to estrogen) of testosterone. Examples of
testosterones that convert are exogenous testosterones (anabolic androgenic steroids) such as Testosterone,
Nandrolone, or Dianabol. There is also a natural source of androgen that converts to estrogen – that
produced by the adrenal glands, in both men and women. When women enter menopause and their ovary-
originating estrogen is no longer produced, the only remaining source of naturally produced estrogen is that
resulting from the adrenals. Examples of AIs are Arimidex, Aromasin, and Letrozole. In practice, both these
and Nolvadex, are all primarily prescribed as breast cancer treatment for post-menopausal women.

Women are more likely to use a SERM like Nolvadex to address the bodyfat associated with estrogen –
specifically the stuff that tends to collect around the hips, thighs, lower abdomen and butt. It is important to
note that each person has her own distribution of fat – estrogen tends to promote a higher concentration of
fat cells in those lower areas as part of a natural preservation strategy to protect a fetus and also to provide
an extra storage of energy source (bodyfat) to help support a growing fetus and the mother if there is any
issue with available food sources (i.e. a drought scenario). This is by design and using an anti-estrogen as a
weight-loss strategy is not a good idea. Estrogen is one of the three basic hormones that make up who we
are, and drive everything from moods to how we look and feel. Estrogen is there for a purpose and should
not be completely suppressed only for the purpose of fat loss.
Nolvadex acts to fake out the estrogen receptors (envision a safety protector that you put into outlets as part
of baby-proofing your house) and essentially cutting off the estrogen process, instead of literally turning it
off. For cycle duration, it is recommended to keep it to 4-8 weeks maximum. Long-term use of Nolvadex has
the potential to introduce health issues as described in this article: Side effects of long-term use of tamoxifen.
In the extreme, full estrogen shut down in women can lead to what is often referred to as the “Female
Athlete Triad” – basically estrogen shutdown as a result of an eating disorder such as anorexia, which leads to
reduction in calcium, and eventually to brittle bones and a host of other issues related to a stopped
 period. Here is an overview of this particular issue. Though this discussion is not focused on eating disorders,
the end result, if someone decided to use medical estrogen suppression as a long-term weight loss protocol,
is the same. This is just to reinforce that this is not a good idea.

The estrogen process tends to be fairly resilient so coming off a reasonable duration cycle can produce an
estrogen rebound when the process is no longer inhibited. There isn’t much documentation about this
rebound, but general guidance is to taper off a cycle by reducing the dose (i.e. in half, every 3 days).

In the context of this article, Aromatase Inhibitors are more specific to the estrogen produced as a result of
using an aromatizing steroid. This means that the steroid cycle is more aggressive and will produce side
effects such as water retention and potentially more mood swings, as the converted estrogen may be adding
to natural estrogen levels, enhancing typical estrogen effects that might be experienced during a menstrual
cycle. AI’s are more commonly used by men who cycle as the increase in estrogen can produce such side
effects in men as gynecomastia (enlarged breast tissue), water retention, mood swings, etc. Estrogen
suppression can help to create a tighter look (i.e. for competition), but full suppression can produce too much
dryness, including painful joints. Plus you typically want some estrogen for other benefits.

Generally speaking AI’s are not recommended for pre-menopausal women who are new to steroid cycling
or using non-aromatizing compounds. If they choose to use an AI, it needs to be very conservatively used,
as it is very easy to shut down estrogen with these compounds.

Typical Use

Primarily Nolvadex is used during the last 4-8 weeks of a contest prep to help reduce bodyfat in the hips /
thighs / waist area. Again, it will not do the heavy lifting, but will support a tight contest prep. It is possible to
experience either immediate interruption of menstrual flow, or breakthrough bleeding within 4 weeks of
starting the cycle. Also once coming off, the effects will not be maintained and the estrogen-pattern bodyfat
depositing will continue again. “Estrogen rebound” is often experienced as well, thus the taper down is
recommended. Because of the potential of this rebound it is recommended to cycle Nolvadex with a specific
end / target date in mind, followed by an expected rebound while your body recovers from the prep phase.
More aggressive aromatase inhibitors are not generally recommended unless you are an experienced cycler
running aromatizing compounds such as NPP. If your cycle is intended for a bulk phase, then don’t use the AIs
as you need the estrogen to build muscle mass and the water gain is minimal with most compounds women
use.

Typical Cycle

• Nolvadex: 10-20mg ED, split in half AM and half PM for maximum of 8 weeks.

• Arimidex: 0.5mg EOD (only with an aromatizing AAS) for maximum of 6-8 weeks – AIs are very aggressive and
will produce dry-feeling joints. If you experience aggressive hot/cold flashes and feeling sick, taper off over a
couple days and stay off.
• Aromasin: 12.5-25mg EOD (only with an aromatizing AAS) for a maximum of 6-8 weeks – AIs are very
aggressive and will produce dry-feeling joints. If you experience aggressive hot/cold flashes and feeling sick,
taper off over a couple days and stay off.

Human Growth Hormone (HGH)

Growth Hormone is often recommended for “fat loss”. It is not a “fat burner” in the same sense as clen or
ephedrine, but instead falls under the larger category of “anti-aging” compounds or “hormone replacement
therapy”. In these contexts, it is intended to be dispensed under the supervision of a qualified physician
based on constant monitoring of IGF-1 levels. This is the indicator used to track growth hormone production
by the hypothalamus. Essentially this is what drives “youthfulness”. The hypothalamus produces optimal
levels of growth hormone around age 18-21. These levels begin to decrease after age 30-35 as the
hypothalamus shrinks with age. The idea behind supplementing with HGH is to return the levels of growth
hormone to optimal levels, as if you were still in the prime of your life.

In practical use, as mentioned above, HGH is used for its anti-aging properties, as a maintenance protocol for
older folks, or to promote those youthful properties with specific interest in promoting fat loss, or rather not
promoting age-related fat depositing, or stacked with an AAS cycle to enhance the overall effect.

Typical Use

GH is often recommended for women for ‘weight loss’. By itself, GH does NOT promote muscle growth in the
same sense as AAS, as it is not sex hormone. Instead, it will work to promote those youthful features such as
healthy hair, improved skin elasticity, better sense of well-being, better healing capability (Study), and more
optimized metabolism to promote a preference for less bodyfat depositing (Study). It might also be viewed as
a support during the extremes of competition prep for the body. With a steroid cycle, such as anavar, it
would work to enhance the effects of that compound. The effects of a GH cycle are not immediate and
dramatic, but rather subtle and slow to show over time.

Typical Cycle

Dose:

• For non-competition use, and more for general maintenance and youthfulness: 1 iu ED

• For competition / with a cycle: 2-3 iu ED

Primarily for cost purposes, 6 days on / 1 day off or 5 days on / 2 days off (not two days in a row) can be used
as well.
Duration: 4-6 months is ideal. Very short cycles such as a month, are not really going to show any particular
results for the cost.
 Potential Sides

• Water retention is a common experience.

• At higher doses (i.e. 4 iu) wrist pain similar to carpal tunnel syndrome is commonly experienced

• Very aggressive use may fall into the extreme category of acromegaly

Anabolic Androgenic Steroids (AAS)

/r/steroids is hesitant to recommend stacking any AAS with more AAS. It is done, but should only be after
you have experience with each individual compound in the stack. For this purpose, we will only cover one
compound at a time. But you may add in a Fat Burner or HGH if your goals could benefit from them.
Virilization

When it comes to steroids and women, there is a universal fear; turning into a man. As you know, anabolic
androgenic steroids derive from the primary male sex hormone testosterone, and as such, while no woman
will turn into a man, if she’s not careful she can easily display masculine traits. Many anabolic steroids cause
what is known as virilization, specifically put, changes that occur due to the high presence of androgens in the
body. Androgens are hormones we all produce, both men and women, and essentially so with Testosterone
and Dihydrotestosterone being primary. Of course, men require about ten times the amount as women, and
when androgen production goes beyond the needed amount for a female, masculine traits can manifest. The
most common virilizing effects include:

• Body-Hair Growth

• Clitoral Enlargement

• Deepening of the Vocal Chords

There is hardly a woman alive who would enjoy such effects, but guess what; plenty of women supplement
with anabolic steroids and never experience a single one. The reason is simple; they’re informed. They’ve
done their homework; they understand which hormones to take and which ones to avoid. They understand if
virilization symptoms begin to show then that particular steroid is not for them; we’ll explain shortly.

Avoiding Virilization

When steroids and women coexist if we’re going to avoid virilization, and we’re assuming you want to, the
first order of business is to choose anabolic steroids that carry low virilizing properties. Some steroids carry
higher virilizing properties, and logic tells us, we’ll need to avoid these; this isn’t rocket science. Even so, let’s
be clear; all anabolic steroids carry a level of virilization concern, some higher and some lower than others.
When we choose anabolic steroids that carry low virilizing properties, in most cases, most women will be
fine, but there is still a risk. As we are all unique individuals, some women will not tolerate some steroids at
all even though another woman may tolerate it perfectly. Look at it like dairy products; most of us can drink
all the milk and eat all the cheese we want, but some of us get sick if we even think about a cow; some of us
are lactose intolerant, but most of use aren’t.

The key to avoiding virilizing symptoms is straightforward; choose steroids that carry a low rate of probability
in this regard. Second, if for any reason virilization symptoms begin to show, discontinue use immediately.
Once you discontinue use, the effects will dissipate rapidly. If you ignore the symptoms and let them set it,
this is where true damage is done, and in many cases, where they cannot be reversed. At any rate, if
symptoms show discontinue all steroid use; in your next go around do some examining of your prior use. Was
your dose of a certain steroid too high? Maybe you simply need a lower dose that is more tolerable; maybe
you need a different steroid altogether. In any case, if you’re smart and pay attention to your body you can
supplement without these effects becoming problematic.

A note about available steroid information:

Most of what is out there on muscle forums and even medical studies is primarily written with men in mind.
The subject of women and steroids is much less studied and published. The detail written here is based on
both published and anecdotal information, and some good guesses based on “what seems to work”. This
puts more of the onus on women to educate themselves to make informed choices for themselves. Always
remember: YOUR body, YOUR results, YOUR sides. Well-intentioned husbands / boyfriends / male friends /
guys from the gym, even experienced, are not necessarily going to be giving you the best or right information
on which to base your decisions. The basic chemistry is different, the dosing is different and the risks are
different. At the end of the day, it is always your own personal chemistry experiment and no one can take
the risks for you.
And a last note on what should be the obvious thought – ANY supplement – over-the-counter, prescribed or
illegal, is always only going to be a SUPPLEMENT to an already existing and functioning diet and training
program. There are no quick fixes and nothing is for free. You will not get the results you envision using any
supplement if you don’t already have your diet and training in place and working. If this is not true, chances
are you are going to end up in a place worse than better. Always consider your diet, training, cardio &
recovery to be your foundation. Constantly optimize these before trying to "fix” things with drugs.
Compound Profiles

This section will include links to the standard steroid profiles for the technical details, with most of the
discussion focused on use, specifically for women. Please note that most steroid profiles are written with
men in mind as the target audience and relative to male hormone profiles. Any dosing recommended is not
going to be appropriate for women unless otherwise specified.

Anavar (Oxandrolone)
Anavar (Var) is probably the most commonly used AAS by women. It might be used by competitors for off-
season building with an appropriate diet, or during contest prep for cutting, preservation of muscle during a
cutting diet, and improved recovery.
 Typical Use

Anavar promotes lean muscle mass with minimal sides and occasional water retention. It is a oral steroid,
though used in small enough doses that its impact on the liver is typically minimal for women. It will mess up
your lipid profile though, as oral steroids do. It is also attractive to women and beginners who are not
interested in dealing with needles. The predictable and minimal sides are also attractive points to those not
wanting to deal with the more individual and androgenic sides of most other AAS.

Typical Cycle

• Dose: 5-10mg ED – split the dose ½ in the AM, ½ in the PM

• Duration: 6-8 weeks for beginners and up to 10-14 weeks for more experienced users

• No need to taper down the dose or follow with post cycle therapy (PCT).

It is generally suggested to start the cycle at 5mg ED (splitting doses as above) for the first 10-14 days to
identify any adverse reaction. (This is strongly suggested if this is your first time with the compound.) After
that time, you can increase to 10mg ED.

Suggested maximum dose is 20mg ED (though more is not better – often 10mg is sufficient). As the dose
increases, sides may increase and results don’t necessarily increase. Anecdotally, if the cycler is interested in
going to doses above 20mg, the sides can begin to accumulate and the impact on your liver becomes more of
a consideration. Based on this and the cost (anavar is typically one of the more expensive compounds), if you
are looking for more aggressive results, this is the point where people will move to a more aggressive,
cheaper, injectable compound.

Potential Sides

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

• You may still experience usual menstrual sides (cramps, bloating, etc.) on your regular menstrual schedule

• Mild acne / bacne

• Clitoral enlargement and increased sensitivity

• Oily hair

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Some experience water retention (though not due to aromatization)

Be careful w/ using diuretics to manage this – continued use of even OTC diuretics is not recommended.
• May cause vaginosis / yeast infection (most any AAS has this potential)

• Occasionally people experience nose bleeds or headaches (due to increased blood pressure – you can google
for OTC supplements to help with BP

Winstrol (Stanozolol)
Winstrol (Winny) comes in both oral and water-based injectable form (but also very rarely an oil based). It is
attractive to women or recommended for women because it is an oral, it has a relatively short half-life and
detection time (i.e it clears the system relatively quickly, reducing the duration of any undesirable sides
following completion of a cycle), and promotes lean muscle mass without water retention. It is most
commonly viewed as a “cutter” for competitors. Winstrol is also attractive as it tends to be both cheaper and
more readily available than others like anavar or primobolan. Because of this, it is also less likely to be faked.

Winstrol is often grouped with anavar as a good steroid for “beginners" or those who don’t want to go into
the more aggressive compounds (i.e. injectables). However it is more androgenic than anavar and sides are
less predictable and more unique to the individual, with the potential of being very androgenic. Because of
this, anavar would generally be the better recommendation, but winstrol is seen as a viable alternative. And
is also known to have a "fat burning" effect.

Typical Use

Winstrol is most commonly used both by men and women, as a cutter during competition prep. It promotes
lean, hard muscle mass without water retention. One might see competitors running a winstrol-only cycle, or
a more advanced physique competitor using it in a stack towards the final weeks of a competition prep.

Typical Cycle

Oral Winstrol: Can be cycled similarly to anavar.

• Dose: 5-10 mg/day- split the dose ½ in the AM, ½ in the PM

• Duration: 6-8 weeks for beginners and 8-12 weeks for more experienced

It is generally suggested to start the cycle at 5mg ED (splitting doses as above) for the first 10-14 days to
identify any adverse reaction. (This is strongly suggested if this is your first time with the compound.) After
that time, you can increase to 10mg ED if desired.

Suggested maximum dose is 15mg ED (though more is not better – often 10mg is sufficient). As the dose
increases, sides may increase and results don’t necessarily increase. Anecdotally, if the cycler is interested in
going to doses above 15mg, the sides can begin to accumulate and the impact on your liver becomes more of
a consideration.

If chosen to include in a competition cutting stack, schedule towards the final weeks of prep. It usually takes
about 2 weeks to really start to “show” itself.
 Potential Sides

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

• May still experience usual menstrual sides (cramps, bloating, etc.) on your regular menstrual schedule.

• Mild to aggressive acne on face or shoulders

• Clitoral enlargement and increased sensitivity

• Oily skin / hair

• Hairloss – A shampoo like Nizoral or Nioxin (find next to the dandruff shampoo in most stores) can help
minimize this.

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Dry joints (result of the anti-estrogenic aspect of winstrol)

• May cause vaginosis / yeast infection (most any AAS has this potential)

• Occasionally people experience nose bleeds or headaches (due to increased blood pressure – you can google
for OTC supplements to help with BP

Turinabol (Tbol)
Turinabol (Tbol) is an oral steroid that has recently become more widely used by women.

Typical Use

Tbol is good to cycle for both cutting or bulking off-season. Lean gains are good for a women looking to build
some size.

Typical Cycle

• Dose: 5-10mg ED – split the dose ½ in the AM, ½ in the PM

• Duration: 6-8 weeks for beginners

• No need to taper down the dose or follow with post cycle therapy (PCT).

It is generally suggested to start the cycle at 5mg ED (splitting doses as above) for the first 10-14 days to
identify any adverse reaction. (This is strongly suggested if this is your first time with the compound.) After
that time, you can increase to 10mg ED if desired.
 Suggested maximum dose is 15mg ED (though more is not better – often 10mg is sufficient). As the dose
increases, sides may increase and results don’t necessarily increase. Anecdotally, if the cycler is interested in
going to doses above 15mg, the sides can begin to accumulate and the impact on your liver becomes more of
a consideration.

Potential Sides

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

• You may still experience usual menstrual sides (cramps, bloating, etc.) on your regular menstrual schedule

• Mild acne / bacne

• Clitoral enlargement and increased sensitivity

• Oily hair

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Some experience water retention (though not due to aromatization)

Be careful w/ using diuretics to manage this – continued use of even OTC diuretics is not recommended.

• May cause vaginosis / yeast infection (most any AAS has this potential)

• Occasionally people experience nose bleeds or headaches (due to increased blood pressure – you can google
for OTC supplements to help with BP

Anadrol (Oxymetholone)
Anadrol (Adrol) is an oral steroid that has recently become more widely used by women when bulking.

Typical Use

Adrol is good to cycle for bulking off-season. Lean gains are good for a women looking to build some size. It
has been found to be a good choice for women who wish to be conservative yet have very effective results.
The medical doses are pretty astonishing. The reason that 50 mg is the tablet size is because that’s the
standard minimal medical dose, including for women and children! It used to be used extensively for
improving red blood cell count. But for bodybuilding purposes, we will always start low with any AAS.

Typical Cycle

• Dose: 12.5-25mg ED – split the dose ½ in the AM, ½ in the PM

• Duration: 6-8 weeks for beginners

• No need to taper down the dose or follow with post cycle therapy (PCT).

It is generally suggested to start the cycle at 12.5mg ED (splitting doses as above) for the first 10-14 days to
identify any adverse reaction. (This is strongly suggested if this is your first time with the compound.) After
that time, you can increase to 25mg ED, which has been found to be a safe dose for women.

Suggested maximum dose is 37.5mg ED (though more is not better – often 25mg is sufficient). As the dose
increases, sides may increase and results don’t necessarily increase. Anecdotally, if the cycler is interested in
going to doses above 25mg, the sides can begin to accumulate and the impact on your liver becomes more of
a consideration. These are just the suggested dosages, medically Anadrol has been given to women at higher
dosages and been fine.

Potential Sides

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

• You may still experience usual menstrual sides (cramps, bloating, etc.) on your regular menstrual schedule

• Mild acne / bacne

• Clitoral enlargement and increased sensitivity

• Oily hair

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Some experience water retention (though not due to aromatization)

Be careful w/ using diuretics to manage this – continued use of even OTC diuretics is not recommended.

• May cause vaginosis / yeast infection (most any AAS has this potential)

• Occasionally people experience nose bleeds or headaches (due to increased blood pressure – you can google
for OTC supplements to help with BP

Primobolan (Methenolone)
Primobolan (Primo), comes in both oral and injectable form. The injectable is most commonly used. Oral
form, primobolan acetate, has recently become more available.

Typical Use

Primo has been listed as one of the top favorites for women. Because it does not aromatize, again it is a
favorite cycle both for cutting or bulking off-season. Lean gains are good for a women looking to build some
 size, but not get “too swole”. Oral Primo is unique in that the oral form is one of the few orals that is not hard
on the liver, but at the same time, it loses a degree of its strength as it passes through your system, thus
higher doses are required.

Typical Cycle

Injectable Primo:

• Dose: 50-150mg / week

• Duration: 6-12 weeks

It is generally good to start the cycle at 50mg / week for the first 4 weeks to identify any adverse reaction.
(This is strongly suggested if this is your first time with the compound.) After that time, you can increase
the dose if desired.

Suggested maximum dose is 150mg / week (though more is not always better). As the dose increases, sides
may increase and results don’t necessarily increase.

Oral Primo:

• Dose: 50-75mg ED – split the dose ½ in the AM, ½ in the PM

• Duration: 6-12 weeks

• No taper or post-cycle therapy is needed.

It is generally good to start the cycle at 50mg ED (splitting doses as above) for the first 10-14 days to
identify any adverse reaction. (This is strongly suggested if this is your first time with the compound.) After
that time, you can increase the dose if desired.

Suggested maximum dose is 15mg ED (though more is not always better). As the dose increases, sides may
increase and results don’t necessarily increase.

This is often the primary component of a prep phase. It can be run all the way up to a show without
promoting water retention issues.
More experienced cyclers will often stack with winstrol or anavar.

Potential Sides

• Notorious for hairloss – A shampoo like Nizoral or Nioxin (find next to the dandruff shampoo in most stores)
can help minimize this.

• Acne

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Clitoral enlargement and increased sensitivity

• Oily hair

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

• May still experience usual menstrual sides (cramps, bloating, etc.) on your regular menstrual schedule.

• May cause vaginosis / yeast infection (most any AAS has this potential)

Proviron (Mesterolone)
Proviron is a highly androgenic compound that is used primarily during the final weeks of a competition
cutting phase to help lean out in the mid-section. It is often stacked with Nolvadex to lean out the
hips/thighs/waist further. Being fundamentally androgenic (as opposed to anabolic), proviron will not
promote muscle growth as much as it promotes leanness and hardness. For short cycles (i.e. 4-8 weeks
maximum), sides are minimal.

Typical Use

Proviron would often be stacked with Nolvadex as a final 4-8 week dial into a competition date.

Typical Cycle

• Dose: 25 mg ED – split the dose ½ in the AM, ½ in the PM

• Duration: 4-8 weeks

• No need to taper the dose when the target date or cycle end date is over.

Potential Sides

• Water retention

• Acne (face or shoulders)

• Oily skin

• Hairloss

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Facial hair growth

• Clitoral enlargement and increased sensitivity

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

Masteron (Drostanolone Propionate)

Masteron (Drostanolone Propionate) is a highly androgenic compound that is used primarily during the final
weeks of a competition cutting phase to help lean out in the mid-section. It is often stacked with Nolvadex to
lean out the hips/thighs/waist further. Being fundamentally androgenic (as opposed to anabolic), Masteron
(Mast) will not promote muscle growth as much as it promotes leanness and hardness. For short cycles (i.e.
4-8 weeks maximum), sides are minimal.

Typical Use

Masteron would often be stacked with Nolvadex as a final 4-8 week dial into a competition date.

Typical Cycle

• Dose: 7-15mg ED or 14-30mg EOD

• Duration: 4-8 weeks

• No need to taper the dose when the target date or cycle end date is over.

Potential Sides

• Water retention

• Acne (face or shoulders)

• Oily skin

• Hairloss

• Increased body hair growth

• Sore or scratchy throat / cracky or deepening voice

• Facial hair growth

• Clitoral enlargement and increased sensitivity

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

Boldenone (EQ, Bold A, Bold C, etc.)

Equipoise (EQ) (Boldenone Undecylenate) is an injectable steroid that includes a small amount of
aromatization. It is seen as a nice compound that produces good gains with minimal water retention. EQ is
 the most readily available (and used), but a shorter ester would be optimal. /r/steroids suggests going with
the short ester version of this compound, Boldenone Acetate (Bold A). This will allow the compound to clear
much faster if sides occur.

Typical Use

For an experienced cycler, as an off-season bulker with low water retention, or at the beginning of a contest
prep, again with low water retention. Anecdotally, some people experience an increase in hunger on EQ, so it
might fit well with a bulker phase.

Typical Cycle

Bold A:

• Dosage: 5-7.5mg ED or 10-15mg EOD

• Duration: 4-10 weeks

It is generally suggested to start the cycle at 5mg ED (or 10mg EOD) (splitting doses as above) for the first
10-14 days to identify any adverse reaction. After that time, you can increase to 7.5mg ED (or 15mg EOD) if
desired.

Suggested maximum dose is 15mg ED (though more is not better – often 10mg is sufficient). As the dose
increases, sides may increase and results don’t necessarily increase.

Equipoise (EQ):

• Dosage: 50-75 mg / week

• Duration: 6-10 weeks

It is generally suggested to start the cycle at 50mg / week for the first 6 weeks to identify any adverse
reaction. After that time, you can increase to 75mg / week if desired.

Suggested maximum dose is 150mg / week (though more is not better). As the dose increases, sides may
increase and results don’t necessarily increase.

Potential Sides

• Acne

• Oily skin

• Hairloss

• Clitoral enlargement and increased sensitivity

• Sore or scratchy throat / cracky or deepening voice

• Increased body hair growth

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

• May cause vaginosis / yeast infection (most any AAS has this potential)

Nandrolone Phenylpropionate (NPP)

There are several different forms (esters) of Nandrolone available. NPP is the shorter-acting Deca Durabolin
(Nandrolone Decanoate) that would be more likely recommended for women. The longer acting Deca will
anecdotally produce more water retention and due to the longer ester it will take longer to clear if sides pop
up. This is a more aggressive cycle for women with some water retention and longer detection time than the
more commonly used injectables such as primo.

Typical Use

For women, NPP falls into the scope of really only for those experienced who are looking for significant
growth and are prepared to deal with the full scope of potential sides. It might be considered an off-season
cycle for a female bodybuilder or used at the beginning of a 16 week prep, to be later dropped and replaced
with a non-aromatizing compound.

Typical Cycle

• Dose: 5-8mg ED or 10-16mg EOD

• Duration: 8-10 weeks

It is generally suggested to start the cycle at 5mg ED (or 10mg EOD) (splitting doses as above) for the first 2-
3 weeks to identify any adverse reaction. After that time, you can increase to 8mg ED (or 16mg EOD) if
desired.

Suggested maximum dose is 15mg ED (though more is not better – often 10mg is sufficient). As the dose
increases, sides may increase and results don’t necessarily increase. As we get into the much more aggressive
cycles, it becomes more of a personal preference on dosing based on goals and any other stacked
compounds

Potential Sides

• Water retention

• Acne

• Oily skin

• Hairloss
• Sore or scratchy throat / cracky or deepening voice

• Increased body hair growth

• Clitoral enlargement and increased sensitivity

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

Testosterone Propionate
There are several esters of testosterone, but only the Propionate ester, also known as Testosterone
Propionate (Test P), would be recommended for women. The other variations commonly used by
men, Testosterone Cypionate, Testosterone Enanthate (Test E), or Sustenon, are considerably longer-acting
esters, producing anecdotally much more water retention and more aggressive sides, taking a much longer to
clear the system.

Typical Use

For women, Test P falls into the scope of really only for those experienced who are looking for significant
growth and are prepared to deal with the full scope of potential sides. It might be considered an off-season
cycle for a female bodybuilder or used at the beginning of a 16 week prep, to be later dropped and replaced
with a non-aromatizing compound. It is reasonably short-acting so will begin to produce results (and sides)
fairly quickly. This compound does aromatize a bit. There is no real need for an aromatase inhibitor with this
compound, but be aware that it does still produce some water retention.

Typical Cycle

• Dose: 3-6mg ED or 6-12mg EOD

• Duration: 4-6 weeks

As we get into the much more aggressive cycles, it becomes more of a personal preference on dosing based
on goals and any other stacked compounds

Potential Sides

• Water retention

• Acne

• Oily skin

• Hairloss

• Sore or scratchy throat / cracky or deepening voice

• Increased body hair growth

• Clitoral enlargement and increased sensitivity

• Interrupted period / flow – may take a few months for the flow to come back as normal. Note this
does NOT mean you won’t get pregnant.

Trenbolone Acetate
Trenbolone Acetate (Tren A) is more recently, being mentioned more frequently with women. It is a favorite
among men because it promotes strength while allowing great cutting results with no aromatization. The
issue is that this compound is extremely androgenic and also can have effects on the liver. Very experienced
female cyclers may use trenbolone acetate as part of a cutting cycle, but should be very careful and diligent
with their bloodwork afterwards.
/r/steroids hesitates to include cycle information her, because you should already have an idea of the cycle
details if you are at a point where you are considering running a tren cycle. Virilization is a major risk here.

Post Cycle Notes

Generally women don’t run aggressive cycles and can just end the AAS cycle. The compound(s) will attenuate
over time as their individual half-lives run their course. During that time, just as at the beginning of the cycle,
there is a big flux in the hormone profile. Drawing a comparison to “that time of the month”, the sides can
seem more pronounced and in particular, some moodiness may result. The range of this is something that is
very unique to each person, and even unique to each compound plus each person’s unique body chemistry.

Anticipating this, pay attention to your general state of mind post-cycle. If you find yourself getting depressed
or moody, step back and acknowledge that it is most likely the effect of the hormones, and not something
else happening in your daily life. If you happened to be using prescription anti-depressants, I would suggest
you be particularly aware of your state of mind. One OTC option to help even out your moods is Inositol. This
is essentially just a B-vitamin, ideally in powder form. For more information about inositol and depression
treatment, here is an article, or you can just google “inositol, depression” for a bunch of information. Powder
inositol is recommended over inositol tabs/caps.

Another obvious effect of coming off a cycle is the reduction (or back to “normal”) in recovery ability and
strength and maybe some of the increased sense of well-being that comes with AAS at times. The loss of
these can be both humbling and frustrating, however it’s important to keep things in perspective as you can’t
stay on a cycle forever without hitting some point of negative effects. It is supposed to be a “cycle” – a phase
with a specific goal, and then letting your body adapt to the change and retain as much as possible. Again,
monitor yourself as the compound(s) clear out of your system in terms of strength and recovery – adjust your
training and your expectations to match this phase of your progress to avoid burnout or injury.
 Things to Remember

In summary, some basic things to keep in mind if you want to play on the dark side:

• Make sure your goals and expectations are appropriate. Just because someone suggested a particular drug
or it is available, doesn’t mean its the right thing to get to your goal.
• More is NOT always better. It’s about finding a workable balance for YOUR hormone levels, your goals and
your experience.
• Never forget that you are self-medicating with hormones – it is always your own personal experiment. Slow
& low is your best approach.
• Don’t stack a pile of stuff you’ve never run each individually before – you have no idea how these
compounds affect your body so you can’t make judgments on what to cut / what is bad / what is good for
your body chemistry. Also there is an accumulated effect when you are throwing all sorts of stuff in the pile.
Fundamentally you are jacking up the amount of DHT in your system. Know the half life of each compound
you are interested in – some are much longer than others so if you don’t like the sides, on longer esters,
tough tit. Now you have to wait for the compound to clear your system before the sides go away.
• Know the potential sides – anything is possible in any degree – there is no such thing as “no sides”- only
those that you don’t experience – it is very individual so you are still running your own personal experiment.
• You need to accept the potential of sides – you either accept them or you don’t. You can’t pick which ones
you want & which you don’t and you can’t predict what you will experience until you try it. It’s more about
managing risk by educating yourself, staying at conservative doses and watching how your body responds. If
you can't accept the risk of sides, you have no business cycling.
• Don’t listen to other people – especially guys. They will have a completely different experience with
different doses & different compounds. A tiny little amount of anything will have dramatic effects on women
compared to men. YOU are responsible for YOUR cycle.
• Women do not need to worry about post-cycle therapy (PCT) like guys do. Women can generally just end a
cycle. There is no need to taper. The compound will clear at the rate specified by its half-life.
• Think in the long term – just like a bulking or cutting diet – it has a place in the ongoing cycle of change that
happens over time. You can’t maintain the state of being “on” so you have to also come off, expect to lose a
little of what you gained, but you will have made a change to your over all body composition.
• Watch your diet – if you are going to bother putting this stuff in your body, you should respect your body
enough to not think you can get away with eating shit – IF the diet is tight, then you will also get the leaned
out effect that everyone wants – but sloppy diet will get you more big than lean.
• Time off = Time on. The general rule of thumb is to allow at least as long as your cycle, to clear your system
and let your body re-establish its own homeostasis. People tend to want to “try more”, but it is important to
remember that there are impacts to your body not immediately apparent that you need to pay attention to,
i.e. kidneys, liver, blood pressure, etc.
• AAS can promote yeast infections / vaginosis. Any AAS or sex hormone manipulator (including AIs) can
promote yeast infections. It is always recommended to supplement with Acidophilus to help prevent these.
• AAS and Birth Control do not interact. However the effects they each promote are opposing – birth control
works to regulate estrogen (including estrogen-pattern bodyfat depositing) while AAS promotes lean muscle
mass.

AAS and Birth Control

One of the most common questions asked is about AAS and Birth Control. Women typically experience an
interruption of their menstrual cycle while on any sex hormone-manipulating cycle (AAS or “anti-estrogen”).
This does NOT mean that you cannot get pregnant. Despite the lack of flow, other typical menstrual sides can
be present when “that time of the month” is expected – including bloating, breast sensitivity, moodiness, etc.

There is very little to nothing published on the topic of the interaction of birth control and anabolic
androgenic steroids so it is hard to say how they truly interact. For the usual purpose of women using
steroids, to cut, it is more than that the effects of birth control and steroids promote opposing results, so the
end result is less than completely optimal effects of either. Birth control’s purpose is to regulate estrogen
levels. For some this may mean controlling higher levels during a period, or for others this might mean
promoting more if they experience irregular periods. This also includes the usual water retention and
estrogen-pattern fat depositing around the stomach, hips and thighs areas. While a steroid is trying to
promote lean muscle mass, and in some cases, even a ‘fat burning’ effect. Even while the steroid may
interrupted the menstrual flow, the birth control will still support prevention of pregnancy.

If a cycle is used for off-season mass-building, the need for staying lean is less of an issue. However for
competition cutting, it can be an issue. The trade-off is to continue using birth control, and possibly not get
the full effect of the cutting in the stomach / hips / thighs area, but still getting the pregnancy
prevention or dropping the birth control, using a back-up birth control method (i.e. condoms) and have less
of an impact from the estrogen-pattern fat depositing. Another option for many is an intra-uterine device
(IUD). The copper IUD is completely non-hormonal, or another option such as Mirena, has a low-dose of
slow-release progesterone to help address bleeding which can be an issue with the copper IUD. IUDs must be
inserted by your OB/GYN and can last 3-6 years for progestin IUDs and up to 12 years for copper IUDs. This is
something you need to discuss with your OB/GYN. The cost tends to vary and may or may not be covered by
your health insurance.

Another concern that women often with steroid use is recovery of the menstrual cycle. Noting I have yet to
see a published study on this, the following paragraphs come with a caveat that this is from anecdotal and
observational information and suggested as practical guidance and not a medical verity. If you have lost your
period for an unusually long time and are concerned, always consult your OB/GYN.
The menstrual cycle tends to be sensitive to changes in its environment – ranging from stress, to increased
physical activity, sudden weight or bodyfat drop, introduction of steroids, or an estrogen manipulator such as
a new birth control dose or use of an anti-estrogen. It will tend to turn off flow (and in the extreme,
amenorrhea) or have breakthrough bleeding or sporadic periods while it deals with the change in its
environment. When things have returned to a state of homeostasis, things will generally return to normal,
including the usual monthly flow and the usual side effects of estrogen-pattern bodyfat depositing, water
retention, cramps, etc.

To gauge roughly how long it should take for an interrupted menstrual cycle to return, look first at the
compound you are using and its half-life. This will help you get an idea of a point where the concentration of
the compound has dropped to where the rest of the body is comfortable and ready to turn things back on.
And then, keeping in mind that the menstrual cycle works on a 28-day schedule, it will generally want a full
month of a stable environment before it may start up again. If you have concern, always consult your
OB/GYN. There are prescriptions that are available to help reintroduce a period.

A last comment is about steroids and pregnancy. Again there are no medical studies available, but general
guidance is to allow a good six months after a cycle to clear before attempting to get pregnant. Be sure to
work closely with your personal physician if you plan to get pregnant and ensure that all of your basic blood
work, and everything else is in order. The concern is that the presence of steroid compounds in the female
system while a fetus is growing, can affect the sex hormones of the fetus, producing androgenic fetal
abnormalities. Some of this mentioned here, but all in all, you would want to ensure a steroid-free
environment for your child. There are many women who have cycled, who then stopped, cleared out and
have had healthy children with no problem. Steroid use will not leave you infertile.

If the father is using steroids when the mother gets pregnant, there is no effect on the fetus itself. The
concern for men using steroids is more related to the steroid-driven suppression of natural testosterone
production, and in the potential for infertility. Again, that said, there are many men who have conceived
while on cycle with no issue.

Androgen Deficiency In Women

If you are a woman and taking non-IUD hormonal birth control and don't take DHEA or some other kind of
androgen replacement you are very probably living with suboptimal hormone levels. More on this:
Here. Obviously this doesn't really apply when on AAS.
FAQ
Will AAS affect my birth control? Short answer: No. There is little/no evidence to show that anabolic or
catabolic steroids will cause your birth control to stop working. However, you may stop ovulating and
therefore stop having menstrual periods while using AAS.
Do women need PCT? For most female cycles, it is advised to simply taper down your dose or stop
completely. Women do not need to use SERMs and AIs and taking them can have very damaging effects.
What is virilization? Technically, virilization refers to the development of male traits by females. For example,
the growth of body hair and loss of hair on head, enlargement of genitals, deepening of voice, acne,
irregularity/loss of menstrual cycle, loss of breast size, and increase in sex drive. Virilization is caused by an
increase of androgens. It is possible to avoid and prevent unwanted virilization by avoiding compounds that
are more androgenic than anabolic, by taking the lowest possible doses to achieve desired results, and by
closely monitoring your body for unwanted physical changes.
What about my genitals? Many women experience an enlargement of the clitoris while using AAS.
Examples: 1, 2
Depending upon the length and dose of the cycle, most women report that this engorgement is only
temporary and that their genitals return to normal within a short period after their last dose. It is a myth that
the common, low-dose cycles will result in "growing a dick."
Am I going to get too bulky/huge? You will only get as big as your eating and training allows. The compounds
and dosages that most women will use will not result in incredible mass.

Related Studies

Most of this wiki page was taken from a blurb written by Sassy69.
Related Thread - Female Cycle Thread.
On the pill, watch out for injuries
Effects of follicular versus luteal phase-based strength training in young women

14 STEROIDS PROFILES, ANDROGENIC AND ANABOLIC RATING

Anabolic steroids, technically known as anabolic-androgenic steroids (AAS), are drugs that are structurally
related to the cyclic steroid ring system and have similar effects to testosterone in the body. They increase
protein within cells, especially in skeletal muscles.

Anabolic steroids also have androgenic and virilizing properties, including the development and maintenance
of masculine characteristics such as the growth of the vocal cords, testicles (primary sexual characteristics)
and body hair (secondary sexual characteristics). The word anabolic comes from the
Greek ἀναβολή or anabole, "that which is thrown up, mound", and the word androgenic from the
Greek ἀνδρός or andros, "of a man" + -γενής -genes, “born”.
See also pages for Insulin, hGH, and other Peptides.

FAQ

Some answers to common questions.

 What is the difference between Testosterone Enanthate and Testosterone Cypionate?
Approximately nothing. Definitely nothing that is going to make a difference in choosing one or the other for
our purposes. Read the specifics below:

• The ester weights are almost identical, with Cypionate being ever so-slightly heavier.
Meaning there is ever so-slightly more actual testosterone hormone (~1%) in Enanthate.
• The terminal half-life's are also almost identical.
Enanthate is 4.5 days.
Cypionate is 5 days.
• For some, they may experience a slight difference in potential Post Injection Pain (PIP). This is due to
Cypionate having a higher melting point than Enanthate, making Cypionate more prone to being able to
cause PIP. This all depends on how your Testosterone was brewed by your source/supplier. Read more on
Post Injection Pain (PIP): Here.
Please See Our Esters Wiki Page: Here

What are esters?

Please See Our Esters Wiki Page: Here

Anadrol (Oxymetholone)

Chemical structure: 17 beta-hydroxy-2-hydroxymethylene-17alpha-methyl-5 alpha-androstan-3-one

Molecular weight of base: 332.482
Active Life: 12 to 16 hours
Anabolic/Androgenic Ratio: 320:45

Originally developed for treatment of severe cases of anemia, oxymethalone soon fell out of favor due to the
development of drugs that had far fewer side effects and were more efficient at treating the disease.
However, in the mid-1990's, researchers found that the compound worked remarkably well with HIV/AIDS
patients due to it's ability to combat muscle wasting.

For bodybuilders and strength athletes, it is the ability of oxymethalone to produce rapid weight and strength
gains that make it such a sought after compound. Some see it as an alternative to methandrostenolone, as it
offers some of the same benefits, and some users report having greater gains with less severe side effects.

It is because of the quick gains and high liver toxicity of oxymethalone, that it is most often used to kick start
a longer cycle, usually during the first weeks of the cycle. However, strength athletes will also use the
compound in the middle or near the end of their cycles to in preparation of a competition when they are
trying to peak in strength.
Use/Dosing

Dosing for most inexperienced users of oxymethalone usually ranges between 50 to 150 milligrams per day.
Experienced users have anecdotally used in excess of this, but side effects are more pronounced as the
dosage increases. The effects of the compound are far weaker than other similar compounds such as
methandrostenolone milligram for milligram, however anecdotally users report that when doses are
increased some individuals react much better to oxymethalone than they have using other compounds with
similar anabolic and androgenic effects.

While using oxymethalone, like any anabolic steroids, it is wise to use a liver protector such as milk thistle,
etc. This is due to the increased strain that a 17 alpha alkylated compound puts on the organ. However, due
to the large doses that a user is ingesting when compared to other oral steroids, this makes it imperative that
precautions are taken to ensure that the health of the liver is maintained. Also, as per all other 17 alpha
alkylated steroids, stacking more than one together is not recommended.

Due to the active life of the compound, two doses per day while administering the drug is recommended.
These should be as evenly separated throughout the day as possible. As well, cycles between four and six
weeks are recommended. Any longer and there is an increased likelihood that damage to the liver could
occur.

Side Effects/Risks

Oxymethalone does not directly convert to estrogen. There is also very little to no progestational-like effects
associated with the compound1. Despite this, individuals using this compound will often report pronounced
estrogen related side effects such as gynecomastia and water retention, among others. Based on this it
would appear that oxymethalone acts upon the estrogen receptors in the body itself2. This theory seems to
hold some weight as aromatase is not involved3, but estrogenic side effects are common during
administration of the drug.
Androgenic side effects should also be expected3. Oily skin, acne, increased body and/or facial hair are all
commonly reported. Also, if susceptible to male pattern baldness, the use of this compound may make the
condition more pronounced. Hypertension is a common side effect of the compound as well, in part due to
the extreme bloat associated with it.

In oxymethalone, virilization symptoms can occur in women who use it (as with any AAS), so women should
be very cautious when using said compound.

Another somewhat unique characteristic of the compound is that it can have a detrimental effect on a user's
glucose tolerance4. This reportedly can actually cause borderline diabetic situations. Obviously this should be
considered by those that have been diagnosed with similar problems in the past as this compound can more
that complicate it.
 Finasteride, a reductase inhibitor, will not be effective in combating some of the androgenic side effects of
oxymetholone. This is due to the fact that while oxymetholone does convert to dihydrotestosterone, this
does not involve the 5 alpha reductase enzyme (2). Oxymetholone is a dihydrotestosterone based steroid. It
differs only from dihydrotestosterone only due to the addition of a 2-hydroxymethylene group. This grouping
can be removed metabolically which in turn would reduce the compound to 17 alpha-methyl
dihydrotestosterone1. It is this biotransformation that can explain, at least partially, the strong androgenic
effect that oxymetholone has.

Oxymetholone is a 17 alpha alkylated compound and includes the usual associated risks and stresses that
those compounds place on the liver. It is because of the high doses of the drug that are required for effective
use that oxymetholone can cause a higher than normal stress level on the liver. However, with moderate
dosing and cycle lengths liver damage should not be an issue for most healthy individuals.

References

1. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition

2. Studies on anabolic steroids-8. GS/MS characterization of unusual seco acidic metabolites of oxymetholone in
human urine. J Steroid Biochem Mol Bio 42: 229-42, 1992
3. Pavlatos AM, Fultz O, Monberg MJ, Vootkur A, Pharmd., Review of oxymetholone: a 17alpha-alkylated
anabolic-androgenic steroid, Clin Ther 2001 Jun;23(6):789-801; discussion 771
4. Woodard TL, Burghen GA, Kitabchi AE, Wilimas JA., Glucose intolerance and insulin resistance in aplastic
anemia treated with oxymetholone., J Clin Endocrinol Metab 1981 Nov;53(5):905-8.

Anavar (Oxandrolone)

Pharmaceutical Name: Oxandrolone

Chemical Structure: 5 alpha-androstan-2-oxa-17 alpha-methyl-17 beta-ol-3-one
Molecular Weight Of Base: 306.4442
Active Life: 8-12 hours
Anabolic/Androgenic Ratio (Range): 322-630/24
Oxandrolone was designed as an extremely mild anabolic, one that could be safely used as a growth
stimulant in children. The compound will not actually aromatize and the anabolic effect of oxandrolone has
been shown to promote linear growth. It was also once prescribed for the treatment of osteoporosis in
women, something that again demonstrates how truly mild it is. However, for the most part it is now
manufactured for the purpose of treating HIV/AIDS related wasting syndrome1 . The expediting of wound
healing, particularly the treatment of burns, is another use but is far more rare2 .

For bodybuilders and strength athletes, the mild nature of oxandrolone is a definite draw to the compound.
The lack of aromatization of the compound makes it ideal for cutting cycles as there is little bloat to deal
with. Oxandrolone does not reduce body fat itself, but can play a major role in the maintenance of lean mass
while dieting. Strength increases are also common and mixed with less than dramatic weight gains, the
compound is very beneficial to athletes participating in sports that have weight divisions or where extra
weight can be a hindrance.

Use/Dosing

Similar to nearly all oral anabolic steroids oxandrolone's half-life is quite short with frequent doses of the
drug being needed to be taken to ensure that blood levels remain fairly constant. Oxandrolone is relatively
quick to be metabolized by the body with concentrations of the drug falling rapidly after ten to eighteen
hours after administration3 . This would indicate that at least two doses should be taken per day so that
blood levels of the compound remain stable and that no major flucuations occur.

The majority of first time male users of oxandrolone tend to take doses ranging from 40mg to 80mg per day,
as reported anecdotally. Experienced users have reportedly used doses up to 150mg per day or more. As is
the case with most anabolic steroids, as one increases the doses one also increases the chances of developing
negative side effects.

Due to the relatively mild nature of the drug, oxandrolone is also a favorite of women. Doses as low as 5mg
per day have reportedly produced dramatic muscle growth and hardness1 . However as with most
compounds doses far larger have also been used with varying degrees of success.

As discussed later, due to the unique nature of oxandrolone and it's relatively mild nature in terms of
hepatotoxicity, this compound can be run far longer than other 17 alpha alkylated oral steroids. Cycles of the
compound lasting ten to twelve weeks are not uncommon, with some users extending their cycles of the
drug further. Of course, risks still remain. They are however less substantial than if a user was administering a
more toxic compound.

Side Effects/Risks

Oxandrolone does not aromatize or convert to DHT and therefore hair loss should not be a concern with this
compound. It causes little or no virilization properties, somewhat surprising since oxandrolone does not
aromatize either. This of course is one of the major reasons why this steroid is so popular with female
athletes.

If used without stacking it with testosterone, oxandrolone can lead to a loss of libido in males as it will shut
down your HPTA. However, some users indicate that no libido problems occur. As usual, it varies from
individual to individual.

Liver enzymes will likely rise while a user is taking this compound, however the actual damage that occurs to
the liver is very minor to non-existent. As noted by William Llewellyn in Anabolics 2004, "One study
comparing the effects of oxandrolone to other agents including as methyltestosterone, norethandrolone,
fluoxymesterone and methAndriol clearly supports this notion. Here it was demonstrated that oxandrolone
 causes the lowest sulfobromophthalein (BSP; a marker of liver stress) retention among all the alkylated orals
tested. 20mg of oxandrolone in fact produced 72% less BSP retention than an equal dosage of
fluoxyrnesterone, which is a considerable difference being that they possess the same liver-toxic alteration".

This would seem to indicate, as stated earlier, that oxandrolone can be run safely for longer periods of time
than most other 17 alpha alkylated oral steroids. However, liver damage is still a possibility and precautions
should be taken. Also, Oxandrolone has been shown to have a negative effect on users' blood lipid profiles,
another indication that long terms use of the compound should be avoided4 .

Bridging with Anavar: Is it possible?

Similar to methandrostenolone, there are some individuals that suggest Oxandrolone can be used in small
doses to "bridge" between cycles. The theory that is proposed tries to argue that by taking a small dose of
Oxandrolone upon awakening, this will provide an anabolic "boost" to an individual's natural testosterone
levels, help combat catabolism, all while supposedly not interfering with the recovery of the HPTA. When one
looks at the evidence, it is apparent however that this theory is not based on any credible information.

The fact that Oxandrolone can be suppressive to the HPTA even at small doses for several hours alone would
prevent it from being useful during PCT or between full cycles. As stated by Sheffeild-Moore et al. in their
study: "Total serum T concentrations were within normal physiological range on day 0 (449 ± 35 ng/dL) and
day 3 (441 ± 44 ng/dL) of OX treatment. However, by day 5, total serum T concentrations were significantly
reduced (282 ± 45 ng/dL; P < 0.05) below day 0 and day 3 values [emphasis mine]..."(3). This means that even
at a dose of 15mg per day an individual will be shut down, thus nullifying any attempt at PCT.

It is for this reason that running Oxandrolone as an attempt to "bridge" between cycles will not aid in
maintaining muscle mass during PCT while allowing your HPTA to recover.

Related Topics

Anavar and lipid levels.

References

1. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp.76-8

2. Demling RH, Orgill DP., The anticatabolic and wound healing effects of the testosterone analog oxandrolone
after severe burn injury., J Crit Care 2000 Mar;15(1):12-7
3. Short-term oxandrolone administration stimulated net protein synthesis in young men. Sheffeild-Moore et al.
J Clin Endocrinol Metab 84(8) 2705-11 (1999)
4. Effects of Oxandrolone on Plasma Lipoproteins and the Intravenous Fat Tolerance in Man. Atherosclerosis 19:
337-46, 1974
Boldenone Undecylenate (Equipoise)
Boldenone aka EQ, Equipoise, Parenabol — Testosterone derivative. Rated 100:50. Metabolites include DHB
(dihydroboldenone). Steady, dry, lean moderate mass gains, EPO-like stamina, strength and endurance,
appetite increase, collagen synthesis, potent aromatase inhibition, IGF-1 boost, stringent estrogen
management requirements. Compound Definition. Comprehensive EQ Guide, Top-level thread. Experience
thread.

Molecular weight of base: 286.4132

Molecular weight of ester: 186.2936 (undecylic acid, 11 carbons)
Chemical structure: 1,4-androstadiene-3-one,17b-ol
Active Life: 14–16 days
Anabolic/Androgenic Ratio (Range): 100:50
Detection Time: 4–5 Months
Compound Experience Thread

History

Boldenone is a highly anabolic and moderately androgenic steroid that was patented and invented by the
pharmaceutical firm Ciba in the late 1940s. The compound was derived from Testosterone by adding a
double bond between the carbons atoms in position C₁ and C₂.

Boldenone is more similar to testosterone than any other anabolic steroid. It was the first synthetic derivative
of Testosterone, long before even Dianabol was conceived of in 1958. Dianabol, or Methandrostenolone,
carries many similarities—it's actually a C17-alpha alkylated version of Equipoise. It differs from Boldenone
only via a methyl group attached to the 17-beta position on the steroid ring. However, this addition
completely changes the chemical properties of Dianabol, making it an entirely different steroid altogether.

After exploring several ester configurations, Ciba introduced boldenone for clinical use in the undecylenate
ester configuration under the brand name Parenabol, which was prescribed by doctors around the world
throughout the late 1960s and early 1970s. However, Parenabol was discontinued before the end of the
1970s, subsequently purchased and introduced by Squibb under the brand name Equipose for veterinary
use. The commercial product is now most commonly sold for administration to horses—though its popularity
with strength athletes and bodybuilders likely exceeds its veterinary applications.

Benefits

Boldenone experiences little aromatization and very limited amount of water retention. An attractive quality
of the compound is the ensuing increase in appetite often reported by users when running this steroid, and it
will often be included in bulking cycles for this purpose.

Boldenone increases hemoglobin and hematocrit—the number of red blood cells and the percentage of red
blood cells1—thus causing greater “pumps” while working out. Although this is true of nearly all anabolic
steroids, the effects are more prominent with boldenone undecylenate. An improvement in vascularity
should also be experienced due these increases if body fat is at a low enough level.

Athletes other than bodybuilders or those concerned primarily with strength may also benefit from
boldenone undecylenate due to the fact that the compound stimulates the release of erythropoietin,
commonly referred to as EPO, in the kidneys. Erythropoeitin signals the body to increase the production of
erythrocytes, red blood cells. Erythrocytes are the carrier of oxygen in the body, and therefore if their
concentration is increased , a higher maximal oxygen capacity is produced. Performance can be improved
due to a delay in the onset of fatigue, including the build up of lactic acid. A user should definitely notice an
improvement in cardiovascular stamina and endurance.

Dosing

A versatile compound, boldenone's effective dose ranges from 300 mg to well over 3 grams depending on the
purposes of the cycle. Its effective dosage range depends entirely on objectives. For cardiovascular
endurance and stamina in competitive sports, as little as 300 mg may make a difference, given the increase in
red blood cell count, i.e., Boldenone as a "poor man's EPO." For the usual bulking purposes, 600, but really
800–1800+ mg/wk. 800 is the minimum recommended dose. Even at 1500 mg, the compound imparts little
by the way of notable effects outside of improvements in vascularity, strength, fullness, metabolism and
appetite. Boldenone's unique dosing requirements are explored in this excerpt from a
2012 IronMag article by Mike Arnold.
Unlike most other steroids, which usually begin to reach the point of diminishing returns at between 500–
1,000 mg per week, EQ tends to reach its optimal dosing range much later on: around 2 grams per week.
Great results will be found between 1.5–3.0 grams. Of course, all steroids will continue to activate more
receptor sites, and thus provide greater muscle growth, up until about 3,500 mg per week, but with
Boldenone, it seems that the gains are just starting to get good at 1 gram per week—while most other AAS
seem to be nearly tapped out by that point, quickly hitting the point of diminishing returns.

One factor which makes higher dosing with EQ possible is its relatively mild nature in terms of side effects.
While many steroids would be rather unpleasant to run at 2 grams weekly, many individuals will find
Boldenone to be rather tame at that dose. This is an important consideration because after all, no one wants
to be miserable on-cycle. It's understandable to think some may initially be put off by these doses, as the
typical steroid user frequently views anything over 1 gram per week (per steroid) as “mega-dosing” and
therefore, excessive. Presumably, this mentality was instilled through the repeated dosing recommendations
of other AAS, which by their intrinsic nature, do not need to be dosed much higher than 1 gram weekly in
order to achieve near optimal results—but with Boldenone, we are dealing with a different animal
altogether.

Boldenone is a steroid which needs to be dosed higher than other AAS if one wishes to take advantage of its
full capabilities. 600 mg per week just isn’t going to cut it if one wants to experience everything that this
compound has to offer. When dosed at the above-mentioned range, Boldenone becomes a formidable
muscle-builder, packing on genuine muscle fiber rather quickly. The next time you consider using Bold as a
part of your cycle, try to look at it from a fresh perspective—as a drug that “needs” to be utilized at higher
dosages in order to experience all that it has to offer. If you do, I can promise you impressive, high-quality,
water-free increases in muscle tissue, along with dramatic increases in vascularity over a 12–16 week period.

Boldenone has been run up to 2–3 grams without diminishing returns or side effects. It's a very mild, safe
compound. Boldenone—and to a certain extent, Primobolan—are the only two AAS mild enough to be
comfortably run at gram-plus levels absent sides or diminishing returns. Boldenone is the only anabolic you'll
find being run at two grams plus in an effectively “normal” cycle, notwithstanding IFBB megadose blasts.

Aromatase Inhibition

The standard ratio for dosing Equipoise is 2:3, but a low aromatizer might need to go with 1:1. An ideal EQ
cycle would be 1000 Test with 1500 EQ, no AI necessary—a very mild, mellow and smooth cycle. A primary
concern will be to balance estrogen, as EQ metabolites ADD, ATD and 1-AD can act as powerful aromatase
inhibitors in those sensitive to these molecules, and hence readily crash E2. EQ anxiety is one symptom of
crashed estrogen levels.

It's important to stack boldenone together with sufficient aromatizing compounds. If estrogen levels get too
low or crash, there's no need to panic. Simply have something on hand to bring E2 levels back up and online:
TNE, short ester or frontloaded test, dianabol, trestolone or HCG. Each of these result in aromatization to
either estrogen—or in the case of dianabol and trestolone, methyl-estrogen.

Due to the compound's active life, injections are usually conducted twice per week to maintain stable blood
levels, although some users prefer injecting only once per week. Most users anecdotally report that the
minimum dose for males is between 800 mg to 1000 mg to see any substantial effects from the drug.
Women, of course, will see results at much lower doses—usually ranging from 50–150 mg per week for less
experienced users.

Like most compounds, the majority of users prefer to stack boldenone with testosterone. This should provide
a potent combination that should result in a dramatic increase in lean body mass. Due to the lack of liver
toxicity associated with the compound, other compounds that can raise liver values, such as 17-alpha
alkylated steroids, can be run with boldenone without any further complications.

Many users believe that boldenone undecylenate can be used in both bulking and cutting cycles, as the lack
of water retention associated with its use and improvement in vascularity can help improve definition while a
user is reducing body fat. At the same time, the compound has a profound effect on lean body mass. Results
can be dramatic when run with a diet high in protein and calories in conjunction with a proper training
regimen.
Not considered a rapid mass builder in comparison to other anabolic steroids, boldenone will add quality lean
muscle consistently throughout a cycle. Anecdotally, users have reported that cycles of at least sixteen to
twenty weeks are needed to see the full effects of the compound.

Side Effects

For the most part, problems such as gynecomastia and a high degree of water/salt retention are unheard of
with this compound—particularly because its natural metabolites function as active aromatase inhibitors.
Boldenone is said to aromatize at about 50% the rate of testosterone, which should make it a fairly
estrogenic drug, prone to causing estrogenic side effects such as gynecomastia and water retention,
especially at higher dosages. However, real-world experience has shown us that it is very unlikely to
propagate serious estrogenic side effects, even when administered at high dosages. This is due to its natural
AI effects.

As boldenone undecylenate is not hepatotoxic to any serious degree, it can be used for extended-duration
cycles. Some side effects that may be experienced are acne and increased body-hair growth, as well as the
usual virilizing effects in women, however these are mild and will likely be at a far-reduced level than other
compounds3 . If a user does not stack the compound with testosterone, they may suffer sexual side effects,
as is the case with the majority of anabolic steroids.
A user's lipid profile will be negatively affected, as with any steroid, but not to the same degree as with a
strong androgen. Boldenone can convert to DHB, a powerful androgenic steroid in its own right, while a very
mild androgen in comparison to DHT, via 5-alpha reductase4,5. Like most other compounds, if you are prone
to male pattern baldness, boldenone can accelerate or worsen the condition. Given the compound's reduced
androgenicity, prostate problems are unlikely to be experienced.
A study on Boldenone's effects on the kidneys, Evaluation of anabolic steroid induced renal damage with
sonography in bodybuilders, showed renal enlargement during blast—but functionality was entirely normal
the whole time, enzyme and metabolite levels weren't elevated or out of range, and all physiological
abnormalities resolved upon cessation. This is of the many animal studies on Boldenone and kidney damage,
which prompted many to claim that Boldenone is particularly kidney toxic. This is nonsense—the results arise
from the fact that at the time, Boldenone was the first steroid whose effect was studied in animals. This
makes sense, as it's a veterinary product. Yet similar detrimental effects on kidney function have since been
observed from other steroids. Case in point: nandrolone, which is more than twice as nephrotoxic as
Boldenone6 at the same dosage. Such damage may be at least in part ameliorated by antioxidants such as
taurine or N-acetylcysteine (NAC).

Hematocrit

Boldenone raises red blood cell count significantly, as it stimulates the release of erythropoietin from the
kidneys. This gives rise to increased hematocrit levels that have been of cause for concern. Some have
 donated blood on cycle to bring the percentage points back in range—however, this is just a quick-fix and a
temporary band-aid solution, nothing that works over the long-term. The body quickly regenerates its RBC
count back to previous levels within a matter of days.

An increase in hematocrit values don't have to be cause for alarm so long as one is otherwise healthy. If there
aren't any sides such as headache or sluggishness from the high HTC, then there's no immediate cause for
alarm. Contra outdated medical consensus of old, elevated HCT in isolation is no longer considered an
independent risk factor.
Nearly every old study reporting the dangers of a elevated HCT analyzes it in the context of polycythemia
vera or another similar condition. These conditions cause a multitude of hematological changes. For
example, polycythemia vera also causes a significant increase in platelets, which is problematic on its own
and further amplified by the synergistic thrombotic action of elevated red blood cells with elevated platelets.

Detectability

The active life of boldenone is 14-16 days; however, it produces detectable metabolites that will appear in
urine for several months after cessation2. This property makes it less than ideal if testing is a concern.

References

1. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition

2. Aromatization of androgens to estrogens mediates increased activity of glucose-6-phosphate dehydrogenase
in rat levator ani muscle, Endocrinol 106 (2), 1980
3. Weisberger, Ho, Activation of the Somatotropic axis by testosterone in adult males : evidence for the role of
aromatization, J Clin Endocrinol Metab, 76, 1993, 1407-12
4. MPB Reserch website, http://www.hairloss-research.org/index.html
5. Rea, Author L., 2002, Chemical Muscle Enhancement: Bodybuilder’s Desk Reference
6. Shabin N., Malik H., et al. (2015). Effect of Nandrolone Decanoate, Boldenone Undecylenate on Renal Status
of Rabbits (Oryctolagus cuniculus). Global Veterinaria 14 (3): 432-438. ISSN 1992-6197. DOI:
10.5829/idosi.gv.2015.14.03.92201.
7. Kantarci, U. H., Punduk, Z., Senarslan, O., & Dirik, A. (2018). Evaluation of anabolic steroid induced renal
damage with sonography in bodybuilders. The Journal of Sports Medicine and Physical Fitness,
58(11). doi:10.23736/s0022-4707.17.06763-9
8. Equipoise, Estrogen, and AI effects (Reddit)
9. Compound Description Page (Reddit)
10. Compound Experience Thread (Reddit)
11. E2 Bloodwork (Reddit)
Deca Durabolin (Nandrolone Decanoate)
Nandrolone aka Deca, NPP — 19-nortestosterone (19-nor). Rated 125:37. Second only to testosterone in
terms of popularity as a bulking compound. Water retention, collagen synthesis, joint relief, more gains.

Formula of Base: C18 H26 O2

Formula of Ester: C10 H20 O2
Molecular Weight of Base: 274.4022
Molecular Weight of Ester: 172.2668
Anabolic/Androgenic Ratio: 125/37
Active Life: 14-16 days
Nandrolone is by far one of the most popular anabolic steroids available. This is due to the compound's affinity
for being highly anabolic but relatively mild in terms of androgenic side effects. Nandrolone is the base steroid
19Nor-testosterone, meaning that it is like testosterone in appearance except for the absence of a carbon atom
in the 19th position. This small change makes a major difference in the characteristics of the
compound1. Notably, this change makes nandrolone a less potent agonist of the androgen receptor. This of
course reduces the chance that a user will experience androgenic side effects. Instead of forming
dihydrotestosterone when encountering the 5 alpha reductase enzyme like testosterone does, nandrolone will
form dihydronandrolone. Dihydronandrolone is extremely mild in terms of it's antagonizing the androgen
receptor. Therefore androgenic side effects should be far less likely to occur with nandrolone than with
testosterone.

It is of note however that nandrolone is believed to have some activity as a progestin in the body. Although
progesterone is a c-19 steroid, removal of this group as in 19-norprogesterone creates a hormone with greater
binding affinity for its corresponding receptor. The compound will stimulate the progesterone receptor, along
with progesterone. Side effects associated with this activity are similar to some of those related to estrogenic
ones including water retention, acne, and gynecomastia among others. However these side effects are fairly
rare in comparison to more androgenic compounds.

Now, with the reduced chance of negative side effects associated with the use of nandrolone one would assume
that the gains in lean body mass that a user could expect to make would also be reduced. This is not true
however. Nandrolone is 2.4 times as anabolic as testosterone when compared gram for gram1. This does not
mean that a user will gain 2.4 times as much muscle if using nandrolone instead of testosterone however. It is
not that easy. It does show how powerful this drug is and how it can help a user make serious gains in muscle
mass.

Use/Dosing

Due to the active life of the compound, users would only need to administer nandrolone decanoate once per
week to maintain fairly stable of the drug. However, since the vast majority of users will stack nandrolone with
testosterone (for reasons that will be discussed later in the Side Effects/Risks section of this profile) and the
most commonly used esters need to be injected more frequently most will simply injected it when it is
convenient, such as twice a week with their testosterone enanthate or cypionate.

Anecdotally most users report that the full benefits of nandrolone decanoate will not be felt until the fifth, sixth
or even seventh week of using the compound. This necessitates that users run the drug for at least eleven or
twelve weeks for a cycle of the compound to have the results that a user expects. Of course, since nandrolone
decanoate is a relatively mild drug many users have run it for extremely lengthy cycles with little in the way of
serious side effects.

Most inexperienced male users will start using about 400mgs of nandrolone decanoate during their first cycles
of the compound. Like most drugs users have used quite large doses of the compound, with diminishing
returns being seen as these doses go higher and higher.

Females also have found that nandrolone can be quite effective while offering relatively mild side effects.
Doses ranging from about 50 to 150mgs per week seem to be the norm for most first time users of the
compound, again with these doses increasing as users try to achieve more and more with the compound.

Side Effects/Risks

Estrogenic effects are not a major concern with use of nandrolone due to it's low rate of aromatization.
However it can cause progesterone-like effects in some users. Commonly reported sides effects associated with
nandrolone are such things as acne/oily skin, insomnia, diarrhea, and nausea. These of course are coupled with
the common side effects most often associated with anabolic steroids including testicular atrophy,
gynecomastia (including lactation in some cases), and sexual dysfunction.

To combat sexual dysfunction most users will stack testosterone with nandrolone. The obvious choice to be
used with nandrolone decanoate is testosterone enanthate or cypionate due to the length of the esters being
similar. How much testosterone one would need to take to ward off side effect associated with use of
nandrolone and lack of natural testosterone production varies from individual to individual. Some have
anecdotally reported that a low dose similar to 200mgs per week is enough. Others state that they need to run
several hundreds more milligrams per week of testosterone than nandrolone to combat the effects. There is a
small minority of individuals that also report having no sexual dysfunction from the drug even while running it
without any type of testosterone. This variance again demonstrates that individuals will react to a compound
differently than others.

This effect also points to the fact that nandrolone is extremely suppressive to a user's natural testosterone
production. Even at relatively small doses, much smaller than those that would be used by those wanting to
reap the anabolic effects that the compound can offer, nandrolone can suppress the natural production of
testosterone of a user so much that it can take up to thirty days after the drug cycle is complete for it to fully
recover2 . For this reason it is imperative that a user run a well planned post cycle therapy after using
nandrolone.
 Nandrolone is relatively safe in terms of a user's lipid profile and cholesterol. In some studies it has even been
shown to actually improve HDL cholesterol levels4 . A major increase in a user's blood pressure or their liver
toxicity should not be noticed with this compound either. Nandrolone is relatively mild in these respects.
Since nandrolone is a progestinic anabolic steroid3,4 . Some special precautions need to be taken to ensure that
side effects do not get out of control as a result of a rise in prolactin levels. Using compounds such as
bromocriptine, cabergoline and/or vitamin b6 have all been shown and reported to help lower prolactin levels.
The drug Femara (letrozole) is also effective for use with nandrolone as it will regulate the progesterone and
estrogen receptors in the body, therefore preventing some of the negative side effects associated with the
compound.

A word of caution also for those that may plan on stacking nandrolone with trenbolone. Trenbolone is a strong
progestin, much stronger than even nandrolone. By running these two compounds concurrently the user will
suffer from extremely high levels of prolactin. This in turn will force the user to pay special attention to
progesterone-like side effects and using compounds to prevent them, as well as having to run a particularly
aggressive post-cycle therapy due to severe suppression of the hypothalamus pituitary testicular axis. Some
users have anecdotally reported that they have suffered no ill effects of running the two compounds together,
but it is a definite risk. One must weigh the costs versus the benefits.

References

1. Sundaram K, Kumar N, Monder C, Bardin CW., Different patterns of metabolism

determine the relative anabolic activity of 19-norandrogens., J Steroid Biochem Mol
Biol. 1995 Jun;53(1-6):253-7
2. Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S. Effect of non
aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Horm Metab Res. 1984 Sep;16(9):492-7.
3. Hochberg RB, Hoyte RM, Rosner W., E-17 alpha-(2-[125I]iodovinyl)-19-
nortestosterone: the synthesis of a gamma-emitting ligand for the progesterone receptor.,
Endocrinology 1985 Dec;117(6):2550-2
4. Sattler FR, Schroeder ET, Dube MP, Jaque SV, Martinez C, Blanche PJ, Azen S, Krauss
RM. Metabolic effects of nandrolone decanoate and resistance training in men with HIV.
Am J Physiol Endocrinol Metab. 2002 Dec;283(6): E1214-22

Dianabol (Methandrostenolone)

Chemical Names: 17a-methyl-17b-hydroxy-1, 4-androstadien-3-one 1-Dehydro-17a-methyltestosterone

methandienone
Molecular Weight: 300.44
Formula: C20H28O2
Melting Point: 159-164 degrees Celsius
Active Life: 3-8hours
Detection Time: up to 6 weeks
Anabolic/Androgenic Ratio (Range): 90-210:40-60

Methandrostenolone has long been a favorite of strength athletes and bodybuilders since it's creation in
1956, with the explicit purpose of it's creation being for the use by athletes. It was the compound's ability to
promote drastic protein synthesis, stimulate strength in a direct and fast-acting way, and it's ability to
enhance glycogenolysis that made it so popular, and why it's popularity remains high today.

In terms of it's medical use, methandrostenolone was/is used in the treatment of conditions such as
interstitial-pituitary insufficiency, chronic adrenocortical insufficiency, thyrotoxicosis, diabetic angiopathies
(retinopathy and nephropathy), steroidal diabetes, and pituitary dwarfism among others1 . However, due to
the U.S. Food and Drug Administration's belief that the compound was being used inside of the bodybuilding
community far more than in the treatment of medical conditions, it ordered that American companies
discontinue it's manufacture in the early 1990's. Numerous drug companies outside of U.S. borders continue
to make the drug however, and it's prevalence on the black market has remained very high.

Use/Dosing

It can be concluded that the best use for methandrostenolone is short-term with most users preferring to use
the product for between four to six weeks, although some will prolong the use with limited consequences to
health, despite its strong hepatoxic effects. For the most part, most recreational users begin administering
methandrostenolone at the start of a longer bulking stack to "jumpstart" gains in mass and strength.
However, it's use prior to various sorts of competitions is also quite common so that it's effects are realized
during a specific period.

Due to the active life, which is three to eight hours, multiple doses throughout the day of
methandrostenolone should be utilized. It is best to maintain blood levels as evenly as possible, therefore
dividing doses throughout the day at even amounts is required. Some argue that administration of the drug
should cease a few hours before you sleep as it will cause further HPTA shut down, as the body's natural
testosterone production during sleep could be affected. However, if you are taking other compounds along
with methandrostenolone, these will already be shutting down your natural testosterone production,
therefore this is not a concern.

In terms of dosing, it has been reported that doses of 10 mg can increase androgen activity by five times, as
well as have an effect of a 50 to 70% decrease in cortisol activity 2 . Despite this, the majority of anecdotal
evidence suggests that twenty to forty milligrams is the norm in terms of first time users (as ascertained from
the anecdotal knowledge gleamed from various users). However, doses ranging from 100-150mg and higher
have been reported by some experienced users. As with the majority of anabolic drugs, the returns are
seemingly diminished and the likelihood of side effects increase as the doses do.

Similar to nearly all oral steroids, the vast majority of users will recognize the fact that methandrostenolone
should not be run alone and only stacked with other compounds. This is due to the fact that most users who
have run methandrostenolone only cycles have reported anecdotally that it is extremely difficult to maintain
gains post cycle. However, the same is true when discontinuing the drug and having your other compounds
"kick in", if they are long ester. It is often the case that the water retention experienced while on
methandrostenolone will be shed but the gains in strength and mass will remain due to the other compounds
being present. It can be argued that therefore, the gains experienced while on methandrostenolone are short
lived no matter what the circumstances and the compound should only be used as a quick fix for either
competition or else simply as a motivator while waiting to notice the effects of long estered compounds.
However, others will argue that the gains they make while using the compound are indeed maintainable.
Therefore, personal experimentation is once again the only way to see how an individual reacts.

Risks/Side Effects

Estrogenic side effects can be a concern with methandrostenolone, as it converts to estradiol via aromatase,
although this is quite modest at best. High blood pressure, water retention, gynocomastia, and acne are all
possible undesirable side effects during use of methandrostenolone. As an aside, a high number of users
have also reported experiencing nose bleeds while using the compound. Some attribute this to an increase in
blood pressure, while others have not noticed a rise in their blood pressure but still experience an increase in
the number of nose bleeds they have while using methandrostenolone.

Use of an aromatase inhibitor such as Arimidex or estrogen blocker such as Nolvadex should help to
counteract some of these side effects. As for potential hair loss, the androgenic metabolite 5-alpha
dihydromethandrostenolone is only produced in trace amounts, and therefore hairloss should not be a
concern3 . In women it is not uncommon for virilizing side effects to occur, including increased growth of
androgen-sensitive hair and deepening the voice, amongst others. There are no ways to minimize these side
effects in women if they are experienced other than to keep the dosage that one is taking to a minimum.
Like most oral steroids methandrostenolone is 17-alpha-alkylated so that it can't be broken down into a 17-
ketosteroid, and therefore rendering the substance ineffective. However, this causes liver values to become
elevated over a short period of time. It is for this reason that long-term use of any 17-alpha-alkylated steroid
is considered dangerous. Despite this however, no long-term damage should be expected if use is kept to
relatively short periods, with liver values returning to previous levels after use is discontinued in nearly all
cases4 .
It should also be noted that methandrostenolone may be less useful to those competing in aerobic events as
it also diminishes cell respiration5 . This may inhibit an individual's ability to perform at their maximum
capacity.
 Bridging with D-Bol: Is it possible?

A widely held belief among some in the steroid using community is that a small dose of methandrostenolone
can be used to "bridge" between cycles. This is due to the fact, as explained above, 10mg taken at once will
increase your average testosterone level by five times and decrease your endogenous cortisone by 50-70%.
This, along with the short active life of the drug, would suggest that by using a small dose first thing upon
waking is thought by some to help to combat the problems associated with coming off of anabolic steroids.
By coinciding the dose of methandrostenolone with the body's own natural testosterone spike upon waking,
many advocates of "bridging" will suggest that the body will somehow be fooled into believing that this spike
is natural and that LH function will remain only partially suppressed, as methandrostenolone has a
comparably small influence on the natural endocrine system6 . The usual suggested dose for bridging is
usually 10mg per day.

Despite appearances, this theory has very little evidence to back itself up with no real scientific evidence to
suggest that a bridge is even possible, although granted that the majority of our working knowledge comes
through trial and error. However, even the proponents of a "d-bol bridge" admit that complete restoration of
LH function will not be achieved until one is completely off of all compounds. With that said, it is unlikely that
a "bridge" will help to maintain muscle mass while you are able to recover both HPTA and LH function. The
only solution is to come completely off all substances and run a proper post-cycle therapy.

Methandrostenolone is an effective steroid, however, it's use must be directed at a specific goal as like most
compounds it's use only fulfills a limited amount of desired effects. With this in mind, methandrostenolone
can be used safely and effectively.

References

1. Metkinen Online Drug Profile, via internet, located

at http://www.metkinen.fi/products/fermentation_technologies/steroids/methandrostenolone
2. Rea, Author L., 2002, Chemical Muscle Enhancement: Bodybuilder’s Desk Reference
3. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 93-6
4. Harrison LM, Fennessey PV., Methandrostenolone metabolism in humans: potential problems associated with
isolation and identification of metabolites, Steroid Biochem 1990 Aug 14;36(5):407-14
5. Blasberg ME, Langan CJ, Clark AS., The effects of 17 alpha-methyltestosterone, methandrostenolone, and
nandrolone decanoate on the rat estrous cycle, Physiol Behav 1997 Feb;61(2)
6. Serakovskii S, Mats'koviak I., Effect of methanedienone (methandrostenolone) on energy processes and
carbohydrate metabolism in rat liver cells, Farmakol Toksikol 1981 Mar-Apr;44(2):213-7

Dymethazine (DMZ, Mebolazine)

Chemical structure: 2,17-dimethyl-5-androstan-17-ol-3,3'-azine

Molecular weight of base: 300.435089 Da
Active Life: N/A
Anabolic/Androgenic Ratio: 210:96-95

Dymethazine, sometimes referred to as DMZ, is an anabolic steroid/prohormone originally brought to the

consumer market covertly as a dietary supplement. It was first described in 1962 and received little interest
from the medical community. Reports claimed an anabolic androgenic ratio of 210:96.

Dymethazine is a rather interesting steroid with a unique molecular structure, which also happens to give
dymethazine its name. The dymethazine molecule is essentially two superdrol (methyldrostanolone)
molecules, with one flipped and then joined at center via a pair of nitrogen atoms. This unique bond has been
termed an azine bond, from the class of organic chemicals known as azines. In the body, this bond is split and
dymethazine breaks down into superdrol, allowing it to bind to the androgen receptor and demonstrate its
anabolic effects.

Use/Dosing

Logically, one would assume that dymethazine would exhibit results similar or identical to superdrol.
However, as usual when it comes to anabolics, things are not that simple. Many users report significant mass
gains on DMZ, though superdrol is often considered a much superior bulking compound.

Dymethazine has little to no ability to aromatize, does not cause estrogen related sides and should be used
along with an aromatizing steroid, the obvious choice being testosterone. It is important to remember that
DMZ’s primary metabolite, superdrol, is DHT derived and thus brings out androgenic side effects, such as the
vascularity and striations pursued by modern bodybuilders. Dymethazine is therefore a “dry” steroid and can
exhibit many of the side effects associated with such drugs.

For aesthetic purposes, dymethazine is usually dosed starting at 20 mg per day, and up to 40 mg, though
doses of up to 60 mg per day are not unheard of.

Side Effects/Risks

Dymethazine is a DHT derivative, so hair loss (alopecia) is a concern. As a dry steroid, DMZ causes little water
retention and is not a progestin. Typical side effects of dry steroids will possibly occur. Anecdotal reports
on /r/steroids report this as a harsh compound. As with almost every oral steroid, liver toxicity is a concern as
dymethazine is 17a alpha alkylated for oral bioavailability. Liver support is necessary and use should be short
term, usually four to six weeks and discontinued if symptoms of hepatotoxicity appear, whichever comes
first. Manufacturers have claimed DMZ exhibits only moderate toxicity, though one study of 20 mg
administered to female test subjects in periods ranging from 45 to 95 days showed mild to moderate cases of
bilirubinemia (excess bilirubin) and significantly raised levels of serum transaminases, demonstrating
significant toxicity. In one case, a 26 year-old causasian male developed cholestatic jaundice (a symptom of
 liver damage) after using an OTC prohormone containing dymethazine for less than thirty days, as per the
manufacturers instructions. His precise intake was 10 mg DMZ stacked with 10 mg methylstenbolone in a
manufactured, OTC prohormone product.1

References

1. Agbenyefia et al. Cholestatic Jaundice With the Use of Methylstenbolone and Dymethazine, Designer Steroids
Found in Super DMZ Rx 2.0 “Nutritional Supplement” A Case Report. Ohio State University. April 22nd, 2014.

Halotestin (Fluoxymesterone)

Active Life: 6-8 hours Chemical structure: 9-alpha-fluoro-11-beta-hydroxy-17-alpha-methyl-4-androstene-3-

one,17b-ol Molecular weight of base: 336.4457 Anabolic/Androgenic Ratio (Range): 1900/80
Fluoxymesterone is a very potent oral steroid that exhibits extremely strong androgenic properties. In the
males, fluoxymesterone has been prescribed for conditions including conditions associated with symptoms of
deficiency or absence of endogenous testosterone and delayed puberty. In the females, fluoxymesterone has
been used to treat androgen responsive recurrent mammary cancer1,2 .

For bodybuilders and strength athletes fluoxymesterone offers several distinct advantages over other drugs.
However, these come with some serious potential side effects. It is because fluoxymesterone is such a strong
androgen that it is such a sought after compound by some individuals, but also so poorly tolerated by others.

Use/Dosing

In terms of use in bodybuilding, the primary application of fluoxymesterone is for cutting cycles. Users often
note improved muscle density and hardness when using the drug in the final weeks prior to competition.
Since the compound does not aromatize there should be no concerns regarding water retention or bloat.

With fluoxymesterone, the majority of users have reported anecdotally that weight gain is minimal while on
the drug, whether it be from water, fat or lean muscle. This can be a benefit to those athletes participating in
sports that have weight divisions or where extra size and/or weight can be a hindrance.

The main reason most strength athletes and bodybuilders use fluoxymesterone is the dramatic increase in a
user's strength while using the compound. Due to these increases in strength and the limited weight gain
associated with the compound, fluoxymesterone has long been a favorite of powerlifters and those
competing in sports where explosive strength is required.

Non-experienced users of fluoxymesterone anecdotally report taking doses between 20mg to 50mg per day.
Cycles of the compound usually will be run for a maximum of six weeks, with four weeks being the norm due
to the risk of liver damage. Due to the active life of the drug, two to three doses of the compound are
required throughout the day to maintain stable blood levels of the compound.
 Risks/Side Effects

Fluoxymesterone is composed of a 17-a methyl group, a 9-a fluorine, and a 11-OH group to help it from being
broken down by the liver, therefore rendering the substance ineffective. It is due to this alteration that
prolonged use of fluoxymesterone can lead to serious liver damage and why it is considered by steroid users
to be one of if not the most hepatoxic anabolic steroids available. However, this is based largely on anecdotal
evidence.

The type of fluorine contained in fluoxymesterone is 9alpha fluorine. It protects substances (in this case
fluoxymesterone) from being broken down by the liver, such as with Sodium fluoride, etc. This type of
Fluorine is considered to be very toxic. Fluoxymesterone also contains the very potent 11-Hydroxyl group.
This group is enzymatically reduced to the 11-hydroxy derivative, thus making it biologically active. This is
accomplished by the 11-hydroxysteroid dehydrogenase isozyme in the liver. This is in itself is a very toxic
process for the liver and renal function in general.

While liver values will undoubtedly be raised while on the compound, like other anabolic agents, these values
should return to normal once the administration of the drug is complete4 . No permanent damage should
occur. As a precautionary measure, a user should use some type of liver protector (such as Milk Thistle,
vitamin b6, etc.). However, one would expect that a steroid user would be using such precautions with any
cycle.

Strong androgenic side effects are to be expected and are for the most part unavoidable if a user is
susceptible to them. Oily skin, along with acne, are commonly reported by users. Hair loss is also probable for
those that are prone to it due to the fact that fluoxymesterone is such a strong androgen.

It is because fluoxymesterone is such a strong androgen that it is advisable that female athletes do not
attempt to use this compound. Virilizing side effects can be very pronounced with this drug, coming on very
quickly. Even those females that experiment with stronger compounds such as testosterone and
methandrostenolone will stay away from fluoxymesterone.

References

1. Pfizer Pharmecutical Group Web Site, Pfizer.com

2. British Columbia Cancer Agency Web Site, Drug Profiles,
hhttp://www.bccancer.bc.ca/HPI/DrugDatabase/DrugIndexPt/Fluoxymesterone.htm
3. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp.109-10
4. Kammerer R., Mardink J., Jangels M et al., Testing for fluoxymesterone (Halotestin) administration to man:
Identification of urinary metabolites by gas chromatography-mass spectrometry. J Steroid Biochem 36 (1990)
659-66
Human Growth Hormone (Somatotropin)

Drug Class: Growth Hormone/IGF-1 Precursor

Active Life: Varies by injection method

Human Growth Hormone is a proteinaceous hormone made up of a chain of 191 amino acids and is produced
by the pituitary gland. It is responsible for the protein deposition, growth of tissues, and the breakdown of
subcutaneous fat stores. Human growth hormone is produced in its highest levels during adolescence, as
should be no surprise since this is when the majority of a person's body growth occurs. In adulthood, growth
hormone still circulates in the body but at much lower levels. The primary medical purpose for administration
of human growth hormone is for those that suffer from a deficiency of the hormone during their adolescence so
that normal growth can occur. However in recent years the popularity of human growth hormone has surged as
a means to treat age-related degenerative conditions, as well as other so-called "anti-aging" therapies.

Human growth hormone first became available in the 1980's. At first it was extracted from the pituitary glands
of cadavers. This practice was discontinued however when it was determined that administration of the
hormone that was collected this way was linked to the spread of a fatal brain disease. All of the human growth
hormone that is now produced is synthetic.

In terms of the use of human growth hormone for strength athletes and bodybuilders, the effects are two fold.
First, it has been demonstrated that consistent administration of human growth hormone can help to promote
loss of body fat. In part this is due to the ability of the compound to cause cells in the body to increase the rate
with which they utilize fats while also decreasing the rate that carbohydrates are used. This fat loss is achieved
because of the ability of growth hormone to stimulate triglyceride hydrolysis in adipose tissue as well2 .

In conjunction with this, human growth hormone helps to promote the movement of amino acids through cell
membranes. This, along with the fact that growth hormone promotes the growth of the cells in the body and
increases the rate at which these cells divide and multiple, obviously indicates that it is also capable of
enhancing anabolism if used at appropriate doses.

Many users also have an interest in using human growth hormone for the ability of the compound to help heal
existing injuries and prevent new ones from occurring. There is some evidence that growth hormone can help
to promote the production of new and regeneration of damaged cartilage when used in conjunction with
insulin-like growth factor. It is actually the insulin-like growth factor that stimulates the production of
cartilage. Insulin-like growth factor is released from the liver in response to circulating growth hormone3 .
It has also been demonstrated that human growth hormone has positive effects on erythropoeisis, i.e. the
manufacture of red blood cells4 . This effect should help to improve the endurance of an athlete and may also
help to promote anabolism. To the degree with which this effect will occur in users varies quite widely, but all
users should show some improvement.
Use/Dosing

Human growth hormone is primarily secreted in rhythmic pulses during sleep. This occurs by the mechanism
of Growth Hormone Releasing Hormone and Somatostatin being released in an alternating fashion. For the
most part users will want to mimic the natural release of growth hormone, while also not disrupting the body's
natural production of the hormone. This is often a delicate balance.

Dosing Schedule
In terms of a dosing schedule for the compound, there is some controversy as to the best method for fat
loss/anabolism. It is thought by many that daily dosing is of primary importance when using human growth
hormone due to the extremely short active life of the drug. Blood concentrations of the hormone reach their
peak within two to six hours of the injection, with the half life being only twenty to thirty minutes3 . This of
course makes it impossible to maintain stable blood levels of the compound.
However a stable level of the hormone is seemingly unnecessary as this does not occur naturally when the
body produces the hormone. In fact there is some research that indicates that administration of the hormone
every other day, instead of injections every day, may result in a more efficient use of the hormone. In a study
using children ranging in ages of two to four, it was demonstrated that administration of the compound every
other day, as opposed to every day, resulted in more growth in the children giving this dosing schedule5 . One
theory as to why this may occur is that injections every other day may simulate the natural pulsile frequency of
growth hormone secretion. This would also allow the growth hormone receptors in the body recover from the
surge of growth hormone that would be circulating and then be better able to make use of the next dose that is
administered the next day.

The only problem with the above theory is that it has never been tested in terms of its effect on muscle growth
and/or fat loss, only in the height growth in extremely young children. For the most part strength athletes and
bodybuilders have administered growth hormone every day and have achieved good results. This method
would seemingly provide a user with a consistent wave of growth hormone throughout their cycle and allow
the body to utilize it rather efficiently.

Another common practice among users is to run growth hormone for five days and then take one or two days
off, or some other similar schedule. This would seemingly be "splitting the difference" between the two dosing
schedules outlined above (as well as save money), but there is no research to indicate that it is of any
significant benefit either way.

As for the time of day a user should inject human growth hormone, it would be least disruptive to the natural
release of the hormone to administer it sometime early in the day. If a user were to inject it close to when they
were going to sleep, this would surely negate any natural release of growth hormone, something that a user
would obviously want to avoid. There is no standard to which most adhere to when deciding how close to
going to sleep that they will administer growth hormone, however mid-afternoon should be early enough that it
does not interfere with the natural release of the hormone during sleep.
 Dosages
In terms of dosages needed to see specific results, there is primarily only anecdotal evidence to be relied upon
when it comes to fat loss and an anabolic response. The relevant research does not discuss these effects in any
great scope. However, most users have indicated that doses of approximately two to four international units (2-
4 iu) per day in men will usually produce a noticeable loss of body fat in most users. In terms of getting an
anabolic response, the experience of users vary considerably. For the most part it can be concluded that most
users will need to administer larger doses than needed to experience fat loss if they wish to see a noticeable
anabolic response from human growth hormone. How much more varies from individual to individual. There
are some users who have indicated that using extremely large doses of the hormone has resulted in dramatic
gains in muscle mass, but often these doses are cost prohibitive for most. Individuals will likely have to
experiment themselves to find a level that they are comfortable with, as well as what they can afford.

Ramping
As a general rule the best way to start an HGH program is to start with a low dose and ease the administration
into the higher doses. This will avoid, or at least minimize, many of the common side effects of HGH such as
bloating, joint pain and swelling. Most people can tolerate approximately 2 i.u.'s with few side effects, so that
would be the recommended starting dose. A scheduled program would look like this:

• Week 1-4: HGH 2i.u.'s one injection

• Week 5: HGH 2.5 i.u.'s one injection

• Week 6: HGH 3 i.u.'s split into two injections of 1.5 i.u.'s each

• Week 7: HGH 3.5 i.u.'s split into two injections of 1.75 i.u's each

• And so forth until you reach your desired dose.

If at any point in this progression unbearable bloating or joint pain becomes an issue, the dose must be reduced
by 25% and held at a lower dosage for a couple of weeks. If the side effects subside, progression may resume
back up towards desired level. If the side effects remain, the dose must be reduced again and held at a lower
level for two weeks before beginning upward progression. This method will keep the HGH experience a good
one with minimal side effects.

Duration
As for the duration of a cycle of growth hormone, it is believed by many that the compound must be
administered for a minimum of 20 to 30 weeks to see results. The action of the compound is slow acting and
therefore lengthy cycles are needed. However due to its relative safety it can be run for several months, and
even years, with little to no negative results. Of course this is dependent on the user and his or her individual
reaction to the compound, along with the doses that they are using.
Administration
Human growth hormone can be administered using either intra-muscular or subcutaneous injections. There is
no difference in the absorption of the compound.

Post Cycle Therapy

No type of post-cycle therapy is necessary when discontinuing growth hormone as it should continue to be
produced naturally by the body of the user. The negative feedback loop that indicates to the body that there is
enough of the hormone circulating is related to insulin-like growth factor. Specifically, when insulin-like
growth factor is secreted by the liver a signal is sent to the pituitary gland and hypothalamus to cease the
production of growth hormone6 .

Although not necessary, some opt to use growth hormone peptides to help promote their release of natural
growth hormone.

Side Effects/Risks

For the most part, human growth hormone is a relatively mild compound with little in the way of side effects
when compared to anabolic steroids. However there are some that can occur. The most common side effects
experienced by users are bloating and/or joint pain. The majority of users anecdotally report that any joint pain
they experience most often ceases after a few weeks of administration of the drug2 .
In addition, it is possible to experience such things are enlarged organs, carpal tunnel syndrome and
acromegaly, which is a thickening of or abnormal growth of the bones7 . For this reason it would be advisable
for users that are in their mid to late 20s or younger to consult with a doctor if they are administering growth
hormone. This is due to the fact that if the growth plates of a user are not yet fused, there is a potential for
disproportionate bone growth. As well if there is a chance that a user has cancer or other tumours it is
imperative that they ensure that they do not begin administering human growth hormone prior to getting
medically cleared. This is due to the fact that growth hormone can help to accelerate the rate at which tumours
will grow.

Some users may also experience some other conditions related to use of growth hormone. Thyroid
suppression, insulin resistance, and prostate growth are all possible side effects that could be experienced.
There are various methods to help deal with these occurrences, ranging from the mild to the very aggressive.
This profile will not go into great detail about these therapies, however it should be noted that most users are
unlikely to have major difficulties with these side effects if their doses remain relatively moderate.

Human growth hormone has also been shown to cause gynocomastia in some users. The exact mechanism that
this occurs is not know, however it is believed to be related to either the a rise in prolactin levels or else the
growth hormone causes breast tissue growth when coupled with a high level of estrogen in the body. To
combat this, the usual protocol can be used, i.e. use of aromatase inhibitors, selective estrogen receptor
modulator and/or compounds that help to reduce prolactin levels.
Does using HGH shut down natural HGH production?

Answer:
The mechanism by which chronic exposure to hGH leads to tolerance, dependence, and a withdrawal
syndrome is unclear and does not involve the suppression of hormone secretion. During the nadir of growth
velocity, which follows the withdrawal of prolonged drug therapy, serum GH levels remain normal, as do
serum IGF-I and IGF-binding protein-3 levels (4). Moreover, endogenous pulsatile secretion of GH resumes
within days even after long-term hGH therapy (7).

http://press.endocrine.org/doi/full/10.1210/jcem.87.8.8721

HGH Brands List

Only brands listed here are the only HGH brands that are the exception to our "No Source Talk" rule. If your
brand isn't listed there just refer to it as "generic HGH."
Brand Amino Acid Purity Available Since Manufacturer (Country)

Ansomone 191 medium 2005 Anke Biotechnology (China)

Fitropin 192 low 2008 - 2010 Kexing Biotech (China)

Genotropin 191 high 1996 Pfizer (USA)

Humatrope 191 high 1998 Eli Lilly (USA)

Hygetropin 191 medium 2008 Zhongshan Hygene Biopharm (China)

Hypertropin 191 high 2007 Neogenica Bioscience (China)

Jintropin 191 high 1997 GeneScience Pharmaceuticals (China)

Norditropin 191 high 1997 Novo Nordisk (USA)

Nutropin 191 high 1997 Genentech (USA)

Scitropin 191 medium 2005 SciGen (Singapore)

Saizen 191 high 1997 Merck Serono (Switzerland)

Serostim 191 high 2002 EMD Serono (USA)

Tev-Tropin 191 medium 2001 Teva Pharmaceuticals (USA)

Zomacton 191 medium 2002 Ferring Pharmaceuticals (Australia)

Zorbtive 191 high 2003 EMD Serono (USA)

 References

1. Viganò et al. Effects of Recombinant Growth Hormone on Visceral Fat Accumulation:

Pilot Study in HIV-Infected Adolescents.J Clin Endocrinol Metab. 2005 Apr 19; [Epub
ahead of print]
2. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 236-8
3. Identification of an insulin-responsive element in the promoter of the human gene for
insulin-like growth factor binding protein-1. J Biol Chem 268:17063-8, 1995
4. Christ ER, Cummings MH, Westwood NB, Sawyer BM, Pearson TC, Sonksen PH,
Russell-Jones DL. The importance of growth hormone in the regulation of erythropoiesis,
red cell mass, and plasma volume in adults with growth hormone deficiency., J Clin
Endocrinol Metab 1997 Sep;82(9):2985-90
5. Lampit, M. Hochberg, Z. Testosterone blunts feedback inhibition of growth hormone
secretion by experimentally elevated insulin-like growth factor-I concentrations.J Clin
Endocrinol Metab. 2005 Mar;90(3):1613-7
6. Yarasheski KE. Growth hormone effects on metabolism, body composition, muscle mass,
and strength. Exerc Sport Sci Rev 1994;22:285-312
7. Growth hormone induced increase in serum IGFBP-3 level is reversed by anabolic
steroids in substance abusing power athletes. Clin Endocrinol (Oxf) 49:459-63, 1998

Insulin

WARNING / DISCLAIMER

Insulin can be very risky if you do not know what you are doing. If you have the mentality that MORE IS
BETTER, it is recommend AVOID even trying insulin. This hormone can be potentially fatal if taken recklessly -
you run the risk of permanent brain damage, coma, or even death.
The risk may not be the worth the reward. /r/steroids should not be your only source for information and is
not responsible for your choices, so know all the facts & research thoroughly BEFORE trying insulin.

Intro

Insulin (/ˈɪn.sjʊ.lɪn/ from Latin insula, 'island') is a peptide hormone produced by beta cells of the pancreatic
islets; it is considered to be the main anabolic hormone of the body. It regulates the metabolism of
carbohydrates, fats and protein by promoting the absorption of glucose from the blood into liver, fat and
skeletal muscle cells. In these tissues the absorbed glucose is converted into either glycogen via glycogenesis
or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both. Glucose production and secretion
by the liver is strongly inhibited by high concentrations of insulin in the blood.
 Circulating insulin affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic
hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low
insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve
body fat. The secretion of insulin and glucagon into the blood in response to the blood glucose concentration
is the primary mechanism of glucose homeostasis.

Insulin and Bodybuilding

In the last half-decade bodybuilders have been getting much larger much quicker. Certain professionals have
added twenty pounds to their contest weight in one season, after having seemingly reached a plateau. The
bodybuilding audience loves to hear that this weight gain is due to some secret drug or some newly
discovered gene therapy. Elaborate theories are developed to explain these rapid weight gains and the
professionals themselves are not helpful; they claim that it's the new X-brand supplement that's doing it and
leave it at that.

The truth is that bodybuilders have discovered one of the most anabolic hormones produced by the body,
insulin. Additionally, insulin has the benefit of being not only legal and over the counter in most states, but it
is very cheap. A bottle costs less than thirty dollars and there is no need to worry about counterfeits. By
correctly using insulin, in conjunction with human growth hormone and anabolic steroids, modern
professionals have added pounds of mass onto seemingly stagnant physiques.

The Overview

Insulin is a peptide hormone, secreted by the pancreatic islets of Langerhans. Insulin promotes glucose
utilization, protein synthesis, and regulates the metabolism of sugar. Insulin travels until it reaches receptor
sites on cells. At these sites insulin facilitates the transport of glucose and amino acids across the cell
membrane to be used inside the cell for energy and protein synthesis. This is insulin's anabolic effect, not
only in super-saturating the cells with nutrients, but also helping to volumize the cell.

Insulin Safety

There are significant risks that accompany the use of insulin. The greatest risk is an over-dose of insulin,
which leads to hypoglycemic shock. This is not an overdose in the typical sense of the word; in this case it
means that too much insulin was administered for the amount of glucose in the bloodstream. To this end, it
is important to choose the correct type of insulin and to know when it peaks and the effective period of
action of the drug in your body. This information is provided later in this chapter.

Symptoms Of Insulin Shock

The symptoms of insulin shock are easy to recognize:

• Distress - is relatively rapid, usually in a matter of minutes

• Hunger
• Sweating
• Cold / Clammy Feeling.
• Paleness
• Trembling / Anxiety
• Rapid Heartbeat
• Feeling Of Weakness Or Faintness
• Irritability & Change In Mood Or Personality
• Loss Of Consciousness

Treatment
Feed the person a source of quickly absorbed sugar. If the person is conscious, table sugar, fruit juice, honey,
a non-diet soft drink, or any other available sugar source will do. If the person is unconscious, do not try to
force sugar or liquid down his throat. Honey, granulated sugar, or a special capsule (such as D-glucose)
containing concentrated sugars, which some diabetics carry, can be carefully placed under the tongue where
it is absorbed into the body. However, this may be difficult to do.

There is another rapid form of intervention that anyone using insulin should know about; a glucagon pen.
Injectable glucagon is a hormone, normally produced in the pancreas, which has effects opposite to those of
insulin. It is commonly used to treat hypoglycemia or low blood sugar. It may also be used to relax parts of
the gastrointestinal tract for certain examinations. It is not a controlled substance. In the event of the onset
of hypoglycemia, this emergency injection will pull your blood sugar back up. If you are using insulin, you
should have one of these pens with you at all times.

Take the person to a hospital emergency room as quickly as possible. Severe insulin reactions can be fatal. Do
not be afraid of getting into "trouble", the use of insulin is legal. You will certainly get a lecture about how
crazy it is to use insulin, but you will not be arrested or detained in anyway.

It is extremely important to have someone who you can trust monitor you when you are using insulin. They
should be aware of the signs of insulin shock as well as the course of action to follow in the event that you do
slip into a hypoglycemic state. Some insulin users will go so far as to purchase a medic alert bracelet that
indicates them as a diabetic in the even that they pass out in public.

During a bulking phase, when calorie intake is deliberately high, insulin shock is not likely to be a problem
assuming that post injection nutrition is precise (as outlined later in the chapter). In the even that you begin
to feel any of the above symptoms immediately begin to consume the most simple sugars you can find,
particularly look for glucose polymers and dextrose. Avoid fructose, as it is ineffective at raising blood sugar
levels rapidly. In the even that you are using insulin in dieting, do not be afraid to "blow your diet" by eating
candy if you feel your blood sugar getting dangerously low. Your diet is not worth your life.
 Types Of Insulin

Insulin Onset Peak Duration Type of Insulin

Humalog <15 min. 30-90 min. 3-5 hours Rapid

NovaLog <15 min. 30-90 min. 3-5 hours Rapid

--- --- --- --- ---

Humulin R 30-60 min. 2-4 hours 4-5 hours Short

Novolin R 30-60 min. 2-4 hours 4-5 hours Short

--- --- --- --- ---

Lantus 60-120 min. No Peak 20-24 hours Long

Levemir 60-120 min. Flat Up to 24 hours Long

--- --- --- --- ---

Humulin N (70/30) 30-60 min. 2-10 hours 10-18 hours Combo/Mix

NovoLog Mix (70/30) <15 min, 1-2 hours 10-18 hours Combo/Mix

There are three important characteristics that differentiate the available types of modern insulin. To properly
use insulin in bodybuilding it is important to know the following characteristics:

• Onset: The time it takes the injected insulin to reach the blood stream and begin to work.
• Peak: The time period in which the insulin is working it's hardest to lower the blood sugar.
• Duration: The length of time the insulin will be working in the bloodstream. It is important to remember that
insulin is an indiscriminate storage hormone. It doesn't care if its storing fat or glucose. Therefore fat intake
should be as low as possible during the effective period of the insulin in the body. This will help prevent
excessive fat gain.

For bodybuilding purposes we will only be concerned with three types of insulin; Rapid, Short, & Long are the
most useful types of insulin for body building purposes. Humulin "N" or NovoLog Mix can be used as well, but
it is only suggested for the most advanced users at the highest tiers of competition due to it's longer peak
and active duration time which can greatly increase the risks of hypoglycemia and improper nutrition intake.

Humulin "R" and Novolin "R" are known as short-acting insulins. The manufacturers claim that this type of
insulin is active in the body for up to six hours; in reality it's closer to four and a half hours. The onset time of
"R" is roughly thirty minutes and the drug peaks in one and a half to two and a half hours after injection.
These are very commonly used at higher levels of body building. It has longer peaks and duration compared
to "log" types, and fits well into most user's eating and workout schedule.
 Humalog and NovaLog are the fastest acting insulin, known as rapid-acting insulins. They have a duration of
about 2 hours, peaks in fifteen minutes, and is ideal for bodybuilding purposes, because it is out of the body
quickly. The speed at which Humalog works is beneficial, because it allows us more precise control and lets us
know exactly when food needs to be consumed.

General Insulin Cycle Rules

HGH
Note that it is NOT recommended to run insulin without HGH (and AAS). Due to insulin's nutrient absorption
properties it will make you very prone to gaining weight. Tren is also beneficial with insulin for its nutrient
partitioning benefits particularly in respect to carbs.

A typical insulin cycle would start after running HGH for at least 4 weeks, ideally the longer you can hold off
on the insulin after starting HGH the better, you want your IGF-1 levels increased before starting insulin, this
can take a few weeks to peak. There is no minimum amount of HGH that must be run, the more the better,
but it is typically suggested to start at at least 6iu/day of HGH if the intent is to run it with insulin.

IGF-1
To be added.

AAS
Since you will be running HGH, your body can also utilize more testosterone than a typical AAS user. The
typical suggested dose is 500mg per week, +100mg per IU of HGH. You want to plan out your insulin cycle so
that it occurs once your body is saturated at its peak testosterone dosage.

"PCT"
A PCT of Metformin is recommended to be run after the insulin cycle. This is to bring your body's insulin
sensitivity back to baseline. Suggested dosing is to start at 500mg/day taken with a high carb meal and to
increase it to 2g-2.5g/day by the start of week 3 for a total of 4 weeks. It is suggested to gradually increase
dosage to avoid unpleasant side-effects.

Other Ancillaries

Shakes
A beginner to intermediate insulin cycle would be based on a 'shake' protocol. There are many different
recipes but they all include: Protein, Carbs, Essential and/or Branch Chain Amino Acids, & Creatine. Now lets
break that down into parts:

• Protein - Whey isolate is recommended. 50-80g

• Carbs - A fast-absorbing carb supplement is added to the shake to ensure we have enough carbs to 'cover'
our insulin dose without risking low blood glucose levels. When first starting out it is suggested to ingest 10g
of carbs per IU of insulin. You should be monitoring your blood glucose levels and over time you will lower
the carbs per IU of insulin. This is also impacted because as you continue your insulin cycle your insulin
sensitivity will decrease, meaning more insulin is needed per carb to get the same effect.

Your carb source is entirely a personal decision, old school guys will say that Waxy Maize is fine, a more
modern approach is to use maltodextrin or dextrose. If you are willing to spend the extra money Karbolyn is
considered a great source, that mixes easily, has a great carb/calorie ratio, and causes minimal bloat. When
looking for a carb source keep in mind the rate of digestion, the calories per carb, and one of the most
important factors is to find a carb source that doesn't cause bloating or stomach discomfort.

• BCAA/EAAs - A high intake of supplemental amino acids is recommended. The most important being leucine,
HGH and insulin both decrease the rate at which it oxidates which leads to a greater anabolic effect.
• Creatine - We are using insulin to shuttle nutrients in our cells, creatine pushes more water into our cells,
they will have a synergistic effect.

Glucose Tablets
You should ALWAYS have a full tube of these on-hand while you are within the peak and duration of your
insulin dose. In the event that your start to experience hypoglycemia symptoms take a few tablets and wait 5
minutes, if you are still experiencing symptoms take a couple more. Each tablet contains 5g of carbs, you
should not be dependent on them, they are just a safety net. If you find yourself using them consistently then
re-evaluate your cycle dosing and carb intake. I suggest you open the tube before you need it, you don't want
to be screwing around trying to open the package when you are experiencing low blood-glucose symptoms.

Before You Start Anything!!!

Blood Glucose Readings

Ranges

Taken first thing on the morning (fasting for 8+ hours):

• 70-110mg/dL - normal range this is individualistic.

• 110-126mg/dL - impaired tolerance range. This means you need to monitor closely as becoming a diabetic is
a problem.
• 126mg/dL & above - You are a diabetic....
Establishing A Baseline

We want to take the time to talk about what you should be doing before you start using insulin. This is really
necessary for anyone who is serious about using Insulin. You are going to want to spend at LEAST two weeks
prior to starting any insulin protocol using a blood glucose meter to determine your morning fasted blood
 glucose and your glucose levels throughout the day. You will want to write these down, as they are important
to you and to your health. Know them, understand what they mean to you and above all while you are using
insulin keep up with the morning fasted glucose levels. This will help you with the question:

How do I tell if I am becoming insulin resistant?

This is of course an excellent question! Well you took your morning FASTED blood glucose readings. These
readings SHOULD be in the 70-80mg/dL range for your average healthy adult, but please note that diabetics
will have a much different reading in which case you should see a doctor if you find your reading is
significantly higher than that after multiple readings, which could indicate that you are pre-diabetic.

You should be continuing to take your morning fasted blood glucose daily even while you are using, you will
notice that as you go on your morning readings will increase. Generally, it's suggested that when you get
above 90mg/dL or so (fasted reading) you want to stop your insulin use for a while and start your "PCT" with
Metformin to allow your body to become sensitized to your natural insulin spikes throughout the day.
Usually, if you do not go overboard with insulin use, you be able to use it for a long while (in some cases
months) before you start to have problems like that.

Blood Glucose Post Shake Baseline

It would be a good idea to eat like you would on Insulin (including shakes listed below) and check your blood
glucose levels. You just have to check it 1-3 times... 15 min after you finish your intra workout shake - post
workout (if using the Beginner's Humulin R / Novolin R Cycle) is great or 15 mins after finishing "Shake 1" (if
using the Beginner's Humalog / NovaLog Cycle).

This will help you know whereabouts you want to be when you start Insulin. You should be taking blood
glucose readings often aiming for 75-110 mg/dL adjust your insulin and carb intake until you are consistently
in that range.

Measuring Your Insulin

You don't want to be that guy who ends up passed out in the squat rack, or the guy that burns down his
house because he passed out while cooking food. Know how to measure your insulin.

Before starting it is important to know what 1 IU of insulin looks like. Typically a vial of insulin is 10 mL. and it
has a concentration of 100 IU/mL. That means each mL of insulin has 100 IU. So if you are dosing 10 IU, that
is 0.1 mL.

• So if you have 1 mL insulin syringes, with 100 ticks on it, each tick is = 1 IU

• If your 1mL insulin syringe has 50 ticks on it, then each tick = 2 IU
• If you have a 1/2 mL insulin syringe, with 50 ticks on it, each tick is = 1 IU
 Insulin Cycle Examples

Your first cycle should be heavily monitored. You should be taking blood glucose readings often aiming for
75-110 mg/dL adjust your insulin and carb intake until you are consistently in that range. The insulin cycles
discussed here will be based on a shake protocol for simplicity. Never take an additional dose of insulin while
your previous dose is still active, this leads to VERY unpredictable blood glucose levels and is very dangerous.

Pre-workout Insulin Cycle Examples

Beginner's Humulin R / Novolin R Cycle

The base of this cycle is taking insulin pre-workout, and it is expected that you have a high-carb meal within
an hour or two after your workout. The longer duration of "R" allows it to be taken pre-workout and still have
it active during your post-workout meal. Just be sure that you do not go to sleep while you are still in the
duration of the insulin dose.
Note: Most users experience two peaks with short-acting ("R" type) insulins. One peak at about 1 hour post
injection and another around 2 hours post-injection.
When starting out, it would be wise to do a test run or two. You will have your blood glucose monitor and
stopwatch handy and start taking readings after 45 minutes post-injection, follow it with another test every
15 minutes. SO, you will act just as you would at the gym, following the instructions below, sipping your pre-
workout shake and timing your intra-workout shake about the same as it will be when you actually are going
to the gym.

Your first cycle will be just insulin pre-workout. With type-R insulin you should pin your insulin and start
drinking your pre-workout shake 30 minutes later and you should finish this shake 15 minutes into your
workout. Then you will start your intra-workout shake sipping it until the end of your workout.

The Shakes
Pre-Workout Shake
• 50% of carbs needed to cover insulin dosage
• 5-7g Creatine
• 4g Glycerol
• 1-5g Taurine
• 1.5g L-Arganine
• 10-20g L-Gluamine (20g may bother your stomach, try less first)
• 5g L-Leucine (plus the 1g from BCAA)
• BCAA - 1g L-Leucine, 500mg L-Isoleucine, 500mg L-Valine

Plus Pre-workout of choice (optional)

Intra-Workout Shake
• 50% of carbs needed to cover insulin dosage
• 50-80g Whey isolate
• 5g Creatine
• 2g L-Glutamine
The Protocol
Day 1-3
• 5iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 50g carbs.
Day 4-6
• 6iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 60g carbs.
Day 7-10
• 8iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 80g carbs.
Day 11-14
• 10iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 100g carbs.
Day 15-18
At this point we start to lower our carbs, do this very carefully, monitor blood glucose and watch for signs of
low blood sugar. If you start to get symptoms, raise your carbs by 10g, if it persists, then raise by a total of
20g.
• 10iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 90g carbs.
Day 19-21
• 10iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 80g carbs.
Day 22-30
• 10iu Short-acting ("R" type) Insulin - 45 minutes pre-workout. 70g carbs.

You should now stop your insulin cycle and begin the one month optional PCT (outlined above). Make sure to
take at least 1 month off to allow your insulin sensitivity to restore. If you intend to follow it with another
cycle, ensure that your morning fasted glucose readings have returned to your baseline before proceeding.
You can also use a ketogenic diet and/or cardio to help restore your insulin sensitivity.

Your following insulin cycles should be augmented by adding an additional insulin dose with breakfast. Just as
with the pre-workout dosing, you should ensure that your meal has enough carbs to adequately cover your
insulin dose. Never take an additional dose of insulin while your previous dose is still active, this leads to
VERY unpredictable blood glucose levels and is very dangerous.

Post-workout Insulin Cycle Examples

Beginner's Humalog / NovaLog Cycle

This cycle is centered around your post-workout meal. Log type insulins are generally considered the easiest
to manage due to the shorter peak and duration, this makes log easier to predict. Log still follows the same
IU/Carb needs as "R" types. Note that your sensitivity to log may vary drastically compared to R. If you are
 trying log do not expect a similar experience to an "R" cycle, treat it as a new insulin cycle and work your way
up with dosing. Just be sure that you do not go to sleep while you are still in the duration of the insulin dose.

This first cycle will be just insulin post-workout. With Log type insulin you should pin your insulin and start
drinking "Shake 1" 5 minutes, then 15 minutes after your injection you should drink "Shake 2." Afterwards,
60-75 minutes after your injection, you will eat a "Protein & Carb Meal."

The Shakes & Meal

Shake 1
• 100% of carbs needed to cover insulin dosage
• 10g Creatine
• 10g Glutamine
Shake 2
• 80g Whey Protein
Protein & Carb Meal

Eat a meal containing:

• 40-50g Protein
• 40-50g Carbs
• NO Fats
• Avoid Fats for 2-3 hours if you inject IM and 3-4 hours if you inject sub-q.
The Protocol
Day 1-3
• 5iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 50g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal
Day 4-6
• 6iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 60g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal
Day 7-10
• 8iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 80g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal
Day 11-14
• 10iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 100g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal
Day 15-18
At this point we start to lower our carbs, do this very carefully, monitor blood glucose and watch for signs of
hypoglycemia. If you start to get symptoms, raise your carbs by 10g, if it persist, then raise by a total of 20g.
• 10iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 90g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal
Day 19-21
• 10iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 80g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal
Day 22-30
• 10iu Rapid-acting ("Log" type) insulin post-workout.
• Injection + 5 minutes - Drink Shake 1 containing 70g carbs.
• Injection + 15 minutes - Drink Shake 2
• Injection + 60-75 minutes - Eat the Protein & Carb meal

You should now stop your insulin cycle and begin one month optional PCT. Make sure to take at least 1
month off to allow your insulin sensitivity to restore. If you intend to follow it with another cycle, ensure that
your morning fasted glucose readings have returned to your baseline before proceeding. It is suggested but
not required to use a PCT of metformin during your time off. You can also use a ketogenic diet and/or cardio
to help restore your insulin sensitivity.

Your following insulin cycles could be augmented by adding an additional insulin dose with breakfast. Just as
with the post-workout dosing, you should ensure that your meal has enough carbs to adequately cover your
insulin dose. Never take an additional dose of insulin while your previous dose is still active, this leads to
VERY unpredictable blood glucose levels and is very dangerous.

Masteron (Drostanolone Propionate)

Chemical structure: 2alpha-methyl-androstan-3-one-17beta-ol

Formula: C23H36O3
Molecular weight of base and ester: 360.5356
Anabolic/Androgenic Ratio: 62/25
Active Life: 2-3 days

Masteron is used by people interested in adding muscle hardness and density to their physiques, nearly
always for the purpose of bodybuilding competitions. The drug is considered to be ideal for this for numerous
reasons.

Masteron, being 5-alpha reduced, cannot form estrogen upon interaction with the aromatase enzyme yet
still shows a very high affinity for it. Because it takes up so much of the aromatase enzyme, yet is refrained
from actually using it by its structural make-up, it reduces the amount of estrogen formed from other
steroids as well because there are less aromatase enzymes to be used by those compounds to form estrogen
with1 . However most will find that drostanolone is too expensive to employ it for that reason alone,
especially when compounds such as Proviron are available for the same purpose at much lower costs.

Masteron can increase muscle hardness and density, giving an individual a more complete appearance when
competing on stage. This is an effect that a lot of pure androgens will exhibit. But with all of them you need
an already rather low body-fat level for it to take full effect. If this is done, drostanolone can promote
increased strength while keeping body fat the same or even lowering it, something can help to prevent
muscle loss while dieting. This can also allow strength athletes or those athletes in sports which have weight
classes to increase performance without the risk of being raised into a higher weight class or add mass that
may hinder performance.

Use/Dosing

Masteron is primarily considered a pre-contest drug for bodybuilders. For it's effects to be fully realized a
user must be at a very low body fat percentage. If a user is not, the muscle "hardening" effect that many look
for when using the compound will not be realized. This, along with the fact that mass gains are unlikely to be
had from the drostanolone, should be a caution to individuals that they may be disappointed with their
results unless they are well conditioned.

As noted previously, it has been suggested that strength athletes or competitive athletes could benefit from
drostanolone as it can improve strength while not adding much mass or weight to the user. However, there
are countless other compounds more effective and better suited for such purposes that the use of Masteron
would seemingly be unnecessary for such objectives.

Since the propionate ester is nearly always used with Masteron it is necessary for users to administer the
compound everyday or at least every other day to maintain a fairly stable blood level of the drug. The
majority of users will do well on the compound using doses ranging from 50-100 mg every day or every other
day, totaling 300-500 milligrams per week. More experienced users of the drug may run higher doses, but
since the compound should be stacked with others to maximize effectiveness, large doses are for the most
part not required.
 Risks/Side Effects

Aromatization is not an issue with Masteron, as discussed previously. Therefore, water retention and
gynecomastia are not a concern with this compound, and as stated it in fact exhibits anti-estrogenic
capabilities by way of being able to compete with other substrates while attempting to bind to aromatase2 .
As well, it shows very little in the way of being hepatoxic and can be run for lengthy cycles without liver
damage likely to occur.
In terms of negative side effects, the only real concern would be from the androgenic properties of
dihydrotestosterone. Things such as oily skin, acne, body/facial hair growth, and hair loss if prone to male
pattern baldness. Masteron is a synthetic form of DHT, therefore Proscar would have no impact on the level
of androgenic effects1,3 . Individuals with a receding hairline and/or those that are predisposed to male
pattern baldness may find it necessary to avoid this compound as it is likely that it will simply aggravate the
condition further. As should be expected as well, users often anecdotally reported that the compound can
exasperate any existing medical conditions concerning the prostate, or cause prostate complications in those
that have suffered none before3 .

There are anecdotal reports that some women have experimented with the compound. However, due to the
virilizing effects that will undoubtedly occur with a compound such as Masteron it is not recommended that
this be attempted. The usual irreversible side effects such as body hair growth, deepening of the voice and
other such symptoms are likely to appear rather rapidly if use of the drug continued on even a short basis by
females.

References

1. Hillier SG, van den Boogaard AM, Reichert LE Jr, van Hall EV.,Alterations in granulosa cell aromatase activity
accompanying preovulatory follicular development in the rat ovary with evidence that 5alpha-reduced C19
steroids inhibit the aromatase reaction in vitro. J Endocrinol 1980 Mar;84(3):409-19
2. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 116-7
3. Rea, Author L., 2002, Chemical Muscle Enhancement: Bodybuilder’s Desk Reference.

Methylstenbolone

Chemical structure: 2,17a-dimethyl-5a-androsta-1-en-17b-ol-3-one

Molecular weight of base:
Active Life:
Anabolic/Androgenic Ratio: 660:90-170
 Description

Methylstenbolone is a DHT-derivative that is dimethylated at C-2 and C-17 (like superdrol) and has a 1-en
(like methyl-1-test). This is NOT a prohormone as many sites claim, as 2,17α-dimethyl-5α-androsta-1-en-17β-
ol-3-one, is active without conversion and orally bioavailable. It is very resistant to degradation, making it
very liver toxic, which the toxicity is up there with that of M1T, SuperDrol, and Pheraplex.

It's important to note that while methylstenbolone is dimethylated at C-2 and C-17 like superdrol, the spatial
configuration is different due to the presence of a delta-1 double bond (the C-2 methyl group is therefore
planar). This means that methylsten is a 2,17a-dimethyl rather than a 2a,17a-dimethyl compound.

Use/Dosing

All cycles should be limited to 4 weeks or less due to the strong hepatoxicity. For beginners, 8mg/day is a
suitable dosage. It can be run up to 16mg/day, though not higher. Users report gaining as much as 22lbs
while bulking during those 4 weeks (take this number with a large grain of salt, as online logs are often
grossly exaggerated. More reasonable evidence points towards 10lbs or so). While cutting, users have
reported losing ~3% bodyfat while gaining 8lbs of lean mass, despite eating at a deficit.

Side Effects/Risks

Methylstenbolone is very hepatoxic, so a liver support like TUDCA/UDCA and short cycles are strongly
advised. It does not aromatize and is not a progestin.

Related Posts

• SOTD post
• /u/entheogenicpersona's experience

References

Metribolone (methyltrienolone)
Methyltrienolone aka Mtren, Oral Tren — 19-nortestosterone (19-nor) derivative. Rated 12000:6000. One of
the strongest AAS in existence—second only to its double methylated cousin, dimethyltrienolone. Said to rank
equally to trestolone for rapid, overnight changes in aesthetics and appearance. Extreme surge in strength
and aggression. Oft-utilized as a pre-workout or for brief cycles of 3-4 weeks. Warning: Highly hepatotoxic.
Can be used orally or injected. For toxicity reasons, injection route is highly recommended. Experience
thread.

Chemical Structure: 17alpha-methyl-17betahydroxyestra-4,9,11-triene-3-one 17alpha-methyl-trenbolone

Androgenic: 6,000-7,000
Anabolic: 12,000-30,000
Estrogenic Activity: None
Progestational Activity: No data available

Description

Methyltrienolone is one of the strongest oral anabolic steroids ever produced. This agent is a derivative of
trenbolone (trienolone), which has been c-17 alpha alkylated to allow for oral administration.This
modification has created a steroid that is significantly stronger than its non-methylated cousin. Its potency
has been measured to be anywhere from 120-300 times greater than that of methyltestosterone, with
greater dissociation between anabolic and androgenic effects.625 626 Milligram for milligram
methyltrienolone is a more active steroid than any agent sold on the commercial market, requiring doses as
little as .5-1 milligram per day to notice a strong anabolic effect. Its potency is only matched by its relative
toxicity, however, which has limited its modern use to that of laboratory research only.

History

Methyltrienolone was first described in 1965.627 It was immediately identified as an extremely potent
anabolic agent, far more potent than the commercially available agents of the time. In spite of its high
relative activity, however, methyltrienolone has seen very limited use in humans. It was used clinically during
the late 1960's and early '70's, most notably in the treatment of advanced breast cancer. Here, its
exceedingly strong anabolic/androgenic action helps the drug counter the local effects of endogenous
estrogens, lending it some efficacy for slowing or even regressing tumor growth. Such application was not
long lived, however, as more realistic evaluations of the drug's toxicity soon led to its abandonment in human
medicine. By the mid-1970's, methyltrienolone was becoming an accepted standard in non-human research
studies, particularly those pertaining to the study of the androgen receptor activity. For this purpose the
agent is very well suited. Its sheer potency and resistance to serum-binding proteins makes it an excellent in-
vitro receptor-binding standard to compare other agents to. Being so resistant to metabolism, active
methyltrienolone metabolites are also not going to greatly interfere with the results of most experiments.
Body tissues can metabolize most steroids fairly easily, which means that even incubation studies can be
complicated with the question of what is causing a particular effect, the steroid or one of its unidentified
metabolites. This is much less of an issue with methyltrienolone. Today, methyltrienolone remains an agent
of research use only.

Structural Characteristics

Methyltrienolone is a modified form of nandrolone. It differs by: 1) the addition of a methyl group at carbon
17alpha to protect the hormone during oral administration and 2) the introduction of double bonds at
carbons 9 and 11, which increases its binding affinity and slows its metabolism. The resulting steroid is
significantly more potent than its nandrolone base, and displays a much longer half-life and lower affinity for
serum-binding proteins in comparison. Methyltrienolone chemically differs from trenbolone only by the
addition of a methyl group at c-17. This alteration changes the activity of methyltrienolone considerably,
however, such that this agent should not simply be considered an oral form of trenbolone.

Administration

Studies have shown that taking an oral anabolic steroid with food may decrease its bioavailability.630 This is
caused by the fat-soluble nature of steroid hormones, which can allow some of the drug to dissolve with
undigested dietary fat, reducing its absorption from the gastrointestinal tract. For maximum utilization,
methyltrienolone should be taken on an empty stomach.

Administration (Men)
Methyltrienolone is no longer used in clinical medicine due to an unacceptable level of hepatotoxicity.This
agent is generally not recommended for physique-or Performance-enhancing purposes for the same reason.
Those absolutely insisting on its use need to take its level of liver toxicity very seriously. At the very least,
routine blood tests should be conducted to ensure the agent is not imparting damage. Drug duration should
also be very limited, preferably to 4 weeks of use or less. The relative potency of methyltrienolone is
extremely high, requiring doses as little as .5 milligram per day. Its effective and tolerable range is usually
considered to be .5 to 2mg per day. Dianabol-type doses of 20-30 mg daily are completely unthinkable, and
should never be attempted. Again, this is an extremely toxic steroid, and all good advice would say to avoid
it. Anyone of the many commercially available steroids would be much safer choices.

Administration (Women)
Methyltrienolone is no longer used in clinical medicine due to an unacceptable level of hepatotoxicity.This
agent is not recommended for women for physique-or Performance-enhancing purposes due to its extremely
strong toxicity and tendency to produce virilizing side effects.

Oral Turinabol (4-chlordehydromethyltestosterone)

Chemical Names: 4-chloro-17b-hydroxy-17a-methyl-androst-1,4-dien-3-one;4-chloro-1-Dehydro-17a-

methyltestosterone; 4-chloro-17a-methyl-17b-hydroxy-1,4-androstadien-3-one
Chemical Formula: C20H27O2Cl
Active life: 16 hours
Anabolic/Androgenic Ratio: >100:0

Oral turinabol was originally developed by East German researchers in the mid-20th century for use by their
athletes during the Olympics and other international competitions. It is believed to be the drug responsible
for much of that country's dominance in many of the athletic competitions of that era, along with their
groundbreaking training techniques. There is no medical use for this drug and as such it has remained
exclusively a performance enhancing compound used by athletes.
Oral Turinabol is a 17-alpha-alkylated compound that is a derivative of methandrostenolone (d-bol). Being a
17AA compound of course means that it is an oral steroid capable of surviving the first pass through the liver,
but this also increases hepatoxicity. For the most part users of oral turinabol have reported minimal bloating
on this compound and achieving the much sought after "hardening" effect associated with some compounds.
This is primarily due to the low level of androgenic activity, and therefore side effects, associated with the
drug. Users anecdotally report that increases in lean body mass free of any bloat should be expected when
using oral turinabol with a proper diet and training regimen.

Oral turinabol features a 4-chloro attachment that inhibits the aromatization of the compound. The
alteration that is done to the compound obviously eliminates much of the worry concerning a user
experiencing any of the typical estrogen related side effects such as water retention, acne, and gynocomastia
among others1 . This is true even at extremely high doses of the drug. Oral turinabol is chemically the same as
methandrostenolone except for this alteration of the 4-chloro. This shows exactly how a simple chemical
alteration to a compound will alter it's effects on a user dramatically.
Oral turinabol also has an advantageous effect in terms of it's ability to reduce the binding of sex hormone-
binding globulin to other anabolic steroids. Even at relatively low doses, it is quite effective at this function
and could improve the action of any anabolics that a user may be running with the compound2 . This would
allow more testosterone to remain active in the body so that it can carry out it's anabolic functions.

Use/Dosing

For the most part, oral turinabol is best used for lean gains in muscle mass as well as maintaining muscle
mass while dieting. Users should not expect to experience major gains in muscle mass, but rather
improvement in muscle "quality". Due to the nature of the compound as well, strength gains will not be
overly dramatic for a user either. However having said this it is a quality compound if used for "cutting"
purposes and to add some lean body weight.

Anecdotally users report that doses ranging from 40 to 60 milligrams per day for inexperienced male users
should produce good results. Of course like most anabolic steroids the doses used by more experienced users
will climb dramatically. Doses in the range of 100 to 150 milligrams per day have been reported by some
users, however doses this high are not recommended.

Female users of oral turinabol should do well using doses ranging from 5 to 15 milligrams per day. At these
levels very little in the way of virilizing side effects should occur. However if these doses are increased the
likelihood of these symptoms will also rise.

Due to the active life of the compound users would only have to take two doses of the drug per day, as
evenly spaced as possible to maintain fairly stable blood levels of the compound. These doses should be of
the same size if possible to avoid fluctuating levels. Most male users will stack oral turinabol with other
compounds for a synergistic effect. Most notably, many will choose to run some type of testosterone with it.
 Since, like all anabolic steroids, oral turinabol will suppress a user's natural testosterone production there is a
chance that some sexual dysfunction and/or reduction in sex drive could occur. However, many users
anecdotally report that when they have run oral turinabol only, no reduction of libido was noticed.

As will be discussed below in the Risks/Side Effects section of this profile there are still risks with the use of
this compound as it can cause toxicity of the liver like all 17 alpha alkylated compounds. For this reason it is
recommended that users do not extend their cycles of the compound too far. However like oxandrolone
(anavar) due to it's relatively mild nature compared to the other 17 alpha alkylated oral steroids it can be run
longer than most. Despite this it is recommended that a user limit their cycle to about six to eight weeks to
limit the stress placed on the liver. However like always many users will run it longer. If this is done for any
lengthy period of time a user should have blood work done to ensure that no damage is occuring.

Risks/Side Effects

Oral turinabol is a relatively mild compound in terms of side effects. Due to the lack of androgenic activity,
androgenic side effects are not an issue. However, there has been at least one case of testicular tumors, It
should be noted though that in that one case study it was found that a case of testicular cancer is an
otherwise healthy male may have been, at least in part, caused by his use of very high doses of oral turinabol
over a five year period3 . However, no other credible links between the drug and cancer have been made as
of yet.
In women virilization may be a concern if higher doses are used. However even in women these effects do
not seem to appear and use of the compound is relatively side effect-free in the majority of individuals as
long as cycles of the compound are kept relatively moderate in duration and doses used are not in excess4 .

Also like most oral steroids liver and cholesterol health should be a concern while running this compound. It
can cause increased liver values, liver damage and reduction in a user's HDL cholesterol ("good" cholesterol)
and increased LDL cholesterol ("bad"). This is why it is not a good idea to run this compound for an extended
period of time.

References

1. Kaufmann G, Schumann G, Horhold C. Influence of 1-double bond and 11 beta-hydroxy group on

stereospecific microbial reductions of 4-en-3-oxo-steroids. J Steroid Biochem. 1986 Oct;25(4):561-6.
2. Schumann W. The pharmacokinetics of Oral-Turinabol in humans. Pharmazie. 1991 Sep;46(9):650-4
3. Froehner M, Fischer R, Leike S, Hakenberg OW, Noack B, Wirth MP. Intratesticular leiomyosarcoma in a young
man after high dose doping with Oral-Turinabol: a case report. Cancer. 1999 Oct 15;86(8):1571-5
4. Franke W.W., Berendonk B. Hormonal doping and androgenization of athletes: a secret program of the
German Democratic Republic government. Clinical Chemistry. 1997;43:1262-1279
Peptides

A peptide is a compound consisting of two or more amino acids linked in a chain, the carboxyl group of each
acid being joined to the amino group of the next by a bond.

Peptide Guide

BPC 157
BPC 157 is a peptide of a sequence of amino acids with a molecular formula of 62 carbons, 98 hydrogens, 16
nitrogens, and 22 oxygen atoms (C62-H98-N16-O22). BPC stands for “Body Protecting Compound”. BPC-157
accelerates wound healing, and, via interaction with the Nitric Oxide (NO) system, causes protection of
endothelial tissue and an “angiogenic” (blood vessel building) wound healing effect. BPC 157 is surprisingly
free of side effects, and has been shown in research that’s been happening since 1991 to repair tendon,
muscle, intestines, teeth, bone and more, both in in-vitro laboratory “test-tube” studies, in in-vivo human
and rodent studies, and when used orally or inject subcutaneously (under your skin) or intramuscularly (into
your muscle). BPC-157 is also known as a “stable gastric pentadecapeptide”, primarily because it is stable in
human gastric juice, can cause an anabolic healing effect in both the upper and lower GI tract, has an
antiulcer effect, and produces a therapeutic effect on inflammatory bowel disease (IBD) – all again
surprisingly free of side effects.

More On This Peptide Below

CJC-1295 with DAC

CJC-1295 is a tetra substituted peptide made up of thirty amino acids. It has been shown through scientific
research studies to bio-conjugate to the protein serum albumin which provides an advanced level of
homeostasis in animals being tested. The use of CJC-1295 with DAC prevents the production of DPP-IV from
occurring as determined in scientific studies with the animal test subjects. This results in the GHRH1-29
experiencing an extended half-life, one which can last over seven days. With the increased stabilization of
GHRH1-29, growth hormones are able to function at greater levels and test subjects are then able to
experience an increased level of stability in the growth hormones. CJC-1295 with DAC is the preferred and
more powerful GHRH component in a peptide protocol. Throughout scientific studies, it has been understood
the presence of CJC-1295 with DAC allows for a few elevated processes test subjects experience. This
includes Muscular Tissue Growth, Increased Bone Density and Body Fat Reduction.

CJC-1295 w/o DAC

CJC-1295 without DAC is a 30 amino acid peptide hormone, better known in the community as a GHRH
(growth hormone releasing hormone). Essentially, what this means is this peptide will release a series of
pulses over a long period of time which usually equates to fewer injections. Even though CJC-1295’s main
function upon creation was found to boost protein synthesis, increased growth of muscle tissue and many
other benefits come with it as well. CJC-1295 also helps injury recovery times, reduce body fat, boost
immune system and bone density and cellular repair (skin and organs). The term CJC 1295 without DAC this is
really means that they are looking at MOD GRF 1-29. And this modification had resulted in a greater peptide
bond, the average user will still likely need to inject two to three times a day with a GHRP to get the
maximum effectiveness for releasing endogenous growth hormone. If you prefer to use shorter spikes of GH
release then the use of the MOD GRF 1-29 (CJC 1295 without DAC) is optimal.

DSIP
DSIP stands for Delta sleep-inducing peptide. This type of peptide is classified as a neuropeptide and it works
by inducing spindle and delta EEG activity and by reducing motor activity. This peptide is utilized in order to
help people fall asleep and stay asleep. This peptide is popular with bodybuilders who have learned about
the power and potential of peptides through their training and supplementation regimens. DSIP lowers basal
corticotropin levels and blocks their release. It also makes it easier for the body to release LH (luteinizing
hormone). In addition, it makes it simpler for the body to release somatotrophin (and somatoliberin
secretions) and to block the production of somatostatin. This peptide may help people to manage stress. In
addition, it may have the power to alleviate the symptoms of hypothermia. It’s also known as an effective
means of normalizing blood pressure and contractions which are myocardial. As well, it may offer anti-
oxidant benefits (slow down cell damage).

Epitalon
Epitalon (a.k.a. epithalon or epithalone) is a synthetically-derived tetrapeptide, meaning that it consists of
four amino acid chains. It was discovered by the Russian scientist Professor Vladimir Khavinson, who then
conducted epitalon-related research for the next 35 years in both animal and human clinical trials. Epitalon’s
primary role is to increase the natural production of telomerase, a natural enzyme that helps cells reproduce
telomeres, which are the protective parts of our DNA. This allows the replication of our DNA so the body can
grow new cells and rejuvenate old ones. Furthermore, Epitalon has been shown to inhibit the growth of
cancerous tumors, enabling a longer and healthier life in the future. And research has shown that epitalon is
a powerful antioxidant that eliminates oxygen-free radicals responsible for damaging and killing cells. As a
result of epitalon’s effect on telomerase production, the benefits are unique and far-reaching. Benefits of
epitalon include: Increase of human lifespan Significant boosting of energy levels Promotion of deeper sleep
Delay and prevention of age-related diseases such as cancer, heart disease and dementia Improvement of
skin health and appearance Healing of injured and deteriorating muscle cells

Follistatin
Follistatin is an inhibitor of TGF-β superfamily ligands that repress skeletal muscle growth and promote
muscle wasting. Accordingly, follistatin has emerged as a potential therapeutic to ameliorate the deleterious
effects of muscle atrophy. In the setting of disease, increasing follistatin expression in musculature has
proven beneficial for improving aspects of pathology in dystrophin-deficient mdx mice that model Duchenne
and Becker muscular dystrophy (DMD, BMD). Administration of recombinant follistatin has also been shown
to promote muscle hypertrophy in wild-type mice, and ameliorate the progression of a mouse model of
spinal muscular atrophy (SMA).

GHRP-2
GHRP-2 is a synthetic agonist of ghrelin, the newly-discovered gut peptide which binds to the growth
hormone (GH) secretagogue receptor. Ghrelin has been shown to have two major effects, stimulating both
GH secretion and appetite/meal initiation. GHRP-2 has been extensively studied for its utility as a growth
hormone secretagogue (GHS). Animal studies have shown its effect on food intake. However, whether GHRP-
2 can also stimulate appetite in humans when administered acutely is not known. When administered either
centrally or peripherally to rodents, ghrelin increases food intake and body weight. Interestingly, its effects
on food intake are independent of GH secretion and appear to be mediated via the NPY/Agouti gene-related
protein (AGRP) neurons in the hypothalamic arcuate nucleus. Peripheral ghrelin administration has recently
been shown to stimulate food intake in lean, healthy men and women and in cancer patients.

Data suggest that circulating ghrelin is also implicated in meal to meal regulation. Ghrelin levels increase in
anticipation of a meal and are suppressed by food ingestion, but the underlying mechanisms are not known.
The meal-related suppression of ghrelin is proportional to the carbohydrate (CHO) content of the meal but
does not appear to be directly related to glucose or insulin, although insulin administration decreases ghrelin.

GHRP-6
GHRP-6 is an injectable peptide in the category of growth hormone releasing peptides, or GHRP’s. The most
common use of these peptides is to increase GH production. Other peptides in this category include GHRP-2,
hexarelin, and ipamorelin. With regard to increasing GH, all of these work similarly, and there is no need or
advantage to combining them. Instead, the one most suited for the particular case is chosen. The principal
use of GHRP-6 is to provide increased GH levels, which also results in increased IGF-1 levels. This aids fat loss
and in some instances aids muscle gain as well. Generally, GHRP use is chosen as an alternate to GH use, and
only rarely is combined with GH. GHRP-6 is most generally used for the same purposes that GH might be
used, but may be chosen where a cost advantage exists favoring GHRP-6, GH is not available, or the individual
prefers the idea of stimulating his own GH production to injecting GH. These purposes can include increased
fat loss, improved muscle gain when used in combination with anabolic steroids, cosmetic improvement of
the skin, and improved healing from injury.

Hexarelin
Hexarelin is a peptide that can promote the secretion of certain hormones. It is a hexipeptide that consists of
six amino acids that can release certain hormones as they are needed. It has a half-life of about 70 minutes.
Some studies have derived several different effects linked to its use, including elevated levels of fat loss,
connective tissues, density of bone minerals, meiosis, mitosis, and elasticity. In turn, these effects have led to
animal test subjects experiencing improved endurance, joint rehabilitation, wound healing, and improved
muscle strength. Studies also conclude that Hexarelin’s functionality can last a long stretch of time.
Furthermore, scientific studies on animal test subjects have determined that Hexarelin does not induce an
increased desire for food consumption. The peptide achieves this because it does not increase the levels of
ghrelin; the amino acid peptide that clears out the gastric system and induces hunger. Further scientific
studies have also determined that the peptide promotes an increase in the secretion of IGF-1 from the liver
of animal test subjects. This additional secretion plays a key role in breaking down fat and improving
strength.

HGH Fragment 176-191

HGH Fragment 176-191 is a fragment of the HGH peptide. Scientists found that if they truncated the peptide
at the C terminal region they could isolate the fat loss attributes associated with HGH. Taking this fragment
from HGH, including the peptide bonds from 176-191, they found they had developed a peptide that
regulated fat loss 12.5 times better than regular HGH. It has an incredibly ability to regulate fat metabolism
without the adverse side effects on insulin sensitivity. By isolating the tail end of the GH molecule, scientists
have found that HGH Frag 176-191 works even better than HGH to stimulate lipolysis (breaking down of fat).
In fact, it actually inhibits lipogenesis; meaning, it stops formation of fatty acids and other lipids. Also, unlike
other fat burning compounds out there, users will not experience hunger suppressing qualities or the jittery
feelings that can be associated with ephedrine like compounds. Since it does not compete for HGH receptors,
multiple studies have shown that HGH Frag 176-191 will not cause hyperglycemia. In addition, it will promote
lean body mass, protein synthesis, increase bone mineral density, and better sleep.

IGF1-DES
IGF-1 DES is a peptide secreted by the liver and consists of 67 amino acids. IGF-1 DES stimulates hormones as
it is a highly anabolic structure. In living organisms, IGF-1 DES offers a number of benefits and is responsible
for creating hyperplasia (or hypergensis), which is a process that regulates the growth of cells. Scientific
research involving IGF-1 DES indicates the peptide is also capable of influencing neurological growth,
maintain nerve cell function, and promote nerve growth. Its ability to create hyperplasia leads scientists to
use animals for researching the ability of IGF-1 DES in relation to growing cells and the development of tissue.
Studies show that IGF-1 DES has the capability to influence the neuronal structure and functions of the brain,
and continuing animal studies are watching the peptide’s effects on muscular and skeletal growth.

IGF1-LR3
The polypeptide IGF-1 LR3, also known as Long R3 IGF-1, is a peptide chain consisting of 83 amino acids. It
contains a molecular weight of 9200, and its molecular structure of C990H1528N262O300S7. Specifically,
scientific studies have determined that IGF-LR3’s relationship with the pancreas and liver can be traced down
to specific secretions. In the case of the pancreas, it has been determined that the peptide can be linked to
the secretion of insulin. This secretion guides the cells that are found within the skeletal muscles, fatty
tissues, and liver to absorb glucose from an animal test subject’s bloodstream. In the case of the liver, it has
been determined that the peptide can be linked to the secretion of IGF-1, also known as Insulin-like Growth
Factor-1 or Somatomedin C. This secretion has been shown to possess highly anabolic properties. What this
means is, the secretion has been determined to play a vital role in muscle and tissue growth as it relates to
muscular and skeletal tissue growth and repair.

Insulin
Insulin (/ˈɪn.sjʊ.lɪn/ from Latin insula, 'island') is a peptide hormone produced by beta cells of the pancreatic
islets; it is considered to be the main anabolic hormone of the body. It regulates the metabolism of
carbohydrates, fats and protein by promoting the absorption of glucose from the blood into liver, fat and
skeletal muscle cells. In these tissues the absorbed glucose is converted into either glycogen via glycogenesis
or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both. Glucose production and secretion
by the liver is strongly inhibited by high concentrations of insulin in the blood.

Circulating insulin affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic
hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low
insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve
body fat. The secretion of insulin and glucagon into the blood in response to the blood glucose concentration
is the primary mechanism of glucose homeostasis.

Ipamorelin
Ipamorelin is a pentipeptide, meaning that its structure is comprised of five amino acids. It contains a
molecular mass of 711.85296, and its molecular formula is C38H49N9O5. It can sometimes go by the
alternate names Ipamorelin Acetate, IPAM, and NNC-26-0161. It is a secretogogue, and is considered to be an
agonist, meaning that it possesses the ability to bind certain receptors of a cell and provokes a cellular
response. Ipamorelin’s operational mechanics enables the peptide to stimulate the production of pituitary
gland-based expression of secretions related to growth amongst animal test subjects. At the same time, the
presence of the peptide has been shown to inhibit the production of a secretion known as somatostatin. In
essence, this peptide is primarily responsible for inhibiting the production of growth secretions. Additionally,
it has been determined that Ipamorelin has the ability to boost the production of IGF-1, or Insulin-like Growth
Factor 1. This particular peptide, which is secreted by the liver, has been shown to be highly anabolic in its
nature. What this means is, its presence plays a key role in the overall growth and repair of muscular and
skeletal tissue.

MGF (Mechano Growth Factor)

Mechano Growth Factor (MGF) also known as IGF-1Ec is a growth factor/repair factor that is derived from
exercised or damaged muscle tissue. What makes MGF special is its unique role in muscle growth. MGF has
the ability to cause wasted tissue to grow and improve by activating muscle stem cells and increasing the up-
regulation of protein synthesis, this unique ability can rapidly improve recovery and speed up muscle growth.
MGF can initiate muscle satellite (stem) cell activation in addition to its IGF-1 receptor domain which, in turn,
increases protein synthesis turnover; therefore, if used correctly it can improve muscle mass over time. MGF
is like a highly anabolic variant of IGF. After you have trained, the IGF-I gene is spliced towards MGF then that
causes hypertrophy and repair of local muscle damage by activating the muscle stem cells as well as other
important anabolic processes, including the above mentioned protein synthesis, and increased nitrogen
retention.

PEG-MGF
PEG-MGF is pegylated mechanic growth factor, which is a research peptide used in a variety of scientific
research conducted throughout the world. The peptide has proved useful with the MGF being a variant of IGF
(insulin-like growth factor), which is responsible for increasing the stem cell count in muscles. This enables
the muscles fibers to mature and fuse. The peptide is being thoroughly tested in patients where muscle fibers
are broken down and need assistance with muscle growth. The PEG-MGF peptide creates new fibers,
promotes protein synthesis and helps with nitrogen retention; this makes it ideal for those who do hard
workouts or suffer from muscular diseases.

PT-141 Bremelanotide
PT-141, also known as Bremelanotide, is a research peptide that has shown promise in scientific studies, on
animal test subjects, to regulate blood flow restriction, inflammation, and helping improve sexual
dysfunction. PT-141 was developed from the Melanotan 2 Peptide, which underwent studies in a laboratory
setting as a sunless tanning agent. It is from this scientific testing that the potential benefits of PT-141 were
discovered. Scientists have determined through rigorous testing on animal test subjects, because of the
ability to regulate blood flow restriction and inflammation by PT-141, it very well may be instrumental in
managing the onset of hemorrhagic shock and reperfusion injury. What this means is it could potentially
reduce, or outright prevent inflammation that may be triggered by a variety of irritants or diseases. This, in
turn, could also help reduce any damage that could potentially occur within blood vessels and surrounding
tissue. Additional studies have determined PT-141 is a potential remedy for the treatment of sexual
dysfunction. Results from early research studies has shown PT-141 does not act on the vascular system like
former compounds, but works by activating the melanocortin receptors in the brain.

Selank
Selank is a peptide that has a molecular mass of 751.9 and a molecular formula of C33H57N11O9. It is
considered to be a heptapeptide, meaning that it is a peptide chain made up of seven amino acids. Its
sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro. According to scientific study that has been based on animal test
subjects, it has been determined that the functional mechanics of Selank gives it the capacity to increase the
secretion of serotonin. This neurotransmitter is noted for its ties to mood regulation, and it has also been
noted to contain links to sleep and appetite regulation. The presence of the peptide and its ability to cause an
uptick in the release of serotonin means that the animal test subject can experience a more efficient means
of homeostasis in terms of mood, hunger, and sleep. In addition to inducing a greater metabolic rate of
serotonin, it has also been determined that Selank has the capacity to modulate the expression of interleukin
6, a white blood cell-secretion that can act as both a pro-inflammatory cytokine and an anti-inflammatory
myokine. This secretion plays a key role in stimulating the immune response during infection and after
trauma, particularly during instances of tissue damage leading to inflammation.

Sermorelin (GRF 1-29)

Sermorelin or GRF 1-29 is a growth hormone secretagogue, which means that it stimulates the pituitary gland
to produce and secrete HGH. It is a form of GRF that contains only the first 29 amino acids. GRF that is
produced by neurosecretory neurons in the brain contains 44 amino acids. Only the first 29 amino acids are
responsible for stimulating pituitary production and secretion of HGH. Sermorelin has highly specific
receptors on pituitary somatotrophs. So it binds to the cells that produce and release HGH. Upon binding,
Sermorelin acts through a cylicAMP second messenger system exactly the same as that used by naturally
occurring growth hormone releasing hormone. Furthermore, it has an excellent safety profile. Its effects are
regulated at the level of the pituitary gland by negative feedback and by release of somatostatin so there are
less safety concerns such as those associated with HGH overdosing. Tissue exposure to HGH released by the
pituitary influence of Sermorelin mimics normal physiology, By stimulating the pituitary it preserves more of
the growth hormone neuroendocrine axis that fails with aging, Semorelin in a complex way, helps preserve
not only youthful anatomy but also youthful physiology, it gives all of the benefits of HGH and more. Another
big advantage of semorelin is that it causes the pituitary gland to up-regulate. This stimulates the gland to
rejuvenate. There are many reports in peer-reviewed medical and scientific literature showing that
GRF/Sermorelin also has a direct effect on the brain to promote non-REM slow wave sleep.

Thymosin Beta 4 (TB-500)

Thymosin Beta 4 or TB-500, as it is called, is an exploration peptide that is tested primarily for its abilities to
increase strength, endurance and restoration in subjects. It is known to have many of the same effects of
growth hormone in animals equating to results in humans that would be related to an increase in
testosterone. It has been shown to inhibit tumor growth making TB-500 an amazing product for research
studies and with further testing, something that may become widely accepted in the minds of many. TB-500
has been proven to speed up the therapeutic process in wounds as well as being used clinically for anti-
inflammatory purposes. This is extremely important when it comes to competitive competitions or events as
well as simple body maintenance. Recovery times and pain relief occur much faster for the duration of use
allowing for peak performance as well as a healthier well being. Subjects have also proven a slight increase in
hair growth which is a positive side effect of TB-500 use. As you can see, research in animals has shown
superior and appealing results in existing studies when it comes to its use. In inclusion to the restoration
aspects of using TB-500 as an exploration peptide, there are several other notable facts that are being
 discovered. Subjects have proven a significant increase in muscle growth which clearly improves strength and
endurance as well as a huge enhancement in muscle tone itself. The improvement in flexibility due to its anti-
inflammation components and known abilities to be able to stretch tissue safely have made this a favorite of
those performing investigation in the area of performance and physical enhancements. Exploration of this
peptide on subjects is simply producing astonishing results in most cases.

The Body's Growth Hormone System & Peptides

Besides Growth hormone (GH) itself, your body utilizes three basic hormones:

• Growth Hormone Releasing Hormone (GHRH)- Released by the brain to tell your bodies growth hormone
storage cells (somatotrophs) to release growth hormone.
• Somatostatin- Acts as the "off switch" and tells your cells (somatotrophs) to cease growth hormone release.
• Ghrelin- Created in the stomach, this hunger derived hormone reduces Somatostatins "off switch" effect and
encourages the brain to release more GHRH.

If GHRH is always around the somatotrophs (GH storing cells) are constantly releasing and unable to store
GH. This results in a constant dribble or "bleed" of GH rather than a big pulse. Growing, development, and
maturity requires GH to be released in a pulsatile manner.

This is where Somatostatin comes into play. It instructs your somatotrophs to cease the GH release allowing
them to begin storing and stockpiling GH. However if Somatostatin is always present the body would never
release enough GH to function. What if GHRH and Somatostatin are trying to work at the same time? For the
most part Somatostatin is stronger and no GH will be released.

Further benefiting this hormonal seesaw is Ghrelin. When Ghrelin makes its way up to the brain it makes it
easier for GHRH to do it's job by suppressing Somatostatins effects. It is possible for Ghrelin on its own to
cause a GH release even with a high Somatostatin presence. However, GHRH and Ghrelin together have a
synergistic GH effect, meaning that the spike of GH released is larger than could have been produced by each
on their own.

Synthetic forms of Ghrelin exist known as Growth Hormone Releasing Peptides (GHRP's) and act in the same
way that natural Ghrelin does.

Growth Hormone Releasing Hormones (GHRH):

• CJC-1295

• CJC-1293

• GRF(1-29)

• Sermorelin
• Modified GRF(1-29)

Which GHRH?
GRF(1-29) and Sermorelin are essentially the same thing. Sermorelin just being the name of a FDA-approved
version of GRF(1-29). The issue here is that these are easily rendered ineffective within minutes of injecting
due to destruction by blood enzymes (unless you could pin directly into your pituitary gland). What remains
of the list are analogs, or altered versions, of the original GRF(1-29).

Using an anolog that is able to survive blood enzymes for around 30 minutes is ideal

CJC-1293 is GRF(1-29) with 1 amino acid swap plus the Drug Affinity Complex (DAC). DAC acts as a velcro
holding the amino acids together for a longer period of time. The single amino acid swap makes the analog
peptide stronger but not by enough. The half-life is maybe double GRF(1-29) in humans. So 5 minutes of half-
life.
CJC-1295 is GRF(1-29) with 4 amino acid alterations and the Drug Affinity Complex (DAC). This version is extra
strong and will last more than 30 minutes and the DAC increases the half-life even more by preventing
breakdown by blood enzymes.

Here is the interesting part: You do not want to use any of the CJC's. The first (CJC-1293) does not survive
long enough after injection and the second (CJC-1295) survives for too long and is always around preventing
Somatostatin from stopping GH release resulting in a GH bleed.

What do you want to use? You want an analog that utilizes those 4 amino acid swaps and mantains the ability
to still be broken down after those 30 or so minutes. This is known as Modfied GRF(1-29).

**There is debate as to whether or not CJC-1295 without DAC is the same as Mod GRF(1-29)

Growth Hormone Releasing Peptides, Ghrelin-mimetics (GHRP):

• GHRP-6

• GHRP-2

• Ipamorelin

• Hexarelin

Which GHRP?
Hexarelin is the strongest in the family known to give the biggest pulse of all. Will create prolactin and
cortisol side effects. Desensitization will happen regardless of the dose.
GHRP-2 has the second strongest GH release, lower hunger effect, and no gastric motility. GHRP-2 will result
in the most bang for your buck. This is a second generation GHRP. Usage of this peptide can also come with
elevated levels of cortisol and prolactin. Desensitization is unclear if used beyond saturation dose.
 GHRP-6 has the second strongest GH release. It can cause an intense hunger effect and gastric motility. This
is a first generation GHRP. Slightly creates prolactin and cortisol issues. Desensitization does not occur.
Ipamorelin does not release as much GH as other GHRPs, but at very large doses was shown to give a large
release of GH without desensitization. Has no almost no hunger effect. This mildest in the bunch, but does
not create prolactin or cortisol.

Dosing Schedules

Injecting a GHRH on its own is not very effective since you are unable to know when your bodies
somatostatin is active. Because of this you'll need to pick a GHRP to be paired with your GHRH of choice. This
ensures that Somatostatin, if present, will be suppressed and the two peptides will synergistically amplify the
natural GH pulse.

Dosing is going to be mostly dependent on your goals and it is generally recommended to asses your
tolerance before diving right into multiple doses per day. Starting slow and gradually increasing to multiple
doses per day may alleviate some side effects

Note: a saturation dose is defined as 1mcg/kg of bodyweight or 100mcg, the latter being the most commonly
used (except in Hexarelin in which 200mcg is considered the saturation dose). Some minority of people have
sleep interruption rather than better sleep from pre-bed dosing. Often a move from GHRP-6, GHRP-2, or
Hexarelin to the smoother Ipamorelin will remedy this. If not moving the pre-bed dose to the morning often
does.

• Minimalist- Dosing below saturation levels pre-bed i.e.: ~50mcg each of a GHRP and GHRH

• Pre-bed Saturation- 100mcg of each GHRP (except Hexarelin) and GHRH. Results in better overall health,
recovery and well being. This is a solid general anti- aging protocol.

• Pre-bed & Post Workout Saturation Dose- PWO serves protein metabolism well and increases protein
synthesis. Twice a day saturation doses has increased recovery, contribution to anabolism, injury healing,
better well being and serious anti-aging properties.

• Pre-bed, PWO, and Morning Saturation Doses- The morning dose, when fasted, engages the release of fatty
acids which can be burned off for energy during activity. Three saturation doses per day further increases
anabolism and decreases catabolism. Local growth factors will rise including systemic IGF-1, but within
physiological levels, resulting in no enhanced health dangers, no abnormal organ or structural growth.

There are more advanced dosing protocols but for simplicity they have been left out of this text.

Administration
For best results doses should be administered on an empty stomach (2 or so hours after eating) or
with only protein in the stomach. Fats and Carbs blunt the bodies GH release. So, administer your dose, wait
 20 minutes for the GH pulse to reach its peak and then you can eat Carbs or fats without having to worry
about blunting the GH pulse. If dosing multiple times per day allow at least 3 hours between administrations.

BPC 157 & Healing Your Body

What is BPC 157?

BPC 157 is a sequence of amino acids with a molecular formula of 62 carbons, 98 hydrogens, 16 nitrogens,
and 22 oxygen atoms (C62-H98-N16-O22).
Should you care to know the nitty-gritty specifics, that comes out to a fifteen amino acid sequence of the
following:

L-Valine, glycyl-L-alpha-glutamyl-L-prolyl-L-prolyl-L-prolylglycyl-L-lysyl-L-prolyl-L-alanyl-L-alpha-aspartyl-L-
alpha-aspartyl-L-alanylglycyl-L-leucyl-; glycyl-L-alpha-glutamyl-L-prolyl-L-prolyl-L-prolylglycyllysyl-L-prolyl-L-
alanyl-L-alpha-aspartyl-L-alpha-aspartyl-L-alanylglycyl-L-leucyl-L-valine.

That's the long, fancy name for BPC 157.

BPC, for reasons you're about to discover, stands for “Body Protecting Compound”. Your body already makes
it in your own gastric juices in very small amounts, where it serves to protect and heal your gut. But if you can
get the super concentrated version and get it into your system, it has an extremely high level of biological
healing activity just about anywhere you put it.

What Does BPC 157 Do?

BPC 157 is surprisingly free of side effects, and has been shown in research that's been happening since 1991
to repair tendon, muscle, intestines, teeth, bone and more, both in in-vitro laboratory “test-tube” studies, in
in-vivo human and rodent studies, and when used orally or inject subcutaneously (under your skin) or
intramuscularly (into your muscle).

Just take a look at the following, all of which was hunted down and identified by Suppversity in their article
on BPC 157. BPC-157 has been shown to:
• Promote tendon and ligament healing by tendon outgrowth, cell survival, and cell migration in a rodent
model of Achilles tendon rupture, and also when administered in drinking water to rats with damaged medial
collateral ligaments.
• Tendon-to-bone healing effective enough that they may actually “successfully exchange the present
reconstructive surgical methods.”
• Counter the damaging effects of NSAIDs like ibuprofen or advil on the gut lining so effectively that scientists
termed BPC 157 “a NSAIDs antidote” one of which they say that “no other single agent has portrayed a
similar array of effects."
• Repair the damage from inflammatory bowel disease (IBD) within just days of oral administration in a rodent
model of IBD.
• Help cure perdidontitis when administered in a rodent model of periodontitis, significantly enough to have
scientists conclude that “BPC 157 may represent a new peptide candidate in the treatment of periodontal
disease.“
• Reverse systemic corticosteroid-impaired muscle healing, in a rodent models where BPC 157 was
administered orally once daily for 14 days to rats with crushed gastrocnemius muscle. Similar benefits were
demonstrated in a rodent study by Novinscak et al.
• Accelerate bone healing in rabbits who suffered segmental bone defect before being treated with BPC 157.

BPC-157 is also known as a “stable gastric pentadecapeptide”, primarily because it is stable in human gastric
juice, can cause an anabolic healing effect in both the upper and lower GI tract, has an antiulcer effect, and
produces a therapeutic effect on inflammatory bowel disease (IBD) – all again surprisingly free of side effects.

As demonstrated in the research studies cited above, BPC 157 also accelerates wound healing, and, via
interaction with the Nitric Oxide (NO) system, causes protection of endothelial tissue and an “angiogenic”
(blood vessel building) wound healing effect. This occurs even in severely impaired conditions, such as in
advanced and poorly controlled irritable bowel disease, in which it stimulates expression of genes
responsible for cytokine and growth factor generation and also extracellular matrix (collagen) formation,
along with intestinal anastomosis healing, reversal of short bowel syndrome and fistula healing – all of which
can extremely frustrating issues in people who have gut pain, constipation, diarrhea and bowel inflammation.

So if you have frustrating joint pain that won't go away, some kind of muscle tear, sprain or strain, or gut
“issues”, you should potentially consider using BPC 157.

How Much BPC 157 To Take

There is an abundance of research on BPC-157 and it has been shown to be effective systematically when
injected once daily at anywhere from 1-10mcg per kg of body weight. In most cases, this comes out to a dose
of anywhere from 200mcg up to 800mcg. Some report the most success dosing twice per day with 250-
350mcg for a total of 500-700mcg per day.

So as you can see, there's quite a bit of variability in dosage recommendations.

How To Inject BPC 157 Or Take BPC 157 Orally

BPC 157 acts systemically.

• This means that whether you inject it subcutaneously – an easier and more-pain free under-the-skin method
that you should do as close to the area of pain as possible…

• ….or you inject it intramuscularly – the more painful and teeth-gritting version of essentially “stabbing” the
needle into the muscle as close to the injury as possible…

• …or you simply spray it into your mouth orally…

• …the BPC 157 going to render some amount of benefit in whichever part of your body needs healing. To what
extent is still unknown.
Side Note: Datbtrue believed the best way of administration was to inject as close to the injury as possible.

Subcutaneous injections are also relatively simple. You can either pinch an area of skin near the injury site
and thrust the needle into that pinched area of skin.

Intramuscular injections will be the more painful option depending on the location of the injury, but again,
you will inject as close to the injury as possible.

Oral administration of BPC 157 is quite straightforward. Just spray it into your mouth (remember: very slowly
to not damage the peptide), hold it in your mouth for 90-120 seconds, then swallow.

How Long To Take BPC 157

Based on the current human studies to date, BPC 157 can be safely administered for four weeks, followed by
a two week rest. Again, this is just using the data we have, some have used longer and not reported any ill
effects, but that doesn't mean there wasn't any.

Use In The Medical Field

Ok, so you may be now wondering why in the heck your physician, physical therapist, surgeon,
gastroenterologist, etc. hasn't told you about this stuff.

Here's the deal: since BPC 157 is a completely natural gastric juice peptides, it's technically not patentable,
period. That means big pharma can't make money off BPC 157, and that means it's not getting marketed to
your local doctor or hospital or anywhere else in the health care system. It's also not available as an FDA
regulated drug, or even considered to be “sellable” for human use.

Studies and Other Links

• GHRP-2 GHRP-2 increases GH levels
• Human Growth Hormone
• Insulin-like Growth Factor 1
• Melanotan II

Datbtrue Article Archive

PEPTIDES BASICS

GHRH (Growth Hormone Releasing Hormone) + GHRP (Growth Hormone Releasing Peptide) = 10 star GH
Release (**********)

GHRP (Growth Hormone Releasing Peptide aka Ghrelin-mimetic) = 3 star GH Release (***)
GHRH (Growth Hormone Releasing Hormone) = 0 or 1 star GH Release (*)

GHRPs (GHRP-6, GHRP-2, Hexarelin, Ipamorelin) are like cardiac shock paddles. You administer a GHRP and a
pulse of GH is created. This is predictable and reliable across all normal people.

GHRH creates no pulse. It only adds to what ever is happening naturally. If there is a pulse occurring then
GHRH increases the GH release. If no pulse is occurring when GHRH is administered then it will have little
effect on GH release.

I can not speak for Dr. Crisler but he indicated that Sermorelin (GHRH) by itself was not very effective at
raising IGF-1 levels. However when he added GHRP-6 with it at saturation dose (I believe administered
together twice a day), IGF-1 levels increase by 1/3.

This underscores the need for both a GHRH & a GHRP.

IF you are 100% sure you have CJC-1295 (and the odds are against it) then because it is a long lasting GHRH
(half-life measured in days) it will always be available which means during natural GH waves & troughs. So it
behaves differently and its effectiveness in terms of absolute GH release is higher then the other forms of
GHRH.

CAVEAT - CJC-1295 raises base levels of GH not the pulses. It is possible that CJC-1295 never gives the
somatotrophs sufficient time to reload stores of GH at the 100% level. Normally Somatostatin by stopping GH
release activity gives the cells sufficient time to build up a big store of releasable GH. So CJC-1295 no matter
how much GHRP you add may not be able to effect as strong a pulse as a GHRP + GHRH.

There is no reason NOT to combine a GHRP such as GHRP-6 with your GHRH, no matter whether the form of
GHRH is Sermorelin, modified GRF(1-29) or CJC-1295. There is only BIG benefit.

On the flip side you can consistently and reliably effect GH pulsatile release with a GHRP alone. Without a
GHRH the amplitude will not be synergistically higher. BUT it will be a strong pulse of GH release.

One more quick point. An iu of synthetic GH is 333mcg of compound. Thats all. A unit of GH doesn't give the
same effect across all normal people and even within a person there is variability.

A far better measure is GH in plasma measured in many multiple intervals over a period of time. By sampling
frequently you can determine the peak of GH in plasma and when it drops to baseline.

You can then measure IGF-1 levels to determine the effect that THAT dosing had on increasing circulating
levels.

You can do the same thing with GHRH & GHRP.

The problem people have is they are stuck on absolute levels of GH in circulation as being of paramount
importance. It isn't.
First it is free GH that is important. Anywhere from 10% to 90% may be bound at any given time with GH-
Binding proteins or prolactin-binding proteins.

Second it is pulsation that is important for growth not absolute levels. Pulses send communicative signals to
the cells. GH is simply the ligand that gives form to the wave. GH has no other value except to be a part of a
communication signal.

The cells respond to this wave of GH by mediating events within the cell that are responsible for metabolism,
protein synthesis, further ligand transcription & synthesis in the form of IGF-1 ...some of these signaling
pathways in the cell carry messages to proliferate, differentiate or induce apoptosis . These intracellular
pathways are common to many different tissue populations and respond to initiation from many different
types of ligands binding to various receptors.

This behavior is optimized by pulsation ...continuous GH desensitizes these pathways (and sends certain
signals that are common to females to mediate certain events such as creation of specific liver enzymes)...

So it is probable that I (and anyone who understands fully) could get more out of a small amount of GHRH +
GHRP then someone who administers large amounts of GH. The validity of this statement is dependent on
the use of other compounds...

Finally to answer your question directly:

I believe that if your CJC-1295 is modified GRF(1-29), coupled with GHRP-6, dosed as described you will
achieve your goal of GH level (i.e. 4ius) and exceed both the quantity & quality of those growth optimizing
events that THAT equivalent level of synthetic GH will be capable of mediating.

BEGINNER: What should I use? ...and why? (GH Releasing System Simplified)

Three Basic Hormones

If you form a V w/ your fingers you have the basics for the GH releasing system modeled before you. One
finger is a hormone called Growth Hormone Releasing Hormone (GHRH) and the other is the hormone
Somatostatin.

The bottom of the V is where both of those hormones converge. At that bottom we have somatotrophs (or
somatotropes or Growth Hormone Releasing cells). These are cells that spend most of their time assembling
Growth Hormone (GH) from pieces and storing it.

So in this simple system we have three hormones. We have Growth Hormone Releasing Hormone (GHRH)
which comes from the brain and contacts Growth Hormone Releasing Cells (Somatotrophs or somatotropes)
and causes the cell to release some of the Growth Hormone (GH) it has made and stored. If we ask the cell to
release GH all the time we end up with no storage of GH. As soon as some is made it is released. This is what I
call GH bleed because you get a constant low flow or dribble of GH but no big pulse, or mass of GH.
What causes GH release? The brain-derived hormone Growth Hormone Releasing Hormone (GHRH). So if
GHRH is always free to act we end up with GH bleed.

However the other brain-derived hormone Somatostatin functions as the "off switch". It also contacts the
Growth Hormone Releasing Cell (Somatotroph) and instructs it not to release Growth Hormone (GH). If
Somatostatin is present and GHRH is not then we will never have GH release. What we will have is plenty of
time for the cells to make and store GH. If we could ever get Somatoststin to go away and GHRH to show up
we'd have a big release or pulse of GH.

As you can see both the "on switch" hormone Growth Hormone Releasing Hormone (GHRH) and the "off
switch" hormone Somatostatin are necessary or we end up with a malfunctioning human being.

You may wonder if we can limp by w/ just GH bleed. We can up until puberty when it is time to grow,
develop and mature. Growth, development and maturity requires pulsatile GH (in conjunction with timed
release of sex hormones).

You may also wonder what happens if GHRH and Somatostatin are together at the bottom of the V at the
same time. What does the cell do? The answer is that for the most part Somatostatin is stronger and GH will
not be released.

From this it is easy to see that a well-functioning GH releasing system depends on both GHRH &
Somatostatin. Somatostatin to hold back release so enough GH can be made and then GHRH to cause a pulse
of GH. Not only must these two brain-derived hormones which oppose each be active, they also must
alternate with one another...GHRH release and a while later somatostatin and then a while later
somatostatin retreats and GHRH is released again... this brings release of some of the GH mass that has been
built up over the course of 3 hours in what looks like a pulse if graphed.

Ghrelin (GHRPs) the 4th hormone in the GH Releasing System

To be complete we need to add a fourth hormone to this system. One hormone Growth Hormone (GH) is the
end-product hormone. It results from all of this activity. That leaves the other 3 hormones as hormones that
determine how, when and how much GH will be released.

If you replace the V you formed with your fingers with a Y, by using the same two fingers to form a V and now
adding your long forearm, you have a very good model of the GH releasing system.

The forearm extends to the stomach and that is where the hormone Ghrelin is made. Ghrelin is a hunger
derived gut-hormone. It is capable of making its way to the pituitary where the GH releasing cells
(somatotrophs) reside. Just like GHRH & Somatostatin it also can contact the cell. When it does it reduces
Somatostatins effect. Ghrelin increases GH release. It does this in several ways -by encouraging the brain to
release more GHRH, amplifying the effect of GHRH when it gets to the somatotroph, benefiting from GHRH
being at the cell to amplify Ghrelin's own effect which is in part an increase in GH release and countering
Somatostatin's stoppage effect at the cell.

In fact Ghrelin can cause GH release all by itself even if Somatostatin is around. But Ghrelin makes the
environment safe for GHRH to act and if GHRH acts when Ghrelin is there the result is what is called a
synergistic GH release. Synergy means the amount is larger then each could have produced on its own. If
Ghrelin would cause 5 units to be released and GHRH 2 units when you put them together synergy means the
result is more then additive (5 + 2). The synergistic result may be 15 units. Why does synergy happen? GHRH
and GHRP help each other... they make each other stronger. More complete fuller treatment of the topic
available on the forum.

Ghrelin is a natural hormone with effects besides GH release. Now a synthetic form of Ghrelin which
primarily just effects GH release is what is known as Growth Hormone Releasing Peptides (GHRPs). These are
man made and are capable of contacting the somatotrophs and causing GH release the same as Ghrelin.

Originally they were called Secretagogues to include a few non-peptide structures as well. So Growth
Hormone Releasing Peptides (GHRPs) may be thought of in our Y model as replacing Ghrelin. They differ from
GHRH primarily in the color I chose. Consistently through most of my posts over the years I label them purple
and GHRH I label green. Wake up! GHRPs are the 3rd hormone/peptide that effects GH release. Its presence
at the somatotroph causes GH release on its own and with the naturally occurring "on switch" it amplifies GH
release. By stopping somatostatin GH is released. Now GHRPs never result in GH bleed. The release they
trigger is always a pulse that is over with within 3 hours.

Will IGF-1 interfere with all of this?

Not really IF you are supplying external GHRH and external GHRPs. IGF-1 primarily exerts negative feedback
by increasing somatostatin release. Somatostatin is stopped by GHRPs. IGF-1 can also reduce release of
natural GHRH from the brain. This is overcome by supplying external GHRH.

What is CJC-1295, CJC-1293, GRF(1-29), Sermorelin and modified GRF(1-29)?

In short they are all forms of GHRH (Growth Hormone Releasing Hormone).

What are GHRP-6, GHRP-2, Ipamorelin, Hexarelin?

In short they are all forms of GHRPs (Growth Hormone Releasing Peptides, Ghrelin-mimetics)

How do I chose? What do I do? Step one: You NEVER know when somatostatin is going to act [Yes but Dat do
I ever need to inject Somatostatin? No... not in our world...don't interupt please.] Again since you don't know
if somatostatin is around you are rolling the dice by injecting GHRH. There will be zero GH release if
somatostatin is around and only some if somatostatin is just starting up or just diminishing. Only if you are
lucky to inject when somatostatin is gone will there be decent GH release. To overcome this, very large
amounts say 2mg (2000mcg) are sometimes used. Injecting GHRH alone is not very effective.

Step two: Choose a GHRP because it can always cause GH release on its own and make the environment safe
for GHRH.

Step three: Choose a GHRH to add to the GHRP because it will synergisticly amplify the GH pulse.

Step four: Choose a dosing schedule. If once a day do it pre-bed. If twice a day then do it pre-bed and post
workout (PWO). If three times a day do it pre-bed, PWO and in the morning. How many times can I dose
before I lose pulsation? Six (6) a day every 3 hours

How few times can I do it for some better sleep, small anti-aging effect? Just pre-bed.

Step five: Assess tolerance by dosing just once w/ a GHRP pre-bed at half of saturation dose. Then if that goes
well go to full saturation dose. If that goes well add a 2nd dosing, If that is fine add a third dosing.

Step six: Decide on a dose. Saturation dose is defined as either 100mcg or 1mcg/kg of bodyweight in the
studies. For the most part it is treated as 100mcg. That is the same for women and men. You will get added
but diminishing benefit by dosing 200mcg, 300mcg perhaps 400mcg. A fuller explanation on why is available
on the forum.

What is Clinical Grade?

American made in a lab that supplies people that do published research. The purity has to be high enough to
allow ethical experiments in humans.

What are all these peptides and what should I choose?

First notice that I referred to GHRH, GH and Ghrelin as hormones. They are naturally occurring hormones
whose structure is just one amino acid such Arginine bonded to another amino acid such as Lysine. They are
both hormones and peptides. Sex hormones are examples of hormones that are not built in the body with
amino acids.

Now GHRPs do not naturally occur in the body but since they are mimickers of a hormone Ghrelin we can
fudge and use the term hormone if we want. Growth Hormone Releasing Petites (GHRPs) as the name
implies are built with attachments of amino acids.

Which GHRH?

The body makes GHRH which 44 aminos long. 15 amino acids are useless so the first 29 amino acids is what is
known as GRF(1-29). Yes GHRH(1-29) makes more sense but someone chose G for "growth hormone", R for
"releasing" and F for "factor". The numbers just tell you which amino acids from GHRH are kept.
GRF(1-29) acts just like GHRH so I'll color it green. GRF(1-29) is an FDA-approved pharmaceutical drug named
Sermorelin.

So GHRH, GRF(1-29) and Sermorelin are basically the same. The problem though is they are easily eaten up
by blood enzymes within minutes. If you could inject directly into the pituitary at the base of the brain then
they will be effective, after-all that is what the brain drops into the pituitary. But circulating in the blood
means they are rendered ineffective within minutes.

That leaves us with analogs. An analog is a modification(s) to the peptide such that a property(ies) is(are)
changed such as longer half-life, receptor binding affinity or receptor binding strength w/o losing the action.
Many analogs can and have been made. However all you need is an analog that survives early blood plasma
enzyme death and lasts say 30 minutes. Note a receptor is how some hormones/peptides interact with a cell.
The hormone/peptide binds to a receptor on the outside of the cell and the message carried in. I purposely
avoided receptor talk so as to avoid confusion and substituted the term "contact" and "contact with the cell".

IGF-1 LR3 is an analog of IGF-1. It survives longer in plasma w/o binding to a binding protein but also has a
lower binding affinity for its contact with the cell or better yet IGF-receptor.

CJC is a term coined & used in a study that tested a newly created velcro type drug complex to attach to
GRF(1-29) to allow it to cling to albumin in blood and give it protection and a long life (albumin has a very
long plasma life).

They tested three peptides/drug compounds. The first was simply GRF(1-29) with the drug affinity complex
(DAC) attached. Think of that DAC as simply the velcro drug component. As you can see the CJCs are not pure
peptides. They called this CJC-1288. It lasted about the same as plain old GRF(1-29). Blood plasma enzymes
killed it in minutes.

Then they took GRF(1-29) and made one amino acid swap plus the DAC (velcro drug) That means they took
Arginine in the 2nd position of the peptide and replaced it with its mirror image form known as the D form.
This makes the analog peptide stronger but not by enough. The half-life is maybe double GRF(1-29) in
humans. So 5 minutes of half-life. This they called CJC-1293.

Then they made 4 amino acid changes in GRF(1-29) to really strengthen it so it would last more then 30
minutes and added the drug affinity complex. This worked well for them because the peptide/drug hybrid
lasted long enough to find the plasma albumin for the DAC part to velcro itself to for a long life of several
days. This they called CJC-1295

You want none of the CJC's. The first two because they do not survive long enough and the last one because
it is always around. True somatostatin does pop up and stop GH release, but as soon as it can CJC-1295 is
inducing GH release. The study itself found it increased base levels but did not increase pulses. That means
there is less GH mass synthesized and stored in the somatotrophs. What are somatotrophs? Remember they
are growth hormone releasing cells. The word may sound like somatostatin but only somatostatin has the
power to stop GH release because? Because it is colored in red.

Somatotrophs are not cells that release prolactin. Prolactin is released by Lactotrophs. Somatotrophs self
organize into networks that coordinate GH release into a pulse. A fuller treatment is available on this forum.

What do you want?

You want the pure peptide part that was used in the third analog. You want those 4 modifications because
they make what is essentially GHRH last for 30 minutes or more. This is a fine peptide to contribute to a GH
pulse. This I call modified GRF(1-29). Since it is basically a 30 minute plus lasting GHRH I color it green.

Which GHRP?

GHRP-6 is sloppier in that it activates a wider array of effects beyond GH release. It causes intense hunger
and gastic motility. It can have a mild effect on cortisol and prolactin. It is a first generation GHRP.

GHRP-2 is less sloppy with a more intense GH release, no gastric motility and less hunger effect. It can have
an effect within the normal range on prolcatin and cortisol. It is a second generation peptide.

Ipamorelin is not sloppy at all. It does not release as much GH as GHRP-2 but it causes virtually no hunger or
gastric motility and for the most part does not effect cortisol or prolactin. It is a third generation peptide

You would choose GHRP-2 unless you wanted GHRP-6 for the hunger effect or for the lower release profiles.

You would choose GHRP-2 normally as the most bang for the buck.

If you are very sensitive to perturbations in cortisol or prolactin you would choose the more expensive
Ipamorelin.

I Datrius B. True use either GHRP-2 or Ipamorelin with modified GRF(1-29) I usually rotate around.

The History of Nutrition (supplements & Steroids) in Bodybuilding

Splendid Specimens: The History of Nutrition in Bodybuilding By Randy Roach

The sport called bodybuilding demands the ex-treme in body presentation. No other athletic endeavor
requires such high levels of regimentation for muscle development and body fat reduction. To outsiders, such
efforts may appear vain and self-centered, even looming out there on the lunatic fringe. Nevertheless, the
sport has had considerable influence on other fields of athletics, not to mention the general public.

We must remember that the men (and women) who sweat it out in the gym year after year were using the
low-carbohydrate diet long before Dr. Atkins made it popular. Many other dietary strategies of today such as
all-raw diets, protein supplementation, eating multiple small meals a day, carbohydrate loading, meal
replacement packages and macro-nutrient balancing all derived their initial popularity from the bodybuilding
field.

PHYSICAL CULTURE

Credit for the Physical Culture movement in North America, the precursor to the bodybuilding movement,
goes to Bernarr Macfadden, an extraordinary entrepreneur who published physical culture magazines,
organized physique competitions, wrote 150 books and accumulated millions in the publishing industry.
Macfadden preached clean living and whole natural foods. He ate vast quantities of raw carrots, beet juice,
fruits, dates, raisins, grains and nuts. He abstained from meat but recommended copious amounts of raw
milk. In fact he even recommended an exclusive raw milk diet for extended periods.

The dominant star of the early years was Eugen Sandow, whose career spanned the late 1890s and the early
part of the 20th century. He did not display the typical burly brute image, but a finely chiseled body,
resembling those of Roman and Greek athletes. With the help of Florenz Ziegfeld, he marketed and displayed
his physique in artistic fashion. In fact, it was through this artistic expression that Sandow inspired
Macfadden in the mid 1890s. In an 1894 interview on his dietary habits, Sandow claimed to abstain from hard
liquor, coffee and tea, but consumed the occasional beer. He ate mostly wholesome foods, but indulged at
selected opportunities. Sandow, along with most of the other Physical Culturists of his day, placed more
emphasis on the mechanical aspects of diet as opposed to the chemical. He believed in doing what was
necessary to facilitate good digestion, including eating at regular intervals, selecting simple foods, applying
thorough mastication, eating slowly and tying it all together with a good night's sleep. He was critical of over-
indulgence and recommended foods with a high nutrient value, although he admitted to eating what he
wanted, when he wanted, and however much he wanted during his younger years.

Earle Liederman, author and friend of Sandow, also advocated whole natural foods. Liederman pointed out
the importance of a strong digestive system enhanced by proper food mastication for men of strength and
large appetites. He described the popularity of "beef juice" or "beef extract" for rapid muscle recovery.
Liederman also felt obliged to mention that ice cream was very popular, referring to one lifter who often felt
it necessary to finish his meals with a quart of vanilla ice cream.

Arthur Saxon of the famous Saxon brothers trio and a contemporary of Eugen Sandow, also recommended
nutrient-dense foods for endurance athletes. He warned against the dangers of hard liquor, but condoned
beer. In fact, Saxon had a reputation for hefty beer drinking as did many men of strength of the time. He
warned against smoking while admitting to being a smoker himself. For gaining muscle, Saxon recommended
milk mixed with raw egg after a workout, milk with oatmeal, cheese, beans, peas, and meat. He called milk
the perfect food.

According to his brother Kurt, all three of the Saxon brothers had very hardy appetites. Along with his
participation in the strength act, Kurt was also the trio's chef. Kurt's list of food consumed by the three
brothers each day indicates substantial daily intake, with little self-denial. Milk is largely absent from Kurt's
menus.

RAW VERSUS COOKED

A debate that has been on-going since the early days of Physical Culture is the relative virtues of raw food
versus cooked. Sandow referred to the eating of raw eggs and under-cooked meats as nonsense and a
practice that was "passing away."

In the raw food corner was champion wrestler George Hackenschmidt, the "Russian Lion," a man rivaling
Sandow's strength, and surpassing him in athletic ability. Like Sandow, he was small by today's standards,
standing just under 5'10" and weighing about 200 pounds. However, he was enormously strong. Both a
gentleman and sportsman, George Hackenschmidt reflected a spiritually conservative philosophy towards
nutrition. In his book The Way to Life, he stated:

"I believe I am right in asserting that our creator has provided food and nutriment for every being for its own
advantage. Man is born without frying-pan or stewpot. The purest natural food for human beings would,
therefore, be fresh, uncooked food and nuts." He stated that a diet of three quarters vegetable food and one
quarter meat would appear to be most satisfactory for the people of central Europe but conceded a hardy
appetite which, in his early training years, was based on 11 pints of milk per day, presumably raw, along with
the rest of his diet. A prophet before his time, he warned about the dangers of refined sugar and meat from
artificially fed and confined animals. He believed that most people ate too much flesh food from these
improperly raised animals and encouraged more emphasis on natural raw foods.

VEGETARIANISM

The early bodybuilders also debated the pros and cons of vegetarianism. Macfadden and Hackenschmidt
inclined towards diets that excluded meat, or that at least derived a preponderence of calories from plant
foods. Juicing was popular among some. In his book Remembering Muscle Beach, Harold Zinkin describes
fellow beach comrade Relna Brewer. At 17, Brewer worked in one of California's first health food stores,
located in Santa Monica. Relna's job was to run the juice press. Because the owners of the store could not
afford to pay much, Relna took out her pay in the celery, watermelon, orange and carrot juice she made each
day.

Jack Lalanne was probably one of Relna's customers. Jack began his carreer as a vegetarian, bringing his own
food, such as apple or carrot juice and vegetables, to train at the beach during the 1930s. However, Lalanne
later ate meat when focussed on bodybuilding. In fact, Armand Tanny says that Jack would visit the local
stockyards to acquire cow's blood to drink while in training. Later Lalanne reverted back to his vegetarian
ways, but allowing some fish and eggs.
Lalanne opened one of the first health studios in Oakland in 1936. A colleague writes that Lalanne would
work 14 hours a day then drive through the night 400 miles so he could be with the gang at Muscle Beach to
participate in all the activities. When it came to pure energy and vitality, Lalanne was, and at 90 today, still is
unbridled.

Another vegetarian was Lionel Strongfort who promoted a system of raw foods based on fruits, vegetables,
eggs and milk. He recommended very little meat and cooked fat. Strongfort suggested eating only two meals
a day, a strategy shared by Macfadden that would re-emerge in the 60s and 70s. Strongfort and Macfadden
both advised against overconsumption of food. They claimed overconsumption created a negative stress on
the body's systems, sensible advice that bodybuilding publications would ignore in the coming years.

Perhaps the most accepted food across all the early eating models for bodybuilders was milk. One of the
most popular protocols for building size and strength was the combination of back squatting and drinking
large quantities of milk. Joseph Curtis Hise was a pioneer of this system in the 1930s and after 70 years this
strategy is still going strong in the drug-free world of bodybuilding.

TONY SANSONE

Another Physical Culturalist who advised against over-consumption was Tony Sansone, but Sansone
understood the importance of flesh foods, including animal fats and organ meats. He wrote extensively on
nutrition for bodybuilders and recommended nutrient-dense "foundation" foods such as milk, eggs, butter,
meat, vegetables, fruits, and some whole grains, in that order. He also stressed the importance of organ
meats such as liver, kidney, heart and cod liver oil and recognized the need to drink whole raw milk instead of
pasteurized and skimmed. He believed goats milk was more nutritious and easily digested than cows milk.
Fresh butter and cream were his preferred fats. He also recommended six to eight glasses of water per day.

Tony Sansone wisely stressed the importance of generous amounts of fat in the diet to allow the complete
utilization of nitrogenous (protein) foods in building muscle tissue--a fundamental and important fact that
would be lost as the era of protein supplements took hold. He also knew that weight loss was not a matter of
simple calorie counting, as cellular uptake or utilization of food varied on an individual basis. In anticipation
of Dr. Atkins, Sansone recommended his foundation foods of milk, eggs, meat, vegetables and fruit for
strength and health, and starchy foods as weight manipulators. His recipe for gaining weight was to add more
high-carbohydrate foods such as bread and potatoes to the diet, and for losing weight to simply reduce or
remove them. Tony Sansone's caveat to lose no more than two pounds of fat per week is still the standard
used in bodybuilding today.

MUSCLE BEACH

Muscle Beach got its start in the 1930s as the meeting place of young athletes who lifted weights, built
human pyramids, tumbled, juggled and engaged in any other athletic endeavor they could think of. That era
gave us many recognizable names such as Harold Zinkin (creator of the Universal weight machine), Joe Gold
(creator of Golds Gym), Jack Lalanne, Harry Smith, and the Tanny brothers, Armand and Vic (who created a
popular gymnasium chain). In fact, it is safe to say that much of the fitness industry grew out of Muscle
Beach--gyms, gym chains, TV exercise programs, fitness equipment, women lifting weights, even aspects of
the natural organic food movement stemmed from this small stretch of sand.

According to Harry Smith, long-time gym owner, ex-pro wrestler and Muscle Beach alumnus, body builders
didn't think much about specialty food or supplements in those days. The emphasis was on training rather
than eating and resting. Harry did state that many of them tried to keep their eating clean, and that on a
number of occasions they would frequent a small deli about one-half block from the beach. The deli offered
freshly ground beef to which some of the guys would mix some raw onions and a little salt and pepper. The
meat was eaten raw along with raw milk. Harry said it was a cheap and easy way to eat hardy and keep out of
the restaurants.

One important Muscle Beach raw food enthusiast was Armand Tanny. Originally a weightlifter, Armand had a
fantastic physique and the strength to qualify him for the wrestling circuit. He visited the Hawaiian Islands
just after the Second World War and came away with a lasting impression of the Samoans. "They ate
everything raw," he noted. "You name it, fish, meat, beetles--everything! They were so strong and healthy."
On his return to the US, he became interested in the work of Weston A. Price, stating that Price's book
Nutrition And Physical Degeneration served as his Bible.

In 1948 he shut off his stove and ate just about everything raw from then on--tuna, beef, liver, lobster,
oysters, clams, nuts, seeds, fruits and vegetables. Armand recalls wading out into the surf along the Santa
Monica Pier and using his feet to kick up 6- to 7-inch Pismo clams, smashing them together to get at the pink
and white flesh. Armand also took brewer's yeast, desiccated liver, yogurt, black strap molasses and wheat
germ oil, all recommendations of Gaylord Hauser, a nutritional guru of the era. Hauser also recommended
fish liver oil, but Tanny felt he was getting plenty from all the raw fish he was consuming.

Armand credited his 1950 Mr. USA and the Pro Mr. America titles to his raw meat diet. In the 1950s, he
helped his brother Vic in the gym business and appeared in a Mae West act. His bodybuilding articles
appeared prominently in bodybuilding publications for the remainder of the century, thus providing a link to
Weston Price during the decade of the 50s.

BULKING UP WITH JOHN GRIMEK

The biggest influence on bodybuilding in the 1930s and 1940s was John Grimek, the second American
Athletics Union (AAU) Mr. America and the first to win back-to-back titles, in 1940 and 1941. Many
commentators believe that Grimek represents the beginning of modern bodybuilding as we know it today,
describing him as the best physique of the mid century.

During the early 1930s, at the start of his career, Grimek came under the influence of Mark Berry, editor of
Strength magazine and an advocate of an eating protocol in which an athlete would bulk up in bodyweight
and then train it off. At one point, Berry had Grimek beef up his 5' 8" frame to 250 pounds. The practice
would become commonplace by the 1950s and maintain a foothold for several decades after.

Grimek bulked up on whatever was put in front of him, reports his wife Angela in a 1956 Health and Strength
article entitled "Life with John." "John has an enormous appetite. . . John has yet to find a restaurant that can
do justice to his appetite. . . . Sometimes he goes on a restricted diet--and it is surprising how little he can get
by on then. But when he goes all out, he can never be filled. . . . but the ‘hog' (our pet name for John) just
eats and eats and still remains trim and muscular."

By the 1950s, Grimek's diet included Hershey chocolate bars and hi-protein tablets manufactured and
promoted by Bob Hoffman, publisher of Strength and Health, a magazine that provided a platform for Grimek
along with the new-fangled supplements coming on the market. Hoffman used Hershey chocolate in his
products, so Grimek and the rest of the York gang had easy access to some empty calories.

PROTEIN POWDERS AND SUPPLEMENTS

In the late 1930s a young pharmacist named Eugene Schiff developed a method of processing whey from milk
for human consumption. He created Schiff Bio-Foods, a whey packaging company. This was a half century
before whey concentrates would emerge as a popular supplement in the bodybuilding scene. For a short
time he sold his packaged whey to local drug stores, then sold his own store to enter into the manufacturing
and packaging of health foods.

Schiff focused on supplements made from natural products. He began to experiment with whole foods such
as brewer's yeast, wheat germ and liver. He found that these foods were naturally rich in vitamins and
minerals. The Schiff company claims that he was first to discover that rose hips was a superior source of
vitamin C. Along with the first rose hip vitamin C supplement, he also launched one of the first multi-vitamin
products, called "V-Complete."

The demand during World War II for non-perishable foods allowed the food industry to expand and
popularize the market for powdered or dehydrated foods and bodybuilders would eventually find their way
into this market. Powdered milk and eggs, and later powdered soy protein, were promoted as an easy way to
get additional protein into the diet. Breakfast drinks based on a protein powder emerged into the diet of the
legendary Steve Reeves who years later wrote about this practice in his book Building The Classic Physique.
Reeves' impressive natural physique landed him starring roles in the films Hercules and Hercules Unchained
in the late 1950s and inspired thousands of young men to adopt weight training. His recipe for a breakfast
drink included fresh orange juice, Knox gelatin, honey, banana, raw eggs and a blend of skim milk, egg white
and soy protein.

The first protein powders "tailored" specifically for athletes appeared around 1950. One of these was called
44, "The Supplemental Food Beverage," produced in California by a company called Kevo Products. The
principle ingredient was dehydrated powdered whole soy beans, along with kelp, wheat germ, dextrose, and
various dehydrated plants, herbs and flavorings. The supplement was sold at health food stores, body-
building studios, and health institutes.

Another popular product was Hi-Protein, "a protein food supplement derived from soya flour, milk proteins,
and wheat. The free amino acids which include natural tryptophan and the other natural essential amino
acids where produced by an acid hydrolysis." The product was developed by bodybuilder and nutrition guru
Irvin Johnson with before and after photographs of weaklings turned musclemen. Bob Hoffman quickly
capitalized on Johnson's success by following immediately with his own soy-based product marketed heavily
in Strength and Health. Hoffman's infamous protein claimed many a victim with hives or gym-clearing gas.

The debates on raw versus cooked and vegetarianism versus meat eating that appeared in bodybuilding
magazines during the 1940s gave way to numerous articles on protein supplements in the 1950s, including
"Building Biceps Faster With Food Supplements (Iron Man, December 1950," "More and Better Protein Will
Keep you Well (Strength & Health, March 1953)," "The Magical Power Of Protein (Mr. America, February
1958)," "Food Supplements Build Rock Hard Definition (Muscle Builder, June 1958)" and "Everyone Needs
More Protein (Strength & Health, July 1959).

Meal replacement products also appeared during the 1950s, with much hype. One product, called B-FIT, was
recommended as a replacement for two or three regular meals per day. According to its promoters, B-FIT "is
scientifically formulated to contain all the needed vitamins and minerals, plus ample supplies of the effective
proteins and yet is so low in calories that the fatty tissue literally melts away. . . . You will not suffer from any
nutritional deficiencies because B-FIT is a complete food insofar as scientific experiment and research is
possible to develop. Approved by dieticians."

Advocates for new diet theories--food combining, alkaline-forming diets, even strict vegetarianism--
promoted their ideas throughout the 1950s, but the big emphasis was on protein powders and supplements.
For the 1954 world weightlifting championships, team coach Bob Hoffman hauled more than 100 pounds of
his Hi Protein powder to Vienna, hailing it as the "secret weapon" for his athletes. But Russia, whose athletes
finished no lower than second place, had a secret weapon of their own.

THE SECRET WEAPON

It was John Ziegler, a doctor accompanying the American team to Vienna, who exposed just what this Soviet
weapon was. Ziegler claimed that after a few drinks, a Russian doctor told him that the Soviet athletes were
using--and abusing--testosterone. Ziegler was no stranger to testosterone. With his background in
rehabilitation therapy and his connection with CIBA Pharmaceuticals, he was already experimenting with
testosterone on himself, his patients and some novice athletes. In fact, author and historian John Fair writes
that even the great John Grimek was cooperating with Ziegler and trying his drugs in the summer of 1954.
Grimek reported disappointing results.
Both American and German research scientists had identified testosterone and noted its effects as far back as
the mid 1930s. CIBA Pharmaceuticals was already targeting bodybuilders with ads for synthetic testosterone
in 1947. With Ziegler's help, CIBA manufactured the most popular anabolic steroid of the 20th century. The
drug was Dianabol, which came out in 1958.

The acceptance of steroid drugs among bodybuilders got off to a slow start. Drinking a gallon of milk or
swallowing 2000 protein pills seemed more logical to them than taking a tiny pill to do the job. Even those
who did take them were slow in accepting or acknowledging the fact that it was the steroids that were giving
them such tremendous gains in muscle mass.

Out on the West Coast, bodybuilding great Bill Pearl was also curious as to what the Russians were doing, so
he took it upon himself to do his own research. During a visit to the University of California at Davis in 1958,
he learned from a veterinarian about the successful use of steroids in beefing up cattle. Bill figured that if it
was good enough for a bull, then it was good enough for him. While continuing to train hard, he took 30 mg
of the steroid drug Nilevar (three times the recommended dose for humans, but an absolute joke by today's
practices) for 12 weeks and brought his bodyweight up from 225 to 250 pounds.

Steroid use among athletes paralleled the challenge to conservative moral standards that characterized the
era of the 1960s. It was a time that seemed ripe for the liberation of one's desires. Individual freedoms took
precedence over the rules, morals and ethics dictated by a long established culture--and by Mother Nature. If
the new generation could take mind-altering drugs, it could take body-altering drugs as well. Anabolic
("building-up") steroids such as testosterone ushered in a new bodybuilding look that was larger and more
muscularly pronounced than ever before.

During the early 1960s, the magazines emphasized caution about steroids. They acknowledged the rumors
concerning Bill Pearl and others but tried to steer their readers away by stating that the drugs didn't work,
wouldn't produce what bodybuilders expected, or were outright dangerous. Both Iron Man and Muscle
Builder magazines warned of side effects and published articles claiming much better results with high-
protein products. But behind the scenes, the athletes knew that they worked. Pearl openly acknowledged
that he used them for a final time in 1961 to prepare for the 1961 National Amateur Bodybuilding Association
(NABBA) Mr. Universe contest. He stated that the drugs by then were no longer underground but well known
to the top bodybuilders.

STEROIDS AND CREAM

Still, most athletes relied on diet for strength-building, and protein occupied a large percentage of that diet.
In the early 1960s, Irving Johnson targeted elite bodybuilders with a milk-and-egg protein blend considered
far superior to competing products--including an earlier product of his own--based on soy. By the mid 60s,
ads for Johnson's protein blend began appearing in the bodybuilding magazines. At that time he changed his
name to Rheo H. Blair. Blair claimed that his protein powder was made from milk and eggs obtained from
animals raised on the rich soil of Wisconsin and that the proteins were extracted at very low temperatures.
Wary of the difficulty some might have digesting all that protein, he endorsed hydrochloric acid supplements,
to be taken with any protein meal. He also sold supplements such as amino acids, liver extract, B-complex
and soybro (a combination of wheat germ, rice germ and soy germ oils). In 1966 he introduced a new protein
formula which he claimed had a biological value resembling mother's milk.

Blair promoted his products with skillful salesmanship but he also made an important suggestion that would
ensure that his products actually worked--he insisted that his protein be taken with raw cream or half and
half. He was smart enough to know that you must replace the fat removed from protein during processing.
He also recognized the benefits of raw dairy products. Athletes of the 1960s used a variety of recipes, varying
the proportions of Blair's protein product with raw cream, raw milk and raw egg yolk. Weight-trainer Don
Howorth remembers eating 3 dozen eggs, 1 quart raw cream, and 2 pounds ground sirloin along with 2-3
cups of Blair's protein powder per day.

Blair had a special method for cooking his eggs. He did not cook them in boiling water but recommended
cooking many eggs at one time in water maintained at 181 degrees for 31 minutes. The eggs were then left in
the water to cool down slowly. Blair claimed that putting the eggs under cold water "shocked" many of the
nutrients, rendering them ineffective and that cooking eggs in this fashion preserved much of their
nutritional value.

It is interesting to read Perry Rader's "Reader Roundup" column in his Iron Man magazine during this time.
He tries to explain the spectacular gains made by some of thepopular bodybuilders who were using Blair's
products. Many of them were eating 6000 to 9000 calories a day in the same fashion as Don Howorth and
gaining muscle while maintaining or even trimming their waist size. Rader published Blair's response in a
1966 issue of Iron Man. Blair claimed that his protein powders, along with all of his other supplements, were
formulated in a special manner to metabolize fat more efficiently. He also warned that taking cream with any
protein powder other than his own would result in fat accumulation.

But Blair could not help knowing that these dramatic results were not achieved on food and protein powders
alone. Bodybuilders knew that they could expect to build muscle consuming 8000 calories per day, but not
lose fat at the same time. That required some additional anabolic assistance. Blair knew his guys were taking
steroids. Don Howorth readily admitted his past use of Dianabol, but was adamant about the importance of
diet along with it. In fact, some bodybuilders were quite open about drugs. When Larry Scott, two-time
winner of Mr. Olympia, was asked about his steroid use he said without hesitation, "Sure, doesn't everyone?"
However, the bodybuilding magazines continued the deception that the new, larger physiques were built on
powders and supplements. Thus steroid use artificially inflated the already marketable commodities of
bodybuilding.

VINCE GIRONDA
One man who had definition dieting mastered and who never used drugs was the Iron Guru Vince Gironda.
Pioneer of a technique involving intense abbreviated training routines rather than long workouts, Gironda
began competing in the 1950s and then trained both athletes and movie stars for many decades after. So
defined was his physique, he often found himself penalized by judges who seemed confused over his
appearance. Says Gironda, "The men who judged physique contests at this time were puzzled by so much
muscularity. Quotes from physique magazines stated I didn't place higher in whatever contest because of too
much muscularity. They thought that this type of cut-up physique was slightly repugnant so I lost most
muscular titles to smoother men who had that type of definition for that day."

Gironda often stated that nutrition was 85-90 percent of bodybuilding. His alternative to drugs was eggs. Like
Blair, he advocated up to 36 eggs a day for 6 to 8 weeks to produce muscle buildup. (He also took, among
many other supplements, "orchic tissue tablets," that is, dried testicles.)

He recommended following this "anabolic phase" with a short-term vegetarian diet to "re-alkalize" the body.
Similarly he alternated a low-carbohydrate diet with periods of carbohydrate loading. He was careful to point
out the difference between natural and refined carbohydrate foods. He presented research data that
strongly indicted refined carbohydrates as the real culprit in much of the century's degenerative disease. His
articles went into surprising detail on the biochemical pathways through which sugar did its damage, pointing
out the relation between sugar and atherosclerosis, abnormal increases in height and weight and skeletal
anomalies.

As for protein, he believed the average American could get along fine with just 45 grams of quality protein a
day. However, he insisted that bodybuilders needed over 300 grams daily for several weeks to force the
growth process. He believed in quality protein powders and used Blair's milk-and-egg blend until he came out
with his own product. When he used the powders, he blended 1/3 of a cup with a dozen eggs and 12 ounces
of raw cream or half & half. He was also big on steak and often ate his meat raw.mmended germ oils, amino
acids, vitamin and mineral supplements, and hydrochloric acid (HCL). He recommended mineral rich sea kelp
for its iodine content and dried liver extract for blood building and oxygen capacity boosting. Many
bodybuilders used desiccated liver after the early 1950s experiments of Dr. Benjamin Ershoff. Ershoff who
conducted the famous liver study wherein rats fed 10 percent desiccated liver swam far longer compared to
controls.

MACRONUTRIENTLAND

In his early years, Blair recommended a very low carbohydrate diet. Later he advocated a diet consisting of
1/3 protein, 1/3 fat and 1/3 carbohydrates to build muscle; then he reversed himself and again urged
avoidance of carbohydrate foods. But other bodybuilders included high levels of carbs in their diets. For
example, teenage sensation Casey Viator, who became the youngest Mr. America ever at age 19, had his own
special peanut butter pudding that consisted of 2 pounds of peanut butter, 1 jar of grape jelly and 3 or 4
bananas. The bananas were optional. This was part of a diet that also included 2 dozen eggs and 2 gallons of
raw milk per day. Casey recalls his father not shedding too many tears when he finally moved out.

A columnist in Strength & Health magazine recommended the following carbohydrate-rich concoction for
"getting big" along with a diet that allowed unlimited meat and eggs:

A one day supply of Hoffman's Gain Weight formula (based on soy protein) 2 quarts milk 2 cups skim milk
powder 2 raw eggs 4 tablespoons peanut butter ½ brick ice cream 1 banana 4 tablespoons malted milk
powder 6 tablespoons corn syrup

By the 1960s, bodybuilders had figured out what they had to do to attain specific goals. Getting lean or
"ripped" for a contest required stripping the diet of all carbohydrates, including milk and cream. Milk was a
favorite for building muscle, but for losing fat, it contained too much carbohydrate and held water under the
skin. Ketogenic diets consisting of meat and water were commonly used to prepare for the shows. During the
1950s, two English researchers--Professor Kekwick and Dr. Pawan--claimed to have isolated a fat-mobilizing
substance that showed up in the urine along with ketone bodies after 24 hours on a no-carb diet. In spite of
considerable scientific debate, the Ketogenic diet remained a constant in the field of bodybuilding until the
1980s.

Yet it was in the early 70s that the lipid hypothesis began to take hold. The result was a series of diets that
emphasized carbohydrates over protein and fats. The pre-game meal of beef was giving way to one of
lasagna or spaghetti.

The magazines of 1970 mirrored this confusion. For example, in an issue of Strength & Health, publisher
Hoffman praises the African Masai tribe for their reverence of whole milk, while in his other publication,
Muscular Development, he recommends skim milk because it is lower in saturated fats. (The vast majority of
the nation was now drinking pasteurized milk--long time strength trainer Jim Bryan remembers avoiding raw
milk because he was given the impression that it was dangerous.) MuscleMag publisher Bob Kennedy told his
readers not to let anyone scare them away from eggs. Frank Zane, Mr. Olympia champion from 1977-79, was
still eating the old way with plenty of eggs, lamb, beef, pork, heart, liver, raw milk, protein powder,
vegetables, fruit with some potato and brown rice, educating his readers on the misconception of cholesterol
and warning against over-consumption of polyunsaturated vegetable oils. But in Iron Man, Sterri Larson was
telling readers that the diet of the bodybuilder was not necessarily one to produce good health. He believed
that eggs were the best for both building muscle and losing fat, but that saturated fat and cholesterol could
prove hazardous. According to bodybuilder Brian Horton, some of the athletes were now eating chicken and
fish instead of beef and eggs.

STEROID USE

Meanwhile, by the end of the 1970s, professional bodybuilders were using a number of metabolism-
enhancing substances such as amphetamines, Armour (Thyroid), human and animal growth hormone, and
multiple steroids (a method referred to as "stacking"). Some of the top pros worked with physicians to
monitor their blood parameters as they prepared for their competitions. During the months before an event,
these athletes would swallow and inject any substance that would facilitate tremendous muscularity. Very
few, if any, bodybuilders could attain such condition without this assistance.

Steroid use suffered a setback with the revelation that 1988 Olympic gold medal sprinter Ben Johnson had
tested positive for anabolic steroids, which had been banned from use in the Olympic games since 1975. In
1990, the Food and Drug Administration added steroids to the Schedule III list of the Controlled Substance
Act. Since then, any athlete seeking to build muscle via anabolic steroids could just as easily find his next
workout conducted in a Federal prison gym -- and several have, to the dismay of many in the legal, medical
and sports arenas.

The ban on steroid use was no surprise to the bodybuilding world since abuse of the drugs, even at the high
school level, was well known. Not only was the number of users growing, but so were the dosages and
arsenals in professions where size and strength really made the difference.

The magazines were not yet labeling heart disease as a side effect of steroid use. However, by 1970 they
were starting to mention the fact that a number of strength athletes were succumbing at their prime.
Columnist Bob Brown described his concern over losing friends at an early age to heart disease and wrote an
article in Iron Man entitled "Will Weight Training Kill You?" Brown compiled some death statistics on
prominent men of the iron game throughout the century and compared them to some mortality stats
supplied from an insurance company. He concluded that even though strength trainers were not immune to
early death, they fared better than the average American and stood a much better chance at living a longer
life.

Others noted the shortened careers of top bodybuilders. The 1967 Mr. America Don Howorth considered a
comeback, but stated he knew his body would not do well with what he had to take at that stage of his life.
Even the genetically blessed Casey Viator who was a serious contender for the Mr. Olympia title, walked from
any more attempts in 1983 knowing that his body had had enough.

NEW DIETARY TRENDS

In the early 1980s, bodybuilders became interested in the glycemic index of carbohydrate foods. A team of
researchers at the University of Toronto, led by Dr. David Jenkins, demonstrated that different foods affected
blood glucose levels at different rates. They developed the Glycemic Index in which many carbohydrate foods
were measured against selected reference foods on how quickly they raised glucose levels.

Many bodybuilders and other athletes used the glycemic index to plan their daily menu and carbohydrate
selection. With the insurgence of carbs into the diet, along with a well-established reverence for protein,
bodybuilders discovered there wasn't much room left for fat. In fact, by the end of the decade, many found
themselves in a competition for who could get their dietary fat the lowest. Some even attempted a
theoretical zero fat diet.

But not everyone was taken in. I interviewed bodybuilder Ron Kosloff who said he didn't change a thing. "I
knew what I saw," he told me. "My grandparents lived on a farm and ate whole milk, cream, eggs, butter,
meat, potatoes and homemade bread. My grandfather often ate 6 eggs a day for years, many of them raw,
along with lard sandwiches. He lived to 98 while my grandmother lived to 101. What astounded me most was
their farmhand who went by the name of Indian Joe. When I first saw him he looked in his 40s and was
incredibly cut and muscular. He looked like Conan. I was shocked when I found out he was well into his 70s.
Indian Joe lived to 115 years of age and ate nothing but meat, glands and intestines!" Kosloff had consumed a
minimum of 6 eggs daily for the previous 20 years with no ill effects. Ron also noted that bodybuilders like
Gironda and Blair were warning him back in the late 60s of the real hazardous fats--hydrogenated oils!

Armand Tanny, now in his 60s, was also writing articles contradicting this new trend. All through the 1980s he
wrote articles for Joe Weider's Muscle and Fitness magazine such as: Caveman Diet (March 1986), Meat and
the Bodybuilder (Dec 1986), Good Nutrition and Sex (June 1987), Streamline Meat (Oct 1987), Uncooked
Delicacies (Dec 1986), and Those Beefs About Meat (Oct 1985).

In the midst of the cholesterol scare in 1984, Vince Gironda released his book Unleashing The Wild Physique,
still recommending 36 eggs a day to produce an anabolic effect. However, he also wrote an article defending
carbohydrates and warning of the potential risks of high protein consumption.

PUTTING THOSE CARBS TO WORK

A major trend in the 80s and 90s was the concept of carbohydrate loading, first popularized by Vince Gironda
back in the 50s and 60s. "I believe that every 3 to 5 days you need to get a ‘carbohydrate loading meal' into
your body

. . . I feel that carbohydrate is necessary every third or fifth day in order to get the glycogen back into the
liver."

Also back in the 1960s, cyclists were using a technique of loading their muscles with carbohydrates to give
themselves an endurance edge. Bodybuilders were also loading their muscles just before a competition to
give them a fuller look. Into the 1980s, the competitive bodybuilders had brought it into a science with their
knowledge of the hormones vasopressin and aldosterone and how they controlled the sodium/water balance
in the body. The challenge was to stand on stage on competition day with as much body fluid sucked into the
muscles with the carbohydrates and not under the skin. The effect of this technique was so dramatic that hit
or missed timing could represent a victory or looking terrible for bodybuilding standards. Often bodybuilders
would be banging their heads off the wall one to three days after a big show when all the fluids would shift
into the right places--too late!
 Similar diets followed including Cyclical Ketogenic Dieting (CKD) variously known as the "Ultimate Diet," the
"High-Fat Diet," the "Anabolic Diet," "Bodyopus," the "Metabolic Diet," "Anabolic Solution," and the
"Ultimate Diet 2.0."

Estrogen - Women & GHRH/GHRP-6

ESTROGEN

Well DHEA conversion to estrogen has a pronounced positive effect on GH.

But I wonder...if you have a big fat pad & are an older guy or even a younger guy with a hormonal profile
skewed toward "excess" estrogen already...whether DHEA will have a positive impact on GH production.

Conversely what happens when we reduce either estrogen or its ability to act...

AND which is more important in regard to negative impact on GH:

• the act of aromatization of testosterone to estradiol or

• absolute estrogen levels

Well that study I posted in post #492 found that the aromatization of testosterone to estradiol was important
and that tamoxifen at 20 mg/day for 3 weeks reduced GH by about 50%, GH pulse by about 40% and IGF-1 by
about 30%.

How about estrogen in general? ...lets look at estrogen supplementation (in females)

Well estrogen impairs the action of GH. Women are less responsive than men to GH treatment.

Oral estrogen especially inhibits GH's actions in dose-dependent fashion. However transdermal estrogen
administration seems to bypass some of the increases in body fat and reductions in lean mass often seen in
postmenopausal women given oral estrogen....so that mode of administration appears to minimize some of
the negative impact of GH.

Oral estrogen administration leads to a reduction in IGF-I levels despite any increase in GH levels (from
supplementation). The reason being that estrogen impairs the ability of GH to stimulate hepatic IGF-I
production because of its negative impact on the growth hormone receptor and signalling.

Estrogen inhibits GH activation of the JAK/STAT pathway. The inhibition is dose-dependent and results from
suppression of GH-induced JAK2 phosphorylation, leading to reduction in transcriptional activity. Estrogen
does not affect phosphatase activity but stimulates expression of SOCS-2, which in turn inhibits JAK2
activation. Thus, esotrogen inhibits GH receptor signalling by stimulating SOCS-2 expression. - Growth
hormone receptor modulators, Vita Birzniece & Akira Sata & Ken KY Ho, Rev Endocr Metab Disord So how
does estrogen effect the use of GHRH and GHRP-6 to effect release of GH?
 It seems that GHRP-6 (assume all GHRPs) induce a greater GH release response in the somatotrophs in the
presence of estrogen then GHRH. Estrogen administration markedly decreases GH release in response to
GHRH. *

So women should always include a GHRP (GHRP-6, GHRP-2, Hexarelin, Ipamorelin) in their therapy. GHRH
(mod GRF(1-29), Sermorelin, CJC-1295) by itself will be inhibited in its action on GH release by the sex
hormone estrogen.

• - Regulation of His-dTrp-Ala-Trp-dPhe-Lys-NH2 (GHRP-6)-lnduced GH Secretion in the Rat,Federico Malloa,

Neuroendocrinology 1993;57:247-256

THE EFFECTS GH AND INSULIN

"I hate people that are gurus because they usually don't know what the hell they are talking about. What I've
always tried to do is point to the science and let people "understand" things on there own.

My thread at PM contains a lot of knowledge about many things beyond just peptides including insulin.

So lets start first with the myth that GH & Insulin can not be used together. Do people even understand that
the GH ligand is only half of the equation? GH needs a receptor to bind to. Do they know how to increase GH-
receptors? How about increasing GH receptor expression.

Since I just now decided to toot my own horn ...toot toot... let me also say the same applies to testosterone.
There is a simple way to increase androgen receptors expression. No I'm not going into that... I just marvel at
the guys who are gurus that don't understand these simple things...

First a response from Dr. Crisler who addressed this doctor myth about separating insulin & GH. He was
responding to my post on how insulin effects GH-receptor expression.

Here is Dr. Crisler's response to my post which I will summarize afterwords:

• So much for the Anti-Aging Medicine doctors out there who tell their patients who take GH in the morning to
not eat until a couple hours after their shot.

Their reasoning (if you call it that LOL) is insulin blocks the IGF-1 receptor, even though the affinity for same is
2 to 3 orders of magnitude less (at appropriate serum concentrations) than it is for IGF-1.

Applying Farmer's Logic, how long would it be then since you last ate?

You need SOME insulin (but not too much), like it is for estrogen

The point is that doctors that perpetuate the "don't eat or increase insulin with GH" are wrong.

Dr. Crisler was responding to my post which discussed a study which focused on the need for insulin to
increase GH-receptors. In other words insulin increases GH-receptor synthesis. However at some point the
 amount of insulin that is administered begins to have a negative consequence. This negative consequence is
that higher amounts of insulin will start to inhibit the birth of those newly created GH-receptors.

So to summarize insulin increases the synthesis of GH-receptors which will be available to bind to the GH
ligands. This is good. At some point though high levels of insulin will stop those newly created receptors from
making their way to the cell surface. This is bad.

So I undertook to calculate the point where insulin would shift from being a positive to a negative. My
conclusion:

• Therefore the point at which the amount of insulin in plasma becomes a negative rather then a positive is
approximately 7.5 to 9 IUs.

So to arrive at a net benefit an insulin amount below that threshold point such as 5-6 ius is desirable.

All of this is only focusing on insulin's effect on increasing GH-receptors. Which is positive to a point and
negative beyond that point.

In addition Dr. Crisler underscores the point that insulin at moderate dose will not interfere with IGF-1
binding to a receptor.

What we didn't discuss was that IGF-1 is not synthesized straight away all at once by GH. Rather GH sets in
motion a chain of events that results in IGF-1 synthesis over a long period of time. Not minutes...but rather
hours even a day+. That is one reason why IGF-1 levels build up every day that you take GH until they plateau
about a week out.

So tell me how insulin use concurrent w/ GH can effect eventually binding of newly created IGF-1 to its
receptor.

If you follow that reasoning you should NEVER take insulin. The truth is you can take it together w/ GH or 30
minutes later or in between GH pulses.

Okay this is one thing that insulin does but there so many more things to that insulin does. Do people even
know what GH does by itself, what insulin does by itself, what all sorts of things do by themselves. How about
if you combine them?

I would copy my posts on this from PM but the formating is lost so I'll just post the links (it is formatted by me
to be highly readable & well worth the time to read by anyone who wants to truly understand):

The above post covers:

• Insulin
• Growth Hormone
• Amino Acid Pool
• Exercise
• Blood Flow
• IGF-1
• IGF-1/IGFBP-3
• Androgens
• Thyroid Hormones"

THE SCIENCE BEHIND: ‘SYNTHETINE – LIPID (FAT) TRANSPORTER’

Synthetine™ is an L-Carnitine based sterile preparation manufactured by a pharmaceutical company in

accordance with the highest level of manufacturing practices. Synthetine is a highly bioavailable form of L-
Carnitine that if used together with SyntheDextrin will activate a “switch” that will reduce carbohydrate
oxidation and increases fat oxidation in contracting muscle, reduce fatigue, reduce muscle glycolysis and
increase glycogen storage during periods that are almost always reserved for carbohydrate oxidation..

The science presented in this article is unique. It details a proven but little known protocol using Synthetine™
and SyntheDEXTRIN™ that immediately enables the regulation of muscle fuel selection in favor of utilizing
fats.

The focus of this article is an attempt to describe the science with enough detail so that the readers can
incorporate this knowledge into their own plans to advance their fitness and health goals. This article is not
about selling the aforementioned products. In the studies a highly bioavailable sterile L-Carnitine such as S
ynthetineâ„¢ was used repeatedly together with either insulin or high glycemic shake such as
SyntheDEXTRIN™ in the protocol that immediately activated the switch. However a second protocol is fully
described herein and it involves low bioavailable oral ingestion of L-Carnitine and high glycemic shake. This
second method is a slow build up process requiring daily use for 100 days to be fully active.

I make no apologies for the length of this article. I have kept the science understandable by introducing key
concepts before explaining their specific relevance to the focus of this article. I have included a table of
contents to make navigation easier.

During the 1990’s a substantial amount of research was undertaken which investigated the effects of L-
carnitine supplementation on exercise performance. The primary hope of the research was that increasing
carnitine availability in the body would lead to increased fat oxidation during prolonged exercise, spare
glycogen stores and, consequently delay the onset of fatigue as well as promote fat loss. Scientific interest in
L-carnitine as a performance enhancement and weight loss tool came to an end when it became apparent
that L-carnitine feeding does not alter fuel metabolism during exercise or, more importantly impact upon the
muscle carnitine pool in humans.

The scientific community for the most part abandoned further research. L-carnitine’s metabolic role had
been thoroughly mapped out and described in the literature. The typical carnivorous diet seemed to supply
sufficient carnitine. Carnitine supplementation proved to be of no additional benefit…it was simply excreted…
end of story.

Despite the failure of science, L-carnitine feeding as a tool to promote weight loss and improve exercise
performance became a multimillion dollar dietary supplement industry with no genuine benefit to the end
users.

Today our understanding of the transport mechanisms that permit cellular membrane penetration are much
more advanced. What was once a saturated transporter and an impermeable membrane are now elements
that are open to favorable manipulation, sometimes in surprisingly simple and physiologically obtainable
ways. The hopes and hypes of yesterday with the scientific approaches described herein are reborn anew.

Synopsis

This article summarizes in understandable language the elements of metabolism that are necessary to
appreciate both the mechanisms and conclusions arrived at through a series of studies published in very well
respected journals by a group of scientists I’ll label the “Stephens Group”. The group of four scientists,
headquartered at the “Centre for Integrated Systems Biology and Medicine” at Queen’s Medical Centre,
University of Nottingham in the United Kingdom examined carnitine’s importance as a regulator of skeletal
muscle fuel selection.

They came to the understanding that because carnitine is vitally involved in both fat metabolism and
carbohydrate metabolism in the cellular mitochondria (where energy production takes place) and because
the pool of available carnitine is restricted at that level, carnitine availability is “the switch” that toggles
between these two systems for energy creation.

There are periods of times when the use of glucose (derive from carbohydrates) as a fuel increases. This
occurs at high intensity exercise and when there is plenty of glucose available. When this occurs this
metabolic pathway calls upon carnitine within the mitochondria for use in the process and this takes away
from the carnitine that is available for fat metabolism. This results in a “switch away” from the use of fats for
fuel in favor of glucose.

The Stephens Group was able to fully describe this process and discover that there exists a “switch back”
which reduces glucose metabolism and increases fat metabolism even during those periods of time (high
intensity exercise, carbohydrate intake and preference for glycolysis) that normally demand otherwise.

In essence they discovered that increasing skeletal muscle carnitine above a threshold inhibited carbohydrate
oxidation.

They then moved forward and also discovered that increasing skeletal muscle carnitine above a threshold
also increased fat oxidation.
Having identified this “switching mechanism” they then discovered that increasing muscle carnitine content
in healthy humans at rest reduced glycolysis, increased glycogen storage and increased fat oxidation.

They then came to the understanding that increasing muscle carnitine content alleviated the decline in fat
oxidation rates during high intensity exercise and reduced muscle glycogen utilization. They were able to
reference in vitro (out of body) studies that reported that increasing muscle carnitine substantially delayed
the onset of fatigue.

Having established the “switching” mechanism and its potential positive benefits they then set about
discovering a method for increasing carnitine in muscle. It is important to remember that this had never been
accomplished before.

Their studies discovered two protocols. One protocol resulted in an immediate and rapid increase in muscle
carnitine levels to the switching threshold. This protocol involved a highly bioavailable method that increased
the influx of carnitine into muscle cells. The second protocol involved a slower day to day build up of
carnitine levels and took 100 days to arrive at the switching threshold. This protocol involved lower
bioavailability but more convenient methods.

The first protocol might be considered by bodybuilders, athletes and fitness enthusiasts while the second
might be better suited for the public at large. Introduction to Fat Oxidation

To sustain life the production of energy is required. This process necessitates the acquisition & concurrent
use of both oxygen and a fuel source. Fuel sources are available from either consumption of carbohydrates,
fats, and rarely proteins or the release of stored fuels from within the body. The ingestion of dietary fat is an
initial energy acquisition process called consumption while the process called oxidation is the final step of
conversion into human energy. Between the initial process of consumption and the final step of conversion
are the processes of storage and eventual release for conversion into energy.

Whether the middle processes of fat storage or fat release are activated depends primarily on the state of
energy balance at any point in time. If there is a surplus of fuel sources from ingested carbohydrates or fats
then fat will not be released from storage in fat cells in appreciable quantities and the body will use its
preferred source of energy carbohydrates followed by newly ingested fats to meet its energy requirements.

When there is a surplus of energy from consumption (i.e. eating outpaces physical activity) the human body
will not readily convert excess carbohydrates into fat stores but will use them for energy. Carbohydrate
ingestion does not always lead to increased fat stores but may do so by being excessive and by crowding out
concurrently ingested fats’ potential to be utilized as energy. As a result ingested fats during periods of
surplus energy consumption will generally be stored in fat cells.

Ingested fats are broken down and converted into free fatty acids, which are then stored in fat cells in a form
known as triglycerides where they remain as potential energy units until called for by negative energy states.
When energy balance is in a deficit (i.e. physical activity outpaces eating) fat oxidation will increase. In order
for this final step of oxidative conversion into human energy to occur the middle step of release of fat stores
(triglycerides) must take place. This process will result in loss of fat mass.

Various hormones will trigger the release of the triglycerides from fat cells. These triglycerides, through a
process labeled lipolysis are broken down into two compounds and released into the bloodstream. The first
compound glycerol is primarily converted to glucose by the liver and provides energy for cellular metabolism.
The second compound fatty acids are transported to the mitochondria, the portion of a cell that produces
energy within each cell.

This is the stage where carnitine plays an essential role in fatty acid oxidation. It is not possible for the newly
liberated fatty acids to penetrate the mitochondria membrane and enter the mitochondria without the help
of carnitine which acts as a transport mechanism.

In general, carnitine transports long-chain acyl groups from fatty acids into the mitochondria where they are
broken down through beta-oxidation in a process that ends up creating adenosine triphosphate (ATP), the
energy-producing fuel.

The research studies have examined the possibility that greater amounts of fatty acids could be oxidized if
carnitine levels were elevated through supplements. Carnitine increases via supplementation were
determined to have no effect on fatty acid oxidization.

It is important to note that what I have described concerning energy balance and fat storage versus release is
a generalized net (or overall) effect. Fat is constantly being stored in and released from fat cells no matter
what the current energy state however the overall net effect very much depends on the state of energy
balance, or as is the focus of this paper L-carnitine can be made to oxidize fat even in the presence of a
positive energy balance.

Summary of the two roles played by Carnitine

In order to understand the relevant conclusions drawn from the Stephens Group’s research detailed from
their studies herein it is necessary to understand a few elementary essentials concerning carnitine’s role in
skeletal muscle fuel metabolism and briefly mention the “competing” metabolic pathway and a second
function of carnitine, which is to act as a buffer during carbohydrate metabolism. When free carnitine is
engaged in its role as a buffering agent for carbohydrate metabolism long-chain fatty acid oxidation
diminishes.

Role 1: Energy Pathway “Fatty acid transport/oxidation” – Two pools of carnitine transport

The Mitochondria (the intra-cellular area where oxidation and energy production occurs) membrane is
impermeable to fatty acyl-CoA (i.e. the long-chain fatty acid liberated from fat cells bonded to an enzyme
named coenzyme A (CoA).) But this is not true if it is bound to carnitine. Carnitine enables the fatty acid to
penetrate the membrane and it does so by binding to it and forming acylcarnitine.

However there are two separate pools of carnitine that need to be utilized to move fatty acids into the
mitochondria. One pool located outside of the mitochondria membrane and one pool located inside the
mitochondria matrix. The one outside the mitochondria is the one that binds to fatty acids and transports
them through the first of 2 layers that make up the membrane and up to the 2nd inner layer but not through
the mitochondria membrane. The pool of carnitine inside the mitochondria is known as “intra-mitochondria
free carnitine”. It moves to the membrane from the inside and is “handed” the fatty acyl-CoA that was
delivered “to the door” by outside carnitine. The handing over process is mediated by an enzyme called
Carnitine palmitoyltransferase I (CPT1) which resides on the 2nd layer of the membrane. We don’t need to
introduce all the various proteins and enzymes involved in the process. Simply understand that CPT1 is akin
to a bouncer at a nightclub who takes a note from someone outside the doorway and gives it to someone
inside the doorway.

In this way two carnitines (one from outside & one from inside the mitochondria) do the work of transporting
the fatty acyl-CoA.

Inside the mitochondria matrix the newly formed acylcarnitine (thanks to the hand off) is reduced back to
two individual components: free carnitine and the long chain fatty acyl-CoA.

So in summary the fatty acyl-CoA thanks to two carnitines has been transported into the mitochondria where
it will be oxidixed and cleaved of the coenzyme A (CoA) which will take two carbon atoms with it. This process
is known as beta-oxidation and results in acetyl-CoA (note: acyl goes in but acetyl comes out).

Acetyl-CoA enters the TCA Cycle (ie. citric acid cycle — also known as the Krebs cycle) where energy is
produced (i.e. ATP is synthesized).

Role 2: Competing Energy Pathyway “Glycolysis” and Carnitine Buffer

While the aforementioned metabolic pathway oxidizes fats and is the route for fatty acid metabolism, the
glycolysis pathway is the carbohydrate metabolic pathway. Glycolysis is the metabolic pathway that converts
glucose into pyruvate.

This is accomplished in the Pyruvate dehydrogenase complex (PDC) which is a complex of three enzymes that
transform pyruvate into acetyl-CoA through a process called pyruvate decarboxylation.

Acetyl-CoA is the same end product arrived at through the fat oxidation pathway and is also “fed to the fire”
to produce energy.

Acetyl-CoA enters the TCA Cycle (ie. citric acid cycle — also known as the Krebs cycle) where energy is
produced (i.e. ATP is synthesized).
Under certain circumstances PDC (Pyruvate dehydrogenase complex) activity greatly increases and makes
acetyl-CoA at a rate faster then the TCA cycle can consume. At that point free carnitine inside the
mitochondria acts as a buffer and binds to excess acetyl from acetyl-CoA and removes it or holds it as a
reservoir. This is carnitine’s other function, the removal of excess acetyl groups thereby ensuring a sufficient
pool of CoA for the continuation of PDC and TCA cycle reactions.

So increased PDC activity can lead to down-regulation of long-chain fatty acid oxidation because it makes use
of carnitine in its second role as a buffer, leaving less carnitine available to act in its role as transporter.

At the beginning of high intensity exercise (but not low intensity) skeletal muscle free carnitine content is
reduced by 75% as a result of it acting as a buffer. This occurs to a greater extent in Type I muscle fibers.

Skeletal muscle free carnitine content is also reduced during moderate intensity exercise when muscle
glycogen content is elevated.

Increased PDC activity whether it is brought about by high intensity exercise or carbohydrate metabolism
results in more carnitine acting as a buffer which reduces its availability to transport fatty acid and thus long-
chain fatty acid oxidation rates go down.

The Switch

Turning down the rate of fat oxidation

Reducing the muscle free carnitine pool during conditions of high PDC flux limits the ability of CPT1 (the
mediator enzyme “bouncer at the door”) to transport long-chain acyl-CoA into the mitochondrial matrix and
thus the rate of fat oxidation.

Support for this understanding is well established and not limited to the Stephens Group’s research. Van
Loon et al. (2001) demonstrated that a 35% decrease in the rate of long-chain fatty oxidation that occurred at
an exercise intensity above 75% VO2 max,was paralleled by a 65% decline in skeletal muscle free carnitine
content.

Roepstorff et al. (2005) showed a 2.5-fold decrease in the rate of fat oxidation, compared to control, during
moderate intensity exercise (65% of VO2 max) when free carnitine availability was reduced by 50% as a result
of pyruvate, and therefore acetyl-CoA, production being increased as a result of pre-exercise muscle glycogen
content being elevated.

Further support for the understanding that free carnitine availability may limit fat oxidation comes from
Achten & Jeukendrup, (2004). Muscle free carnitine content has been shown to decrease from approximately
11 to below 5.5mmol (kg dm)-1 between the exercise intensities of 60 and 80% of VO2 max, and it has been
calculated that maximal and minimal fat oxidation rates during exercise are achieved at exercise intensities of
around 65% and greater than 80% of VO2 max, respectively.
Reversing the Switch – Turning up the rate of fat oxidation & turning down the rate of carbohydrate
oxidation

Putmanet al. (1993) supply evidence by demonstrating that during bicycle exercise at 75% of VO2 max to
exhaustion, both muscle free carnitine content and fat oxidation rates were markedly higher when pre-
exercise muscle glycogen content was lowered compared to control.

In one of the Stephens Group’s studies they found that a 15% increase in skeletal muscle carnitine content…
resulted in a 30% decrease in muscle PDC activity and a 40% decrease in muscle lactate content, leading
them to conclude “These results suggest that an acute increase in human skeletal muscle total carnitine
content results in an inhibition of carbohydrate oxidation in conditions of high carbohydrate availability, due
to a carnitine-mediated increase in fat oxidation.”

As an explanation

Philip Randle in the 1960s undertook a series of landmark and controversial studies detailing the workings of
the balance between fatty acid oxidation and glucose oxidation in what he called the glucose–fatty acid
cycle (Randle et al. 1963, 1964; Garland et al. 1963; Garland & Randle, 1963). Therein he laid down the
fundamental concept of reciprocal substrate competition between glucose and non-esterified fatty acids (the
major fuels that are oxidized to provide ATP in mammals) in normal physiology in muscle.

In describing the competition between glucose oxidation and fatty acid oxidation he specified that an
increase in beta-oxidation would result in an elevation of muscle acetyl-CoA concentration and,
consequently, an increase in muscle citrate and glucose-6-phosphate content. This, in turn, would result in
the down-regulation of carbohydrate flux [activity], due to product inhibition of PDC, phosphofructokinase
and hexokinase, respectively.

The Stephens Group acknowledge Randle’s important work in their elaboration of the results of their own
study stating “In support of [Randle’s description] muscle long-chain acyl-CoA content returned to basal
overnight during the L-carnitine infusion visit (whereas it remained suppressed during the control visit),
which suggests that Beta-oxidation was indeed increased…while there was a 30% decrease in muscle PDC
activity”

Athletic Performance, fatigue & the first few seconds of muscle contraction

It is well established that there is a lag in oxidative ATP delivery at the onset of exercise and muscular
contraction. This is attributable to a lag in mitochondrial ATP production brought about by a lag in PDC
activity which results in an insufficient acetyl-CoA supply to match the demands of the TCA cycle (Krebs cycle
– energy producing). The fuel supply is lacking at that moment in time.

According to a study by Roberts et al. (2002) a lag in acetyl group provision (predominately in the form of
acetylcarnitine) occurs during the initial 20 seconds of contraction. Remember acetylcarnitine is created as a
result of its role as a buffer during high PDC activity and held as an acetyl reserve. If PDC activity is not high
enough at the start of contraction there will be very little acetyl group available to feed the cycle that
produces energy (ATP).

So at the onset of contraction there is a lack of fuel in the form of acetyl groups.

“This is a rate-limiting step in the rate of rise in mitochondrial ATP re-synthesis in skeletal muscle at the onset
of exercise, which in turn will dictate the magnitude of oxygen-independent ATP delivery, and thereby the
rate of fatigue development during intense exercise.” – Stephens Group

This can be overcome by “priming” through manipulating muscle carnitine pools at rest so as to make
available sufficient energy substrate and by activating the PDC prior to the event by warming up before
intense exercise.

The Stephens Group Research: Summary of Findings

How to increase muscle carnitine

Plasma carnitine is not specifically lacking The transport mechanism and membrane gradient for carnitine
flow into muscle cells are restrictive Increasing the amount of carnitine is of no value in and of itself
Increasing the transport mechanism/membrane gradient + the amount of carnitine = increase in muscle
carnitine The methodolgy for increasing flow of carnitine in to cells is via changing the membrane
permeability to allow more carnitine transport Methodology

Insulin is a method for effecting this increased flow Intravenously administered L-carnitine + insulin =
increased carnitine in muscle cells There is a threshold concentration for the stimulatory effect of insulin on
skeletal muscle accumulation blunts PDC activity (carbohydrate oxidation) reduces muscle lactate content
increases glycogen content in muscle (i.e reduces oxidation of glucose in favor of storage) reduces muscle
glycolysis increases fat oxidation Results: Using this methodology carnitine content increases by 13% to 15%
and:

Alternative Methodology

For the reason that the determined insulin threshold is low enough to be reached via non-pharmacological
methods, oral ingestion of glucose may be used. For the reason that the carnitine turnover rate in skeletal
muscle is low (190 +/- 20 hours) daily carnitine increases will result in a continued build up of total muscle
carnitine. This allows the use of low bioavailable methods such as daily ingestion of oral carnitine w/ glucose
load to increase carnitine in muscle at an incremental rate such that within 100 days carnitine content will
have increased by 10%. blunt PDC activity (carbohydrate oxidation) reduce muscle lactate content increase
glycogen content in muscle (i.e. reduce oxidation of glucose in favor of storage) reduce muscle glycolysis
increase fat oxidation Results: This amount of carnitine is sufficient to:
How do you increase carnitine in muscle?

Studies have consistently failed to increase skeletal muscle carnitine content either through oral
supplementation or intravenous L-carnitine administration. Watcher et al (2002) fed 2 grams of L-carnitine
twice a day for 3 months to normal people and failed. Similar studies by Barnet et al. (1994) and Vulkovich et
al. (1994) demonstrated similar failures with oral feedings of l-carnitine for 3 months.

Intravenous infusion of L-carnitine for up to 5 hours similarly failed to have any effect on muscular carnitine
content (Brass et al. (1994); (Stephens Group, Insulin stimulates… (2006)).

How carnitine is normally transported into the cell

The reason for these failures is very simple. Normal people have no deficiency in circulating plasma levels of
carnitine. What they have is a fully saturated transport mechanism. No amount of carnitine load is sufficient
without a concurrent increase in the ability of the transport mechanism to transport carnitine across the
cellular membrane.

The cellular membrane is a lipid bilayer easily permeable to water molecules and a few other small,
uncharged, molecules such as oxygen and carbon dioxide but little else. The cellular membrane is not
permeable to ions such as K+, Na+.

In the normal course of things molecules and ions move about spontaneously down what is known as their
concentration gradient (i.e., from a region of higher to a region of lower concentration) by diffusion.

Molecules and ions are capable of moving against their concentration gradient, but this process requires a
process known as active transport.

It is the active transport that is lacking in regard to carnitine movement and unless this is changed additional
carnitine will not be allowed to enter the cell.

Active transport is the pumping of molecules or ions through a membrane against their concentration
gradient. It requires: a transmembrane protein (usually a complex of them) called a transporter and energy.
The source of this energy is ATP.

The transmembrane protein responsible for carnitine transport into skeletal muscle is OCTN2. The half-
saturation concentration of L-carnitine uptake by OCTN2 is 4.34 umols (Tamai et al. (1998)). In the normal
state skeletal muscle carnitine uptake is saturated since plasma total carnitine concentration is 50 umols.

OCTN2 has a high affinity for carnitine and sodium ions (Na+) and readily binds to both and so carnitine is
transported into skeletal muscle against a substantial concentration gradient via a transport process involving
sodium Na+ flow. In essence carnitine hitches a ride on OCTN2 which hitches a ride on Na+.
A detailed description of this process is beyond the scope of this article so a general reduction will suffice.
One method of direct active transport across the cellular membrane is the Na+/K+ ATPase pump.

The concentration of potassium ions (K+) is as much as 20 times higher inside the cell then outside.
Conversely, the fluid outside the cell contains a concentration of sodium ions (Na+) as much as 10 times
greater than that within the cell. Because of this difference a concentration gradient amenable to flow exists
and the Na+/K+ ATPase pump effects the transfer of these two ions pushing out 3 Na+ ions for every 2 K+
ions pumped back into the cell. This activity establishes a net charge across the plasma membrane with the
interior of the cell being negatively charged with respect to the exterior.

So with this basic understanding that OCTN2 is a cotransporter of sodium & carnitine and that under normal
conditions it is fully saturated and thus unable to benefit further carnitine inflow via Na+/K+ ATPase pump
activity, lets examine how insulin overcomes this equilibrium and brings about an increased inflow of
carnitine into skeletal muscle.

How insulin increases the flow of carnitine into muscle

The Na+ dependent, active transport of carnitine into human skeletal muscle is mediated via a high-affinity,
transporter OCTN2.

The Stephens Group found that the combination of increased carnitine and increased insulin (above a
threshold) increased skeletal muscle OCTN2 mRNA expression by 2.3 fold (Stephens Group, Insulin
stimulates… (2006)) in addition to increasing the activity of Na+/K+ ATPase pump. This results in an increased
availability of transporter which potentially increases the amount of carnitine that may be carried into the
muscle cell.

The action of insulin however is most important in changing the membrane permeability in favor of carnitine
inflow.

It has been demonstrated that the Na+ dependent uptake of other nutrients into skeletal muscle is increased
by insulin, for example amino acids (Zorzano et al. 2000) and creatine (Green et al. 1996; Steenge et al. 1998).

Insulin is able to increase the flow of carnitine into skeletal muscle as follows.

Insulin increases Na+/K+ ATPase pump activity by increasing translocation (or movement) of alpha2 and
beta1 pump subunits from an intracellular storage site to the plasma membrane (Sweeney & Klip, 1998), and
through an increase in the sensitivity of the Na+/K+ ATPase pump to intracellular Na+ (Clausen, 1986, 2003;
Ewart & Klip, 1995).

OCTN2 has equal affinity for sodium ion (Na+) and carnitine and bonds to both. With an increased Na+/K+
ATPase pump activity brought about by an increase in circulating insulin concentration intracellular Na+
concentration is lowered which increases the electrochemical gradient for Na+ and therefore increases
Na+/carnitine cotransport.

This results in an increase of carnitine inside the muscle cell.

Methodology and results

The Stephens Group undertook a series of experiments building on each to create an overall understanding.
In Insulin stimulates L-carnitine accumulation in human skeletal muscle, they were able to increase muscle
total carnitine content by 13%. They achieved this by using what I will call an “overkill amount of L-carnitine”
administered by infusion. They administered a 15mg/kg bolus w/in the 1st 10 minutes rapidly achieving a
supraphysiological plasma concentration of about 500 umol/L. This was followed by 10mg/kg infused over
the next 290 minutes to maintain hypercarnitinemia.

In addition they infused insulin at a dose I will call an “overkill amount”. The aim of study was to determine
whether insulin could increase Na+/dependent skeletal muscle carnitine up-take in healthy human subjects
as a result of increasing Na+/K+ ATPase pump activity. They were very much successful. The positive results
of the study are incorporated in the previous section.

Using an identical protocol and intravenous L-carnitine & insulin amounts they undertook another study
reported in An Acute Increase in Skeletal Muscle Carnitine Content Alters Fuel Metabolism in Resting Human
Skeletal Muscle with the broader aim of determining the effect that an increase in skeletal muscle carnitine
content would have on the integration of muscle fat and carbohydrate oxidation during and after hyper-
insulinemia.

As in the previous study total carnitine content increased in skeletal muscle, this time by 15%.

This resulted in a 30% decrease in muscle PDC activity (carbohydrate metabolism) and a 40% decrease in
muscle lactate content. After an overnight fast, muscle glycogen and LCA-CoA (long-chain acyl-CoA) content
had increased by 30% and 40% respectively, in the carnitine group compared with control. The difference
between the control and carnitine visits was not attributable to a difference in the amount of carbohydrate
administered.

“Taken together, these findings lead us to conclude that the increase in muscle carnitine content observed in
the present study inhibited glycolytic flux (decrease in lactate) and carbohydrate oxidation at the level of the
PDC, thereby diverting muscle glucose uptake toward glycogen storage (nonoxidative glucose disposal).”

“The reciprocal relationship between carbohydrate and fat oxidation in skeletal muscle would suggest that
the apparent decrease in carbohydrate flux observed was the result of, or resulted in, an increase in fat
oxidation. Thus, these findings could be of major importance in the treatment of insulin-resistant states, such
as obesity and type 2 diabetes, because both conditions are associated with an impaired ability of skeletal
muscle to oxidize fatty acids, both at rest and during exercise. Furthermore, reducing or preventing
intramuscular lipid accumulation increases insulin sensitivity.”

The implications of these results should be clear and having read the previous portions of this article and
examined the figures, self-explanatory. To reiterate the decrease in PDC activity indicates a substantial drop
in carbohydrate metabolism, while the decrease in muscle lactate indicates a decrease in glycolysis activity.
The increase in muscle glycogen storage given the constants of the study indicate that glucose was
preferentially stored not metabolized. This also indicates that existing muscle glycogen stores where
enhanced rather then drawn upon.

The reciprocal relationship between carbohydrate oxidation and fat oxidation indicates that fuel sources
utilized for energy where fats.

The meaning of the one item that may not be readily apparent is that of LCA-CoA (long-chain acyl-CoA)
increasing overnight. Remember from the early discussion in this article that carnitine transports long-chain
acyl groups from fatty acids into the mitochondria where they are broken down through beta-oxidation. The
fact that these groups had increased strongly indicated that carnitine is increasing its activity as a transporter
in fatty acid oxidation and that fatty acid oxidation is increased.

In the words of the Stephens Group in an overall review of their work:

“…the apparent reduction in glycolytic flux and carbohydrate oxidation… (decreased PDC activity and lactate
content, and increased glycogen accumulation), in the face of high carbohydrate availability, could have been
caused by a carnitine-mediated increase in skeletal muscle long-chain fatty acid oxidation, i.e. an increase in
long-chain acyl-CoA translocation into the mitochondrial matrix via CPT1, resulting in an increase in beta-
oxidation.

According to Randle’s glucose–fatty acid cycle (Randle et al. 1963, 1964; Garland et al. 1963; Garland &
Randle, 1963), a concept proposed in the 1960s from experiments involving rat heart and diaphragm muscle,
an increase in beta-oxidation would result in an elevation of muscle acetyl-CoA concentration and,
consequently, an increase in muscle citrate and glucose-6-phosphate content. This, in turn, would result in
the down-regulation of carbohydrate flux, due to product inhibition of PDC….

Indeed, the decrease in PDC activity observed in our study was paralleled by a reduction in muscle lactate
content and resulted in an accumulation of muscle glycogen overnight, conditions which are both consistent
with the premise that glycolytic flux, and therefore carbohydrate oxidation, was inhibited. In support of this…
muscle long-chain acyl-CoA content returned to basal overnight during the l-carnitine infusion visit (whereas
it remained suppressed during the control visit), which suggests that beta-oxidation was indeed increased.”

Alternative Methodology

Obtaining a lower insulin threshold

In an attempt to discover the lowest amount of insulin needed to drive carnitine into muscle and activate the
switch from carbohydrate oxidation to fatty acid oxidation, the Stephens Group undertook a study the
reports of which are discussed in A threshold exists for the stimulatory effect of insulin on plasma L-carnitine
clearance in humans.

They reasoned that while their previous studies with insulin infusion in an amount in the upper physiological
range were successful, it would be difficult to achieve by dietary means alone.

They discovered that administered insulin will not stimulate muscle carnitine retention unless a serum insulin
concentration greater than 90 mU/l is achieved during hypercarnitinemia. This level was substantially lower
(and obtainable via dietary means) then the previous high concentrations used and stimulated muscle
carnitine transport to a similar degree.

Extrapolating from data, skeletal muscle total carnitine content in this study with this threshold insulin
amount would have been increased by about 10%.

Orally ingesting lower bioavailable L-carnitine together with high glycemic index carbohydrates

The Stephens Group in a study the results of which are reported in Carbohydrate ingestion augments L-
carnitine retention in humans, investigated whether physiologically significant increases in skeletal muscle
carnitine content can be achieved through the use of L-carnitine feeding in conjunction with a dietary-
induced elevation in circulating insulin.

They examined serum insulin levels achieved from glucose ingestion, the plasma total carnitine level and the
urinary total carnitine excretion levels in order to determine the amount of carnitine taken up in muscle by
performing both a one day study and a 14 day study.

Both studies used oral ingestion of:

4.5 g L-carnitine L-tartrate (3 g L-carnitine) dissolved in 200 ml of water

followed by

94 g of simple sugars (CHO) either ingested twice at 1 hour & 4 hours after L-carnitine ingestion as in the 14
day study or as in the one day study four time across a 5 hour period.

Serum insulin concentrations during the period when simple sugars were ingested are graphed below.
Surprisingly peak serum insulin concentrations of about 70mU/l proved to be sufficient.

The graph below indicates that the rise in insulin eliminated carnitine from plasma. The control subjects had
more carnitine in plasma then those on the protocol. See below.

If the carnitine is not in plasma is it excreted? The graph below indicates that urinary excretion rates were
lower over the measured 14 days in those following the protocol. See below.
“We suggest, therefore, that the lowering of plasma total carnitine (TC) concentration occurring immediately
following CHO ingestion, and the lower urinary TC excretion during the CHO visit, collectively indicate that an
increase in whole body carnitine retention occurred when L-carnitine feeding was accompanied by CHO
ingestion. Given that skeletal muscle is the major site of carnitine storage within the body, and that
maintaining hypercarnitinemia for 5h in the presence of hyperinsulinemia increases skeletal muscle TC
accumulation (other Stephens Group studies), it is not unreasonable to suggest that this greater retention
occurred mainly in this tissue.”

Extrapolating an accumulation strategy

Given that the increase in muscle carnitine content following a single dose, or 2 weeks, of L-carnitine feeding
in the presence of elevated circulating insulin is likely to be small due to the poor bioavailability of orally
administered L-carnitine (less then 20%), muscle carnitine accumulation was estimated indirectly from
measurements of plasma and urinary carnitine concentration.

In this study 3 grams of carnitine results in at most 560 mg of absorbable plasma carnitine.

“Assuming all absorbed carnitine was either taken up into skeletal muscle tissue or excreted in the urine, it
can be calculated that L-carnitine feeding in conjunction with CHO ingestion would have increased skeletal
muscle total carnitine concentration by a further 0.1% (i.e., 60 mg) compared with L-carnitine ingestion
alone.”

In fact “urinary total carnitine excretion was on average 70 mg/day lower in the CHO group over the 14 days
of study. Consequently, if maintaining a daily L-carnitine feeding regime with CHO has an additive effect on
muscle carnitine content, L-carnitine feeding for 100 days could increase muscle carnitine content by an
additional 10%, which we believe could have a significant metabolic impact in contracting skeletal muscle.”

In the other comprehensive Stephens Group study they found that muscle total carnitine content was not
reduced 24 h after a 15% increase, suggesting that a daily increase in muscle carnitine content can be
maintained. In addition release of carnitine from skeletal muscle is a slow process, with skeletal muscle
carnitine turnover time of 190 +/- 20 hours (Rebouche (1984)).

“Taken together with the maintained effect on whole body total carnitine retention observed in the 14 day
study, these findings would suggest that daily L-carnitine and carbohydrate administration could well have an
additive effect on skeletal muscle total carnitine accumulation. Importantly, if L-carnitine supplementation is
to be used as a tool to modify skeletal muscle energy metabolism, the findings in the 14 day study also
suggest that, at most, only two 500-ml CHO drinks (2 x 94 g CHO) are required to achieve the effect on L-
carnitine retention.”

In conclusion:
“…muscle free carnitine availability becomes limiting to carnitine palmitoyltransferase I (CPT1) at a
concentration of about 6 mmol/kg dry muscle….

Thus, assuming the average 70 mg/day retention in the present studies resided within skeletal muscle and
that daily L-carnitine/carbohydrate feeding for 100 days would have an additive effect, then muscle carnitine
content would increase by about 2 mmol/kg dry muscle, which could alleviate the decline in fat oxidation
rates routinely observed at exercise intensities above 70% VO2 max, which could be of major relevance to
exercise performance due to the sparing of muscle glycogen.

In line with this theory, increasing skeletal muscle carnitine availability has been reported to delay fatigue
development by 25% in rat soleus muscle strips in vitro (Brass (1993)).”

Further more it is worth reiterating that the Stephens Group has demonstrated in the study involving
intravenous L-carnitine administration that a 15% increase in skeletal muscle carnitine content, achieved
during hyperinsulinemia, resulted in a 30% decrease in muscle PDC activity and 40% decrease in muscle
lactate content compared with control. Furthermore, following an overnight fast, muscle glycogen and long-
chain acyl-CoA content was 30% and 40% greater than control, respectively, despite carbohydrate
administration over the previous 24 hours being exactly the same.

This is the first study to demonstrate that the retention of orally supplemented L-carnitine can be increased if
accompanied by carbohydrate ingestion and that this retention is likely to reside in skeletal muscle, because
insulin is known to stimulate muscle total carnitine accumulation. “These findings could have a significant
effect on the integration of fat and carbohydrate oxidation in contracting skeletal muscle.”

Final Note

An immediate threshold amount of increase in muscle carnitine concentration can be had with
administration of highly bioavailable Synthetine™ (sterile L-Carnitine) with insulin or oral ingestion of two
high glycemic index drinks such as SyntheDEXTRIN™ (Maltodextrin Pure Carbohydrate).

An accumulation strategy of daily oral ingestion of low bioavailable l-carnitine with oral ingestion of two high
glycemic index drinks such as SyntheDEXTRIN™ (Maltodextrin Pure Carbohydrate) will lead to a threshold
amount of muscle carnitine concentration within 100 days.

These strategies should enable reversing the switch – Turning up the rate of fat oxidation & turning down the
rate of carbohydrate oxidation.

THE SCIENCE BEHIND: ‘SYNTHEROL – SITE ENHANCING OIL’

Syntherol™ is a caprylic acid based proprietary formulated sterile site enhancement oil. It is manufactured by
a major pharmaceutical company in accordance with the highest level of manufacturing practices. No other
seller of site enhancement oil can guarantee that the product they sell is sanitary, hygienic, bottled and
sealed under pharmaceutical conditions that assure the health and wellbeing of the end user..

Syntherol™ is a proprietary formula whose constituent parts do not deviate from that which is necessary to
effect muscular change as described in the science summarized herein. As a result Syntherol™ is highly
effective.

No other site enhancement oil currently available can claim to be both pharmaceutically sterile and
scientifically effective.

What follows is a summary of the science that makes Syntherol™ a muscle building agent and the basic
protocol developed by IFBB Pro Big A in regard to applying Syntherol™. What is Fascia?

The fascia is not extremely well studied. It is basically a three-dimensional matrix of tissue which may be
thought of as both a body casing or sheath (think about a tight rubber body suit) and a separate deeper
tissue which penetrates muscle and is attached to muscle via septa (or offshoots).

Fascia seems to function as a way to transmit applied force information from one muscle grouping to the
next. Fascia also seems to function as a method by which the force generated by load is applied to muscle
fiber and reduced in bone.

When a muscular contraction occurs fascia or rather fascicle (a fascia bundle of muscle fibers) curves. The
greater the contraction the greater the curvature. When this curving takes place pressure is produced on the
concave side. Curving of the fascicle increases intramuscular pressure and therefore affects blood flow. In
addition fascicle curving reduces the force transmitted to the bone.

So a contracted muscle which bulges can be understood to have increased pressure inward.

There really are two distinct classes of fascia. The superficial fascia (the body wrap) is connected to the
dermis and the upper torso is enveloped in this tissue from the pectorals to the rib cage area & stomach, up
under the lats, from the pectorals up over the delts and down the arms.

This body sheath is capable of transmitting information to various parts of the body concerning the amount
of pressure that is occurring on other regions of the body as a result of force generation.

The second class of fascia is specific to the region and yet this deeper tissue also connects to other regions as
described above and transmits force/pressure data. The pectoral fascia is firmly connected to the underlying
muscle by many intramuscular septa, which originate from the inner surface of the fascia and penetrate
between the muscular fibers, dividing the muscle itself into many bundles.

Pectoral fascia thickness varies greatly between people. The lower pectoral fascia is thicker then the upper
with the upper pectorial region averaging .49mm in thickness and the lower averaging .60mm in thickness.
There is a significant deviation from these averages in both the thickness & pliability among individuals. One
study found lower pectoral fascia thickness varied from a high of .99mm to a low of .24mm.

So from this brief summary we can understand that:

There is a wide variability in fascia thickness and this in part can explain the difference in fullness of muscle
bellies between individuals that lift weights. We can visualize that application of oil will apply pressure to the
fascia as it creates curvature even at rest.

We can further visualize that application of oil will increase pressure in the region and as a result increase
blood flow.

Consequently if you follow weightlifting lifting techniques that maximize the generation of peak force on a
targeted muscle you will also be creating additional maximum pressure inside the muscle worked.

Below are three images showing the superficial fascia (the body wrap); the pectoral fascia; and an image
demonstrating how fascia coordinates balance and contraction between the two pectoral sides.

Autopsy of superficial fascia pectoral fascia

Coordinated force transmission across fascia

References:

The pectoral fascia: Anatomical and histological study, Antonio Stecco, Journal of Bodywork and Movement
Therapy (2008)

In vivo determination of fascicle curvature in contracting human skeletal muscles, Tadashi Muramatsu, J Appl
Physiol 92:129-134, 2002

Anatomy and Clinical Significance of Pectoral Fascia, Lin Jinde, M.D., American Society of Plastic Surgeons
Volume 118, Number 7 Pectoral Fascia

Fascia Stretching

Therapists utilize deep and painful tissue manipulation techniques to loosen up stiff fascia, which can impinge
certain areas. They call their techniques myofascial release.

In the world of bodybuilding John Parrillo may have been the first one to use the term “fascial stretching.” He
developed a technique which basically involved pumping the muscle with blood to engorge it, followed by
extreme and painful stretching of the engorged muscle and then a pose to you cramp style of holding the
engorged muscle in a contraction. He even went so far as to create and sell fascia stretch machines.

Tom Platz appears to be one of the earliest practitioners of this technique. He would use the entire weight
stack of the old school leg extension machine (where you could lay flat if you wanted) and he would pump
out as many full and then partial reps as he could followed by assisted reps. Then he would immediately get
on the floor on his knees and lay back grimacing in pain and he would hold this deep stretch. Then do it
again…

The problem with this technique, although beneficial, is that the pressure which is being applied to curvature
of the fascia is short lived albeit intense.

It is likely that fascia will become more pliable (it is simply layers of collagen and elastin in a water-based
matrix) the longer it is held in a curved position. This is the reason applied oil has proven superior.

Clearance rate of applied oil

I was once wondering about the clearance rate of oils. I have seen it stated at various times that MCT
(Medium Chain Triglycerides) could be deadly because it stays around forever.

No it doesn’t. I went through a lot of studies and although there is variability among animal models it seems
MCT oil (Fractionated coconut oil) possesses about a one week half-life in muscle and the rate of
disappearance remains linear.

The key determinant seems to be the general viscosity of the oil. Here is a good example:

From, Intramuscular rate of disappearance of oily vehicles in rabbits investigated by gamma-scintigraphy,

Kirsten Schultz et al, International Journal of Pharmaceutics 169 (1998) 121-126

Viscosities and muscular disappearance rates of various oily vehicles

Oily vehicle Viscosity at 37°C T1/2 Ethyl oleate 3.9 10 days Fractionated coconut oil 15 1 week Sesame oil 35
1 month Arachidis oil 35.2 23 days Castor oil 286 Indefinitely Apparently the volume of the oil applied doesn’t
effect the clearance rate. That remains constant.

In addition both fractionated coconut oil (MCT) and sesame oil spread approximately 25% along the muscle
fibers (beneath the fascial sheaths) during the first 24 hours after administration (primarily in the first few
minutes) and then virtually no more spreading. So MCT oil is effective at creating a volume depot capable of
fascial stretching.

More importantly the studies show that MCT oil is not deadly. It has half the viscosity of sesame oil so if it
gets into the blood stream it probably isn’t going to clog any arteries or cause blockages in and around the
heart. In fact MCT oils ingested orally pass into the body without much change and circulate in plasma
eventually acting as an energy substrate with no apparent health concerns.

It has a half-life (i.e. degradation rate) of a week and a linear continual clearance rate so MCT oil will not stay
around for a long period of time. Only about 1% remains after 6 weeks.

What determines absorption of administered oil & how is it absorbed?

Lymphatic (minor role)

A maximum of 5% of the applied dose of sesame oil and Viscoleo (brand of MCT oil) in rats and dogs was
accounted for via lymphatic absorption (Svendsen and Aaes- Jorgensen, 1979)….Lymphatic absorption might
be expected to take place more efficiently from the subcutaneous layers than from the intramuscular
application sites, since the lymphatic system is better developed in the former region (Ballard, 1968).
Although some absorption into the lymphatic system may occur it appears less likely that this route of
absorption plays a dominant role in the clearance of oil vehicles.

Surface area

The surface area of the oil depot is likely to affect the clearance of the oil vehicle from the application site.
Thus, the distribution of the oil vehicle at the application site can be an important variable. The spreading
characteristics of the oil vehicle appear to be influenced by the viscosity of the oil (Howard and Hadgraft,
1983). …the more viscous oil the more resistant to spreading at the application site and consequently a
slower clearance rate would be expected.

Other Factors

Biological and physiological factors such as vascularisation (Zuidema et al., 1988) and body movement
(Ballard, 1968) might also influence the absorption rate of the oil vehicles.

Phagocytosis (the cellular process of engulfing solid particles by the cell membrane) might constitute another
possible absorption mechanism (Ballard, 1968). Phagocytosis is likely to be related to the tissue response to
the applied oil material (Ballard, 1968).

Metabolic degradation of oil vehicles has been suggested by Svendsen and Aaes-Jorgensen (1979) to play a
role in the removal of oil vehicles from the site of application. As a result of the inflammatory response,
several enzymes might be present at the application site. Degradation of oil vehicles mediated by lipases
might therefore also contribute to the disappearance rate of oil vehicles where the rate of degradation might
be influenced by the composition of the oil vehicles:

Source: Determination of the disappearance rate of iodine-125 labelled oils from the application site after
intramuscular and subcutaneous administration to pigs, Susan Weng Larsen et al, International Journal of
Pharmaceutics 230 (2001) 67-75

For the specific studies written by the authors mentioned above, see the references cited in the
aforementioned study.

Caprylic Acid (MCTs)

So what happens when MCT oil moves into the blood stream?
 It is a good thing and is a significant dietary aid. It has a “direct inhibitory effect on fat storage in adipocytes
under conditions that normally favor lipogenesis”.

Medium-chain fatty acids are unique because they are metabolized differently from either long-chain fatty
acids or carbohydrates. Dietary Medium-chain triglycerides (MCT) have been found to inhibit body fat mass
growth in both animals and humans. They do this through two distinct mechanisms.

The first mechanism involves MCTs in their role as an energy source. They are rapidly absorbed and oxidized
in the liver, and used as a quick source of energy, which reduces the circulating fatty acids available to
adipocytes (fat cells). Unlike long chain fatty acids (LCTs), they are able to pass through the mitochondrial
membrane without the assistance of the primary mode of transport, carnitine. As a result MCTs are capable
of quickly and directly entering into a metabolic process that results in the production of ketones thereby
increasing available energy.

The second mechanism involves the portion of MCTs that do find there way into adipocytes (fat cells).
However they are not stored but rather act to suppresses lipogenesis (fat storage) by inhibiting gene
expression. Technically they inactivate the key adipocyte transcription factor, peroxisome proliferator-
activated receptor y (PPARy). Simply stated caprylic acid (MCTs) induces a metabolic state in adipocytes (fat
cells) mimicking a fasting condition without actual hormone/nutrient deprivation. In fact they are able to do
this even in the presence of insulin and glucose (conditions that normally favor lipogenesis (fat storage).

“Compared to the pharmaceutical inhibitors of lipogenesis, the effects of octanoate [caprylic acid] can be
considered as moderate and yet might be more desirable for physiological regulation of body fat mass
without adversely affecting normal fat tissue functions.” – *

• – Modulation of adipocyte lipogenesis by octanoate: involvement of reactive oxygen species, Wen Guo,
Weisheng Xie and Jianrong Han, Nutrition & Metabolism 2006, 3:30

This is one reason why MCT oil works well in those in pre-contest mode. It is used for site enhancement but it
also acts as an energy substrate with very little fat storage and a positive effect as an inhibitor of lipogenesis.

Why site application of Caprylic Acid may work (In addition to increasing fascia pliability).

STUDY ** The study set out to determine what effect if any does an extract of the bark of the tree Eucommia
ulmoides have on creating synergism between sex steroids receptors, sex hormones and lipids derived from
plants.

What they discovered is that the extract demonstrated androgenic activities by weakly activating Androgen
Receptors (AR) in a dose-dependent manner. The scale that is used to measure androgenic activity is such
that a saturation dose of the androgen receptor’s native ligand (testosterone) will produce a 100 fold
Luciferase assay (LUC) activity. The extract produced a 6.4 fold LUC activity.

Androgenic of Eucommia ulmoide by itself

The extract also demonstrated a weak activation of the estrogen receptor.

However when they combined a saturation dose of testosterone and the extract they found synergy. When a
saturation dose of androgen, either DHT or testosterone is added together with the extract the increases in
Androgen Receptor (AR)-mediated reporter gene expression goes up beyond what the saturation dose of
testosterone or DHT alone could produce. The synergy with DHT moved up above the 200% mark while the
synergy with testosterone moved androgen receptor activity close to the 240% mark. The extract acted as an
amplifier of androgen receptor transcriptional activity.

In the words of the study “This is highly unusual as normally, androgen mediated AR transcriptional capacity,
akin to all ligand dependent steroid receptors, plateaus at saturating doses of its cognate ligand.”

So to restate, testosterone activates androgen receptor transcriptional activity to their normal capacity of
100%. The extract by itself weakly activates the androgen receptor by 6%. Together the extract and
testosterone activate the androgen receptor and propel it to transcribe at a rate more than twice what it is
normally capable of. In this case increasing activity to 240%.

A similar effect was demonstrated on the estrogen receptor.

Synergy between testosterone and Eucommia ulmoide

Having demonstrated a synergistic relationship in human and mammalian cells they carried out a second
study this time in vivo.

To test the anabolic effect in vivo prostate growth was measured in an animal model (rats). Saturation dose
for testosterone defined as 5mg was administered IM and 50mg of E. ulmoides (EU) extract was given orally.
The results graphed below again indicate that extract amplifies testosterones effect on the androgen
receptor-mediated transcriptional events that lead to growth.

In vivo anabolism between testosterone and Eucommia ulmoide

The study then attempted to ascertain the components of the extract responsible for the synergism. To this
end they fractionated the extract into components and found two active components. One component was
found to exert its effect (labeled phytoandrogenic activity by the authors) on the Androgen Receptor by
changing its binding characteristics. That compound is completely unrelated to caprylic acid.

The second active fraction contained 8-carbon polysaturated fatty acid, caprylic acid, and other lipids. In the
words of the authors:

“Bioassays using pure caprylic acid and other polysaturated fatty acids (PFAs) correlated with the augmenting
effect of E. ulmoides on the AR [androgen receptor] in varying degrees. Ethanolic extract of coconut (Cocos
nucifera) flesh, rich in C-8 caprylic acid and other polysaturated fatty acids, replicated the hormone
potentiating effect of both E. ulmoides extract and pure caprylic acid in AR bioassays (data not shown).”
In my words,

Equally effective were:

Ethanolic extract of coconut;

Pure caprylic acid; and

E. ulmoides.

The major constituent in all three is caprylic acid which as the authors show in the figure below had the
strongest augmenting effect of all the lipids.

So a blend of PFAs in ethanolic extract of coconut the vast majority of which is caprylic acid replicated the
hormone potentiating effect of E. ulmoides extract whose primary constituent is caprylic acid which all by
itself in pure caprylic acid form replicated the hormone potentiating effect of E. ulmoides extract.

Caprylic acid is the strongest lipid augmenter of androgen receptors

In an attempt to explain why caprylic acid had an augmenting effect the authors state:

“Okadaic acid, a known phosphorylation promoter, is able to strongly augment androgen-dependent AR

activity. Interestingly, fatty acids can also promote phosphorylation. One instance is oleic acid, a C-18 cis-
monosaturated fatty acid. It is possible that AR [androgen receptor] and ER augmentation by both E.
ulmoides extract and caprylic acid arise from a common tripartite synergism between the steroid receptors,
sex steroids and fats, based on a phosphorylation mechanism.”

The action of caprylic acid labeled a “lipid augmenter” by the authors is postulated to result from increased
phosphorylation. This differs from the action of the other non-caprylic component labeled a
“phytoandrogen” which changes the ligand binding characteristics.

The study concludes, “the novel discoveries reported in this study add phytoandrogens and lipidic
augmenters to the emerging list of hormomimetics (such as phytoestrogens) known to exist in plants.
Pharmaceutical utility of lipidic augmenters in the treatment of hypogonadal conditions such as menopause
or andropause could be exploited based on this mechanism of tripartite synergism. The link between excess
dietary lipids, hyper-androgenism and hormone-related disorders should also be further explored in the light
of these findings.”

** Source: Novel phytoandrogens and lipidic augmenters from Eucommia ulmoides, Victor YC Ong and Benny
KH Tan, BMC Complementary and Alternative Medicine 2007, 7:3

Site administration of sterile caprylic acid

MCT oil’s primary constituent is caprylic acid. Consuming it orally or administering IM should have the effect
of synergizing with natural levels of testosterone (hopefully) and externally administered testosterone.

Site administration maintains MCT oil in a particular area and has a high likelihood of specifically increasing
androgen receptor-mediated transcription events locally.

Those that have administered MCT oil have experienced site growth. This may result from both the fascia
stretching and the possible accelerated growth brought about by the synergy described herein.

Site Enhancing Oils – A How to Guide by Big A

The following protocol was developed by IFBB Pro Big A many years ago and has proven over the years to be
highly successful with positive, even ecstatic feedback from more then a thousand users. In his own words
what follows is the original methodology for maximizing muscle gain with Syntherol™ as related to all who
dared to discover newfound muscle gain… gather around discover what has been holding you back. Big A, …
Syntherol™ can be used for two purposes – to increase the size of a muscle or to shape a muscle.

To increase size – using the biceps as an example:

You need to apply Syntherol™ to EVERY head of the muscle, while rotating the applications daily within that
muscle head. This is the only way to ensure that the added size keeps to the natural look/shape of that
particular muscle.

Since some bodybuilders prefer various ways of using Syntherol™, they usually tailor dosages to suit the
individual.

Some bodybuilders use 1ml per muscle (that is 1ml per muscle head – ie. inner head, outer head, etc). 1ml is
used per day, every day, for a period of 2 weeks followed by a one week rest period. Then repeated.

Other bodybuilders use 1ml per muscle 3 times a week for the first week, followed by 2ml per muscle 3 times
a week the second week and 3ml per muscle 3 times a week the third week. That is followed by one or two
week break, after which the usage pattern is repeated.

The quickest way to increase a muscle’s appearance to maximum size is by following the regimen below:

1ml per muscle head every day for 10 days

2ml per muscle head every day for 10 days

3ml per muscle head every day for 10 days

If you would be using Syntherol™ in both biceps and triceps simultaneously, you can add up to 3 inches on
your arms in those 30 days.
It is EXTREMELLY IMPORTANT that you HAVE to massage SEVERELY the muscle that you just applied with
Syntherol™!

You have to make sure that there is not a lump forming. The muscle should always be soft. You should NEVER
feel like you have a lump. It is also a good idea, to apply Syntherol™ just before going to the gym, so as soon
as you get to the gym, you should be doing a couple light weight, high rep sets for that muscle, to get the
blood moving. This again will minimize lump formation. Keep in mind, that as soon as lumps form because
you did not massage, scar tissue will form as well as you want to avoid scar tissue at all costs!

If you find that you cannot keep the lump build up away, but you are due for another application, wait until,
by massaging, the lump goes away (it should not be more than a couple of days) and then resume from
where you left off.

If you have all the size you wish and just want to shape the muscle, as adding a peak on the biceps, then
apply Syntherol™ to the spot, in the peak of the muscle, with 1ml every day or every second day until you
obtain the peak that you desire.

Where to apply Syntherol™:

BICEPS: inner and outer head. One can feel the “split” in between the two heads of the biceps when a bicep
is felt with the other hand. Apply the Syntherol™ on each side of that split. If you want to increase the
length/thickness of the bicep, apply Syntherol™ more in the inner head (closer to the body). If increase of the
peak is desired then apply Syntherol™ more in the outer head.

TRICEPS: One does not need to apply Syntherol™ in the outer/horseshoe head, unless it is really lacking
development behind the other tricep heads. Syntherol™ is applied in the middle and rear heads of the
triceps. Generally, at the back of the arm, the upper portion is the rear head and the lower portion is the
middle head, as the two heads overlap each other somewhat.

DELTOIDS: Apply Syntherol™ straight into whatever head is lacking in size.

CALVES: Natural calves, regardless of how big they are, have a “flat” look to the muscle. As such, one would
want to keep that look, as it is not wanted to have the calves looking round like someone stuck an air hose in
there. As such, Syntherol™ is applied in multiple applications, on the outside edges of the muscle. That will
make the calf go outwards, while keeping the flat, natural look.

QUADS: With muscles this large, one needs to do multiple daily applications. Where in the biceps 1ml per
head per day is used to begin with, on quads it is needed to start with 1ml per site, 7 sites per quad. That is to
avoid the “lumpy” look and keep the quad uniform. Again, to keep the natural look of the thigh, Syntherol™
should be applied to the “peak” of the outer quad, along the crest. If the teardrop is lacking, then Syntherol™
should be applied straight into it, rotating sites daily.
PECS: Again, these are very large, “flat” looking muscle groups, as such the entire muscle has to be covered
evenly with Syntherol™, so 3 rows of 3 applications per day per pectoral should be used. Dosage would be
0.5ml per day per application site for 10 days, followed by 1ml per day per application site for 10 days and
finished off with 1.5ml per day per application site for 10 days.

We strongly recommend that Syntherol™ users obtain some anatomy charts and study the muscles and the
nerves that are in the area that Syntherol™ is to be applied.

How does Syntherol™ work?

To begin with, Syntherol™ does not stay in the muscle for 3 to 5 years as wrongly assumed. Syntherol™ gets
dissipated gradually within months. However, during this time, Syntherol™ will stretch the fascia of that
muscle. The fascia is a great constrictive factor in muscle growth. The more stretched the fascia is the more
the muscle will grow and the more it will have that “popping” look. Syntherol™ stays in there long enough for
the fascia to stretch.

As the oil starts to dissipate, the “space” left by Syntherol™ is replaced with new muscle tissue growth, if the
user is in a proper anabolic environment. That is an environment conducive to muscle growth, ie. resistance
training, proper nutrition, recovery and supplementation. The new muscle tissue growth in the space left by
Syntherol™ is the reason that when x-rays where performed on some of the people that have 25+ inch arms,
there was no Syntherol™ found to be present. Syntherol™ dissipated and it was replaced by real muscle.

Pain – obviously, any fascial stretching will hurt. The pain will minimise the more Syntherol™ is applied, until
it will not hurt any more at all.

All SEOs hurt, Syntherol™ has been reported to hurt the less due to its high level of refinement, as such
making for a very thin oil.

And again, we strongly suggest that the muscle be stretched and vigorously massaged throughout the day
after every application with Syntherol™.

Basic Peptide Primer

What is a peptide?

Peptides (proteins) are present in every living cell and possess a variety of biochemical activities. Some
peptides are synthesized in the ribosomes of a cell by translation of mRNA (messenger RNA) into hormones
and signaling molecules for example. Other peptides are assembled (rather then synthesized) and become
enzymes with a vast variety of functions. Peptides also make up the structure of receptors which await
binding of hormones & signaling molecules.

A peptide is a molecule created by joining two or more amino acids. In general if the number of amino acids
is less than fifty, these molecules are called peptides, while larger sequences are referred to as proteins.
So peptides can be thought of as tiny proteins. They are merely strings of amino acids.

Raw Constituents of Peptides (Amino Acids)

Amino acids are small molecules made up of atoms. As part of their structure they posses a grouping of a
Nitrogen (N) atom bonded to two Hydrogen (H) atoms. This is called an amino group and written as (NH2). In
addition their structure is also made up of a second grouping of a Carbon (C) atom bonded to two Oxygen (O)
and one Hydrogen atom. This group is called a carboxyl group and is written as (COOH).

Between these two groupings are atoms and bonds unique to each amino acid. In other words all amino acids
possess the two groupings (amino& carboxyl) as end-points between which are sandwiched a unique set of
atoms.

Amino Acids

Inside the human body there are twenty standard amino acids used by cells in peptide biosynthesis (i.e. the
cellular creation of peptides from amino acids). Our genetic code specifies how to synthesize peptides and
proteins from these amino acids.

Amino acids are classified into two groups: essential amino acids and nonessential amino acids.

An essential amino acid is an indispensable amino acid which cannot be made by the body and must be
supplied by food. These include isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan,
and valine. Another amino acid - histidine is considered semi-essential because the body does not always
require dietary sources of it.

Nonessential amino acids are made by the body from the essential amino acids or the routine breakdown of
proteins. The nonessential amino acids are arginine, alanine, asparagine, aspartic acid, cysteine, glutamine,
glutamic acid, glycine, proline, serine, and tyrosine.

All twenty amino acids are equally important in maintaining a healthy body. They are the raw constituents of
peptides and proteins.

The standard abbreviations for amino acids come in two forms: a one letter form and a three letter form.
They are:

A - Ala - Alanine C - Cys - Cysteine D - Asp - Aspartic Acid E - Glu - Glutamic Acid F - Phe - Phenylalanine G - Gly
- Glycine H - His - Histidine I - Ile - Isoleucine K - Lys - Lysine L - Leu - Leucine M - Met - Methionine N - Asn -
Asparagine P - Pro - Proline Q - Gln - glutamine R - Arg - Arginine S - Ser - Serine T - Thr - Threonine V - Val -
Valine W - Trp - Tryptophan Y - Tyr - Tyrosine

Amino acids exist in either D (dextro) or L (levo) form. Most of the amino acids found in nature (and all within
human cells) are of the L-form. As a generality all amino acids except glycine have a mirror image of the L-
 form. This mirror image is called the D-form. It is common when referring to the L-form (naturally occurring
form) to leave off the "L" designation whereas the "D" designation is always explicitly written.

D-amino acids are found naturally in bacterial cell walls and used in some synthetic peptides to make a
peptide more stable or more resistant to degradation.

Amino Acid + Amino Acid = Peptide

The amino acids are joined together by what is known as a "peptide bond". A "peptide bond" is a linkage in
which the nitrogen atom of one amino acid (from the amino group (NH2) binds to the carbon atom of
another amino acid's carboxyl group (COOH).

During this binding process a molecule of water is released. This is called a condensation reaction.

The resulting CO-NH bond is called a peptide bond, and the resulting molecule is called an amide.

On the following image note that the COOH group gives up an Oxygen Hydrogen (OH) bond and the NH2
group gives up a Hydrogen (H). This forms H2O, which is a water molecule which is not part of the newly
created peptide. NOTE: in the following image the C (carbon) symbol is missing as it is assumed so I indicate it
with a blue square.

This reaction creating a peptide bond between two amino acids creates a peptide. We can call this peptide
(made up of two amino acids) a dipeptide.

This process can be repeated using the twenty amino acids as raw material to create longer peptide chains.
Sometimes peptide chains consisting of fifty to 100 amino acids are called polypeptides. Often a peptide
chain beyond 100 amino acids is called a protein.

GHRP-6 is a peptide made up of just six amino acids. It's structure is often written as His-DTrp-Ala-Trp-DPhe-
Lys-NH2

Note that the Carboxyl grouping (COOH) is assumed in the first position and is usually not written. The amino
group (NH2) is wrtitten in the last position. The "meat" or the part that makes GHRP-6 distinct is the seqence
in the middle of histadine bonded to the "D" form of Tryptophan bonded to Alanine bonded to Tryptophan
bonded to the "D" form of Phenylalanine bonded to Lysine.

Pepdide bonds are formed by water (H2O) condensation (removing water). The converse is also true. A
peptide bond can be broken down by hydrolysis (adding water).

The Amino Acid Structures of Peptides discussed in this thread

Growth Hormone Releasing peptides (GHRPs) (GH pulse initiators):

• GHRP-6 (His-DTrp-Ala-Trp-DPhe-Lys-NH2)
• GHRP-2 (DAla-D-2-Nal-Ala-Trp-DPhe-Lys-NH2)

• Hexarelin (His-D-2-methyl-Trp-Ala-Trp-DPhe-Lys-NH2)

• Ipamorelin (Aib-His-D-2-Nal-DPhe-Lys-NH2) - Ref-1 NOTES: Aib = Aminoisobutyryc acid D-2-Nal = "D" form of
2’-naphthylalanine

Growth Hormone Releasing Hormone (GHRH) (amplifies the GHRP initiated pulse):

• Growth Hormone Releasing Hormone (GHRH) aka GRF(1-44) (Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-

Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-Gln-Gln-Gly-Glu-Ser-Asn-Gln-Glu-
Arg-Gly-Ala-Arg-Ala-Arg-Leu-NH2) = half-life "less then 10 minutes", perhaps as low as 5 minutes. - Ref-2

• GRF(1-29) aka Sermorelin (Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-

Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH2) - the biologically active portion of the 44 amino acid GHRH = half-
life "less then 10 minutes", perhaps as low as 5 minutes. - Ref-3

• Longer-lasting analogs of GRF(1-29): -- replace the 2nd amino acid Alanine w/ D-Alanine only to modify
GRF(1-29), D-Ala2 GRF(1-29) (Tyr-DAla-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-
Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH2) =half-life "closer to 10 minutes" - Ref-4

-- replace the 2nd, 8th, 15th & 27th amino acids & get modified GRF(1-29) or CJC-1295 w/o the DAC (i.e. the
part that will bind to albumin & make the half-life days) (Tyr-DAla-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-
Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH2) = Half-life at least 30 minutes or
so - Ref-5

-- CJC-1295 (Tyr-DAla-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-
Gln-Asp-Ile-Leu-Ser-Arg-Lys-(Maleimidopropionyl)-NH2) = Half-life measured in days, - Ref-6

NOTES: Lys = linker to the Drug Affinity Complex (aka (Maleimidopropionyl))

"Since GH is released in a pulsatile manner and a higher level of GH is observed between 15 and 30 min after
subcutaneous administration of GH-RH analogues, hydrolysis by trypsin-like enzymes could not affect the
result of stimulation." - Potent Trypsin-resistant hGH-RH Analogues, JAN IZDEBSKI, J. Peptide Sci. 10: 524–529
(2004)

The analog in the above quoted study resisted degradation for 30 minutes. The quote implies that if your
analog can last 30 minutes it has tapped out the potential for a single pulse.

Since another pulse won't be generated for about 2.5 - 3 hours analogs that last more than 30 minutes up to
3 hours are not any more beneficial.

You would need an analog that kept growth hormone releasing hormone around beyond 3 hours to have it
trigger a second pulse.
Otherwise dosing the 30 minute analog every 3 hours will maximize GH output OR you could just use an
analog such as CJC-1295 which lasts for many days and will trigger several GH pulses a day for several days on
a single dose.

References:

Ref-1 - "lack of effect on ACTH and cortisol plasma levels" - Ipamorelin, the first selective growth hormone
secretagogue , K Raun, European Journal of Endocrinology, 1996 Vol 139, Issue 5, 552-561

Ref-2 - Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to
a biologically inactive product cleaved at the NH2 terminus, Frohman LA, J Clin Invest. 1986 78:906–913
andIncorporation of D-Ala2 in Growth Hormone-Releasing Hormone-( l-29)-NH2 Increases the Half-Life and
Decreases Metabolic Clearance in Normal Men, STEVEN SOULE, Journal of Clinical Endocrinology and
Metabolism 1994 Vol. 79, No. 4

Ref-3 - Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to
a biologically inactive product cleaved at the NH2 terminus, Frohman LA, J Clin Invest. 1986 78:906–913
andIncorporation of D-Ala2 in Growth Hormone-Releasing Hormone-( l-29)-NH2 Increases the Half-Life and
Decreases Metabolic Clearance in Normal Men, STEVEN SOULE, Journal of Clinical Endocrinology and
Metabolism 1994 Vol. 79, No. 4

Ref-4 - Incorporation of D-Ala2 in Growth Hormone-Releasing Hormone-( l-29)-NH2 Increases the Half-Life
and Decreases Metabolic Clearance in Normal Men, STEVEN SOULE, Journal of Clinical Endocrinology and
Metabolism 1994 Vol. 79, No. 4

What is growth hormone?

Synthetic Growth Hormone is an artificially created hormone "identical" to the major naturally produced
(endogenous) isoform. It is often referred to by its molecular mass which is 22kDa (kilodaltons) and is made
up of a sequence of 191 amino acids (primary structure) with a very specific folding pattern that comprise a
three-dimensional structure (tertiary structure). This tertiary structure is subject to potential shape change
through a process known as thermal denaturation. While many labs are capable of generating growth
hormone (GH) with the proper primary structure not all will be capable of creating a tertiary structure
identical to the major naturally occurring growth hormone. The tertiary structure can determine the strength
with which the growth hormone molecule binds to a receptor which will in turn affect the "strength" of the
intracellular signaling which mediates the events leading to protein transcription, metabolism, IGF-1 creation,
etc. It is this inconsistency that accounts in part for the differences in effectiveness of various non-
pharmaceutically produced synthetic growth hormone.

Naturally produced Growth Hormone is produced in the anterior pituitary and to a far lesser extent in
peripheral tissue. It is made up of a blend of isoforms the majority of which is the 22kDa (191 amino acid)
 variety with which most are familiar. In addition an isoform that is missing the 15 amino acids that interact
with the prolactin receptor is also produced. This form is known as 20kDa and although it binds differently to
the growth hormone receptor it has been shown to be equally potent to 22kDa. It appears that 20kDa has
lower diabetogenic activity then 22kDa. The pituitary releases a blend of these two isoforms with 20kDa
averaging perhaps 10% of the total although this percentage increases post-exercise. Currently there is no
synthetic produced for external administration for this isoform.

Growth hormone (GH) in the body is released in pulsatile fashion. It has been demonstrated that this pattern
promotes growth. The pituitary is capable of rather quickly synthesizing very large amounts of growth
hormone which it stores large amounts in both a finished and unfinished form. Adults rarely experience GH
pulses (i.e. releases of pituitary stores) that completely deplete these stores. As we age we do not lose the
ability to create and store large amounts of growth hormone. Rather we experience a diminished capacity to
"instruct" their release. The volume of GH that is released can not be properly equated to the exogenous
administration of synthetic GH for the reason that a set of behavioral characteristics accompany natural GH
that differ from those of synthetic GH. Among those characteristics are concentrated pulsatile release which
upon binding in mass to growth hormone receptors on the surface of cells initiate signaling cascades which
mediate growth events by translocating signaling proteins to the nucleus of the cell where protein
transcription and metabolic events occur.

These very important signaling pathways desensitize to Growth Hormone's initiating effects and need to
experience an absence of Growth Hormone in order to reset and be ready to act again. The presence of GH
released in pulsatile fashion is graphed as a wave with the low or no growth hormone period graphed as a
trough. Therefore attempting to find a natural GH to synthetic GH equivalency is not very productive because
in the end what is probably import is:

• the quantity & quality of intracellular signaling events; and

• the degree to which GH stimulates autocrine/paracrine (locally produced/locally used) muscle IGF-1 & post-
exercise its splice variant MGF.

Synthetic GH versus Natural GH in IUs

An attempt has been made on my part and can be found at:

Growth Hormone Administration vs. CJC-1295/GHRP-6 + GHRH (part I of II)

Growth Hormone Administration vs. CJC-1295/GHRP-6 + GHRH (part II of II) Rather than demonstrate
absolute values this comparison articles should serve to demonstrate that the body can produce
pharmacological levels of growth hormone.

Brief overview of natural GH release

The initiation of growth hormone release in the pituitary is dependent on a trilogy of hormones:
Somatostatin which is the inhibitory hormone and responsible in large part for the creation of pulsation;

Growth Hormone Releasing Hormone (GHRH) which is the stimulatory hormone responsible for initiating GH
release; and

Ghrelin which is a modulating hormone and in essence optimizes the balance between the "on" hormone &
the "off" hormone. Before Ghrelin was discovered the synthetic growth hormone releasing peptides (GHRPs)
were created and are superior to Ghrelin in that they do not share Ghrelin's lipogenic behavior. These GHRPs
are GHRP-6, GHRP-2, Hexarelin and later Ipamorelin all of which behave in similar fashion. In the aging adult
these Ghrelin-mimetics or the GHRPs restore a more youthful ability to release GH from the pituitary as they
turn down somatostatin's negative influence which becomes stronger as we age and turn up growth
hormone releasing hormone's influence which becomes weaker as we age.

The exogenous administration of Growth Hormone Releasing Hormone (GHRH) creates a pulse of GH release
which will be small if administered during a natural GH trough and higher if administered during a rising
natural GH wave.

Growth Hormone Releasing Peptides (GHRP-6, GHRP-2, Hexarelin) are capable of creating a larger pulse of
GH on their own then GHRH and they do this with much more consistency and predictability without regard
to whether a natural wave or trough of GH is currently taking place.

Synergy of GHRH + GHRP

It is well documented and established that the concurrent administration of Growth Hormone Releasing
Hormone (GHRH) and a Growth Hormone Releasing Peptide (GHRP-6, GHRP-2 or Hexarelin) results in
synergistic release of GH from pituitary stores. In other words if GHRH contributes a GH amount quantified as
the number 2 and GHRPs contributed a GH amount quantified as the number 4 the total GH release is not
additive (i.e. 2 + 4 = 6). Rather the whole is greater than the sum of the parts such that 2 + 4 = 10.

While the GHRPs (GHRP-6, GHRP-2 and Hexarelin) come in only one half-life form and are capable of
generating a GH pulse that lasts a couple of hours re-administration of a GHRP is required to effect additional
pulses.

Growth Hormone Releasing Hormone (GHRH) however is currently available in several forms which vary only
by their half-lives. Naturally occurring GHRH is either a 40 or 44 amino acid peptide with the bioactive portion
residing in the first 29 amino acids. This shortened peptide identical in behavior and half-life to that of GHRH
is called Growth Hormone Releasing Factor and is abbreviated as GRF(1-29).

GRF(1-29) is produced and sold as a drug called Sermorelin. It has a short-half life measured in minutes. If you
prefer analogies think of this as a Testosterone Suspension (i.e. unestered).
To increase the stability and half-life of GRF(1-29) four amino acid changes where made to its structure.
These changes increase the half-life beyond 30 minutes which is more than sufficient to exert a sustained
effect which will maximize a GH pulse. This form is often calledtetrasubstituted GRF(1-29) (or modified) and
unfortunately & confusingly mislabeled as CJC-1295. If you prefer analogies think of this as a Testosterone
Propionate (i.e. short-estered).

Note that some may also refer to this as CJC-1295 without the DAC (Drug Affinity Complex).

Frequent dosing of either the aforementioned modified GRF(1-29) or regular GRF(1-29) is required and as
previously indicated works synergistically with a GHRP.

In an attempt to create a more convenient long-lasting GHRH, a compound known as CJC-1295 was created.
This compound is identical to the aforementioned modified GRF(1-29) with the addition of the amino acid
Lysine which links to a non-peptide molecule known as a "Drug Affinity Complex (DAC)". This complex allows
GRF(1-29) to bind to albumin post-injection in plasma and extends its half-life to that of days. If you prefer
analogies think of this as a Testosterone Cypionate (i.e. long-estered). However this is not accurate. CJC-1295
results in continual GH bleed. Although natural pulsation still occurs CJC-1295 does nothing to increase those
pulses. Instead it raises base levels of GH and creates a more feminized pattern of release. This not desirable.

Modified GRF(1-29)however when combined with a GHRP brings about a substantial pulse which has
desirable effects.

A Brief Summary of Dosing and Administration

Dosing GHRPs

The saturation dose in most studies on the GHRPs (GHRP-6, GHRP-2, Ipamorelin & Hexarelin) is defined as
either 100mcg or 1mcg/kg.

What that means is that 100mcg will saturate the receptors fully, but if you add another 100mcg to that dose
only 50% of that portion will be effective. If you add an additional 100mcg to that dose only about 25% will
be effective. Perhaps a final 100mcg might add a little something to GH release but that is it.

So 100mcg is the saturation dose and you could add more up to 300 to 400mcg and get a little more effect.

A 500mcg dose will not be more effective then a 400mcg, perhaps not even more effective then 300mcg.

The additional problems are desensitization & cortisol/prolactin side-effects.

Ipamorelin is about as efficacious as GHRP-6 in causing GH release but even at higher dose (above 100mcg) it
does not create prolactin or cortisol.

GHRP-6 at the saturation dose 100mcg does not really increase prolactin & cortisol but may do so slightly at
higher doses. This rise is still within the normal range.
GHRP-2 is a little more efficacious then GHRP-6 at causing GH release but at the saturation dose or higher
may produce a slight to moderate increase in prolactin & cortisol. This rise is still within the normal range
although doses of 200 - 400mcg might make it the high end of the normal range.

Hexarelin is the most efficacious of all of the GHRPs at causing an increase in GH release. However it has the
highest potential to also increase cortisol & prolactin. This rise will occur even at the 100mcg saturation dose.
This rise will reach the higher levels of what is defined as normal.

Desensitization

GHRP-6 can be used at saturation dose (100mcg) three or four times a day without risk of desensitization.

GHRP-2 probably at saturation dose several times a day will not result in desensitization.

Hexarelin has been shown to bring about desensitization but in a long-term study the pituitary recovered its
sensitivity so that there was not long-term loss of sensitivity at saturation dose. However dosing Hexarelin
even at 100mcg three times a day will likely lead to some down regulation within 14 days.

If desensitization were to ever occur for any of these GHRPs simply stopping use for several days will remedy
this effect.

Chronic use of GHRP-6 at 100mcg dosed several times a day every day will not cause pituitary problems, nor
significant prolactin or cortisol problems, nor desensitize.

GHRH

Now Sermorelin, GHRH (1-44) and GRF(1-29) all are basically GHRH and have a short half-life in plasma
because of quick cleavage between the 2nd & 3rd amino acid. This is no worry naturally because this
hormone is secreted from the hypothalamus and travels a short distance to the underlying anterior pituitary
and is not really subject to enzymatic cleavage. The release from the hypothalamus and binding to
somatotrophs (pituitary cells) happens quickly.

However when injected into the body it must circulate before finding its way to the pituitary and so within 3
minutes it is already being degraded.

That is why GHRH in the above forms must be dosed high to get an effect.

GHRH analogs

All GHRH analogs swap Alanine at the 2nd position for D-Alanine which makes the peptide resistant to quick
cleavage at that position. This means analogs will be more effective when injected at smaller dosing.
The analog tetra or 4 substituted GRF(1-29) sometimes called CJC w/o the DAC or referred to by me as
modified GRF(1-29) has other amino acid modifications. They are a glutamine (Gln or Q) at the 8-position,
alanine (Ala or A) at the 15-position, and a leucine (Leu or L) at the 27-position.

The alanine at the 8th position enhances bioavailability but the other two amino substitutions are made to
enhance the manufacturing process (i.e. create manufacturing stability).

For use in vivo, in humans, the GHRH analog known as CJC w/o the DAC or tetra (4) substituted GRF(1-29) or
modified GRF(1-29) is a very effective peptide with a half-life probably 30+ minutes.

That is long enough to be completely effective.

The saturation dose is also defined as 100mcg.

Problem w/ Using any GHRH alone

The problem with using a GHRH even the stronger analogs is that they are only highly effective when
somatostatin is low (the GH inhibiting hormone). So if you unluckily administer in a trough (or when a GH
pulse is not naturally occurring) you will add very little GH release. If however you luckily administer during a
rising wave or GH pulse (somatostatin will not be active at this point) you will add to GH release.

Solution is GHRP + GHRH analog

The solution is simple and highly effective. You administer a GHRH analog with a GHRP. The GHRP creates a
pulse of GH. It does this through several mechanisms. One mechanism is the reduction of somatostatin
release from the hypothalamus, another is a reduction of somatostatin influence at the pituitary, still another
is increased release of GHRH from the brain and finally GHRPs act on the same pituitary cells (somatotrophs)
as do GHRHs but use a different mechanism to increase cAMP formation which will further cause GH release
from somatotroph stores.

GHRH also has a way of reciprocally reinforcing GHRPs action.

The result is a synergistic GH release.

The GH is not additive it is synergistic. By that I mean:

If GHRH by itself will cause a GH release valued at 2 and GHRP itself will cause a GH release valued at 5

Together the GH is not 7 (5+2) it turns out to say 16!

A solid protocol

A solid protocol would be to use a GHRP + a GHRH analog pre-bed (to support the nightime pulse) and once
or twice throughout the day.
For anti-aging, deep restful restorative sleep, the once at night dosing is all you need. For an adult aged 40+ it
is enough to restore GH to youthful levels.

However for bodybuilding or fatloss or injury repair multiple dosings can be effective.

The GHRH analog can be used at 100mcg and as high as you want without problems.

The GHRP-6 can always be used at 100mcg w/o problems but a dose of 200mcg will probably be fine as well.

Again desensitization is something to keep an eye on particularly with the highest doses of GHRP-2 and all
doses of Hexarelin.

So 100 - 200mcg of GHRP-6 + 100 - 500mcg+ of a GHRH analog taken together will be effective. This may be
dosed several times a day to be highly effective.

A solid approach is a bit more conservative at 100mcg of GHRP-6 + 100mcg of a GHRH analog dosed either
once, twice, three or four times a day. When dosing multiple times a day at least 3 hours should separate the
administrations.

The difference is once a day dosing pre-bed will give a youthful restorative amount of GH while multiple
dosing and or higher levels will give higher GH & IGF-1 levels when coupled with diet & exercise will lead to
muscle gain & fatloss.

Dose w/o food

Administration should ideally be done on either an empty stomach or with only protein in the stomach. Fats
& carbs blunt GH release. So administer the peptides and wait about 20 minutes (no more then 30 but no less
then 15 minutes) to eat. AT that point the GH pulse has about hit the peak and you can eat what you want.

Basic Guide: CJC-1295

Partial explanation (Oct 21, 2009) "Cell-to-cell communication is also likely to reflect the density and
proximity of adjacent cells as GH responsiveness (but not sensitivity) to GHRH is enhanced at higher densities
and basal GH release is greatest at low densities."

"Cell-to-cell contact may therefore affect the cellular integrity of somatotrophs because GH synthesis or
secretory granule storage may be better maintained in high density cell concentration then in low-density
concentrations." - Growth Hormone, Stephen Harvey What happens is cells in the pituitary communicate.
They self organize and create a firing network for coordinated growth hormone release. This communication
creates a high density of GH releasing cells. They are in close proximity through their communicatory
network. The cells have specific spatial relationships that may be modulated by peripheral endocrines. These
include sex steroids, thyroid hormones, glucorticoids and even the pancreatic and gut hormones. Their
spatial relationship is also effected by physiological state such as nutrient status, age and pregnancy.
As a quick example, corticotroph, thyrotrophs and folliculostellate cells are in close proximity to
somatotrophs and communicate with them through gap junctions (almost like just reaching out and touching
signaling). They have the potential to effect and be effected by their neighbors.

What happens when you have GHRH always around is you force these somatotrophs to release GH because
they are sensitive to the GHRH binding to them and effecting release. By constantly occupying you are
preventing them from coordinating with surrounding cell populations. You force these cells to act as low
density subpopulations. Basal GH release is greatest when you can disperse the spatial relationship between
somatotrophs and that is what an always on GHRH will do.

CJC-1295 as an always on GHRH will force upon somatotrophs loner behavior with a single constant chore.
This reduces GH responsiveness as this only occurs when somatotrophs can communicate, self organize and
maintain social relationships with the surrounding community. These types of social somatotrophs are better
able to make and store GH then the loner cells.

So CJC-1295 seems to disperse somatotrophs and enslave them getting less from them then if it had just let
them congregate in towns and cities.

Aging has an effect on the vitality of city centers as well and as we age these somatotroph population centers
become less vigorous. By using a more physiological GHRH such as modified GRF(1-29) together with a
modulator GHRP-2 we revitalize that inner city and allow our cells to be more social and thus more
productive. If instead we choose to use CJC-1295 we not only fail to remedy the problem associated with age
, but we may end up exacerbating it.

I conjecture that it also makes them better neighbors to corticotroph, thyrotrophs and folliculostellate cells
as well.

Revision 2 [8/31/08]

Restoring Growth Hormone "It has been argued that the age-dependent decline in sex steroid, Growth
Hormone, and IGF-I production is nature’s way of protecting us from cancer and heart disease, but a far more
likely scenario is that once we reach our reproductive capacity, nature begins programming us for death."-
Roy G. Smith, Ph.D. Director, Huffington Center on Aging; Professor, Department of Molecular & Cellular
Biology; former Vice President for Basic Research at Merck Research Laboratories, Merck & Co Such
programming begins as the second decade of life draws to a close, the negative consequences of which
become more noticeable with each passing year.

We begin to experience a steady decline in immune function. (1,2) Our bodies increase production of
glucocorticoids (catabolic hormones) and cytokines (inflammatory) which negatively impact metabolism,
bone density, strength, exercise tolerance, cognitive function, and mood. (3,4–8)
The hormones of sex, dehydroepiandrosterone (DHEA), Growth Hormone (GH), and Insulin-like Growth
Factor (IGF-1) are positively correlated with the health and well-being of the body in general and the specific
functioning of metabolism, the cardiovascular system, the musculature skeletal system, cognitive function &
the immune system. However these hormonal levels naturally decline as we age and as a consequence those
systems necessary to maintain optimal health decline as well. (1-4,9)

"Hence, if we wish to maintain quality of life during aging we must oppose nature." - Roy G. Smith, Ph.D.

A progressive decline in lean body mass, atrophy of its component organs & reduction in their function and
increased deposition of adipose tissue mass characteristic of the aging human body result partially from the
body's diminished secretion of growth hormone. (10-13) These negative changes resulting from growth
hormone deficiency have been shown to be reversible by replacement doses of growth hormone. (14-21)

Growth Hormone is a vital anabolic hormone whose positive stimulatory effects on protein synthesis
(particularly in the liver, muscle, bone, cartlidge, spleen, kidney, skin, thymus, and red blood cells) and on
lipolysis (the breakdown of fat stored in fat cells) contributes greatly to growth, repair & well-being. (10)

Growth Hormone (GH) secretion is primarily regulated by the release of two peptides, Growth Hormone-
Releasing Hormone (GHRH) andSomatostatin. The hypothalamus region of the brain releases these
hormones in response to signals from the central nervous system. GHRH once released makes its way to the
receptors on the somatotrope cells of the pituitary gland below the brain where it stimulates Growth
Hormone release.

Somatostatin once released makes its way to the receptors on the somatotrope cells of the pituitary gland
below the brain where it inhibitsGrowth Hormone release. (15)

The primary physiological action of somatostatin is to inhibit synthesis and release of GH. (16-19) The primary
physiological action of Growth Hormone-Releasing Hormone (GHRH) is to stimulate synthesis and release of
GH.

The end product of this cascade, Growth Hormone (GH) once secreted exerts its effect in the body as a whole
both directly and indirectly through its initiation of Insulin-like Growth Factor (IGF-1) synthesis in the liver.
IGF-1 in turn exerts its effect in the body and its rise in turn begins to inhibit any further GH release.

Growth Hormone (GH) is released periodically within the body in a controlled pulsating fashion. This periodic
pattern plays an important role in transmitting the GH "growth, repair & well-being" message to tissue. A
review of several studies involving GH replacement in GH-deficient animals reveals the biological significance
of episodic secretion. These studies conclude that GH released in a pulsatile pattern is far more efficient in
improving mammalian growth and repair than the method of GH administration by constant infusion.

In males GH pulses occur approximately every three (3) hours, a frequency that appears across most
mammals. The secretion bursts are preceded and followed by almost undetectable levels of plasma GH.
In females however GH pulses occur more frequently and the base level of plasma GH remains higher than
males who have fewer GH pulses but the amplitude of which are more pronounced.

GH pulse amplitudes are increased during slow wave sleep such that particularly in males, most GH secretion
occurs at night. (22)

Growth Hormone secretion is highest during the growing years of youth and early adulthood. In humans the
secretion rate starts to noticeably decrease during the third decade of life and strongly decreases during the
fourth decade of life. As we age the daytime secretory pulses diminish first, while the sleep associated GH
pulse persists and diminishes gradually.

Nudging Nature

Growth Hormone levels may be increased either by exogenically administering Growth Hormone or by
administering Growth Hormone-Releasing Hormone which then endogenically stimulates the somatrope cells
of the pituitary to secrete additional Growth Hormone. The primary advantage of GHRH is that GH ends up
being released in physiological conformance to the body’s natural biorhythm. This biorhythm is pulsatile.

Studies have concluded that endogenous Growth Hormone Releasing Hormone (GHRH) is the principal
regulator of pulsatile GH secretion in humans and that continuous GHRH infusion augments pulsatile GH
release. Whereas exogenic administration of GH raises overall GH levels but has no effect on amplifying the
pulses.

People of all ages naturally continue to possess the ability to secrete GH from stores within the pituitary.
Most studies are in agreement on this point. One study in particular examined the effects of administration
of GHRH & a Growth Hormone Releasing Peptide on all adult age groups from those in their 20's to those
above 75 years of age. They observed substantial increases in GH release as a direct result of administration
of GHRH & GHRP-6. This prompted them to conclude, "...that the lack of side-effects & safety of the protocol
and the discovered lack of age-related decline in the 'GHRH-GHRP-6-mediated' GH release opens the
possibility of using it as a therapeutical tool to revert some deleterious manifestations of aging in man." (23)

Long-lasting GHRH analog CJC-1295

While the studies have demonstrated repeatedly that administration of GHRH does increase GH secretion
and amplifies the release pulse there does remain a significant drawback. GHRH has a very short half life,
measured in minutes with a fairly short clearance rate measured in hours. (24) While this is a sufficient
amount of time to exert a positive effect on GH secretion, particularly if GHRH is administered multiple times
a day, the result is less than optimal. (25,26)

It is for this reason that longer-lasting analogs of GHRH were researched and developed. (28) The most
effective of which is CJC-1295.
Exposure of native GHRH to blood plasma results in rapid degradation. CJC-1295, a synthetic human GHRH
analog avoids rapid degradation by possessing the ability to selectively and covalently bind to endogenous
albumin after subcutaneous administration. Albumin possesses a half-life of 19 days in humans and so
modified GHRH bound to albumin greatly extends its half-life and duration of action. (27)

In a recent (2006) study "Prolonged Stimulation of Growth Hormone (GH) and Insulin-Like Growth Factor I
Secretion by CJC-1295, a Long-Acting Analog of GH-Releasing Hormone, in Healthy Adults", Sam L. Teichman,
et al. Journal of Clinical Endocrinology & Metabolism 91(3):799-805, CJC-1295 was found to result in
"sustained, dose-dependent increases in GH and IGF-I levels in healthy adults and was safe and relatively well
tolerated, particularly at doses of 30mcg/kg or 60 mcg/kg."

It has been demonstrated repeatedly in various studies that GHRH is effective at instigating GH release and
longer acting analogs do increase the overall effectiveness. So it is no surprise that the results of this CJC-
1295 study comport with what has been previously demonstrated.

What was unknown was what effect persistent elevation of GH by a long-lasting GHRH analog would have on
the pulsatility of release. This was explored in a follow up study, "Pulsatile Secretion of Growth Hormone
(GH) Persists during Continuous Stimulation by CJC-1295, a Long- Acting GH-Releasing Hormone Analog",
Madalina Ionescu, et al. The Journal of Clinical Endocrinology & Metabolism 91(12):4792-4797.

That study found that pulsatility was not interfered with and was in fact preserved in all subjects both
immediately after administration and continuing 7 days post-administration.

This is obviously a very beneficial characteristic to preserve. In fact episodic release appears to be imperative
to growth and repair of tissue in mammals.

The study further found that while growth hormone secretion was increased by almost fifty percent there
was no increase in pulse amplitude or frequency. All of the increase came from a substantial elevation of
trough levels with preserved pulsatility.

One further note of interest is that study participants were all of young age with lower lean body masses
which may indicate that GHRH in the form of CJC-1295 is an effective avenue for growth hormone release for
those of young age.

The results of the study charted above show that administration of single doses of CJC-1295 remained in high
concentration for 7 days with measurable concentration for 14 subsequent days. (29)

As seen in the chart below this resulted in substantial increases in mean serum GH levels in all dosing groups,
which were dose incremental and persisted for up to 7 days.

As seen in the chart below this chronic elevation in CJC-1295 levels resulted in substantial increases in mean
serum IGF-1 levels in all dosing groups, which were dose incremental and persisted for up to 7 days.
The results from a toxicology study wherein 50mcg/kg of CJC-1295 was administered subcutaneously to
monkeys for a period of six months found no ill effects and no indication of presence of neutralizing
antibodies. They concluded that the Drug Affinity Complex (DAC) a technology that enables covalent binding
(conjugation) of a drug to albumin produced no evidence of immunogenic or immunotoxic effects in
monkeys. (30)

In summary, although the added Drug Affinity Complex adds complexity and increases the expense of CJC-
1295 peptide synthesis, it does add tremendously to both the dosing convenience and the biological activity
of GHRH without any identifiable adverse toxicity.

References:

1 - Hadden JW, Malec PH, Coto J, Hadden EM 1992 Thymic involution in aging. Prospects for correction. Ann
NY Acad Sci 673: 231–239

2 - Mackall CL, Gress RE 1997 Thymic aging and T-cell regeneration. Immunol Rev 160:91–102

3 - Ershler WB, Keller ET 2000 Age-associated increased interleukin-6 gene expression, late-life diseases, and
frailty. Annu Rev Med 51:245–270

4 - van Eekelen JA, Rots NY, Sutanto W, de Kloet ER 1992 The effect of aging on stress responsiveness and
central corticosteroid receptors in the brown Norway rat. Neurobiol Aging 13:159–170

5 - Martignoni E, Costa A, Sinforiani E, Liuzzi A, Chiodini P, MauriM, Bono G, Nappi G 1992 The brain as a
target for adrenocorticalsteroids: cognitive implications. Psychoneuroendocrinology 17: 343–354

6 - Liu J, Mori A 1999 Stress, aging, and brain oxidative damage. Neurochem Res 24:1479–1497

7 - Sapolsky R, Armanini M, Packan D, TombaughG1987 Stress and glucocorticoids in aging. Endocrinol Metab
Clin North Am 16:965– 980

8 - Heffelfinger AK, Newcomer JW 2001 Glucocorticoid effects on memory function over the human life span.
Dev Psychopathol 13:491–513

9 - Murialdo G, Barreca A, Nobili F, Rollero A, Timossi G, Gianelli MV, Copello F, Rodriguez G, Polleri A 2001
Relationships between cortisol, dehydroepiandrosterone sulphate and insulin-like growth factor-I system in
dementia. J Endocrinol Invest 24:139–146

10 - Rudman D. Growth hormone, body composition, and aging. J Am Geriatr Soc 1985; 33:800-7.

11 - Meites J. Neuroendocrine biomarkers of aging in the rat. Exp Gerontol 1988; 23:349-58.

12 - Finkelstein JW, Boyar RM, Roffwarg HP, Kream J, Hellman L. Age-related change in the twenty-four-hour
spontaneous secretion of growth hormone. J Clin Endocrinol Metab 1972; 35:665-70.
13 - Rudman D, Kutner MH, Rogers CM, Lubin MF, Fleming GA, Bain RP. Impaired growth hormone secretion
in the adult population: relation to age and adiposity. J Clin Invest 1981; 67:1361-9.

14 - van Buul-Offers S, Van den Brande JL. The growth of different organs of normal and dwarfed Snell mice,
before and during growth hormone therapy. Acta Endocrinol 1981; 96:46-58.

15 - Parra A, Argote RM, Garcia G, Cervantes C, Alatorre S, Perez-Pasten E. Body composition in hypopituitary
dwarfs before and during human growth hormone therapy. Metabolism 1979; 28:851-7.

16 - van der Werff ten Bosch JJ, Bot A. Effects of human pituitary growth hormone on body composition.
Neth J Med 1987; 30:220-7.

17 - Crist DM, Peake GT, Mackinnon LT, Sibbitt WL Jr, Kraner JC. Exogenous growth hormone treatment alters
body composition and increases natural killer cell activity in women with impaired endogenous growth
hormone secretion. Metabolism 1987; 36:1115-7.

18 - Jorgensen JOL, Pedersen SA, Thuesen L, et al Beneficial effects of growth hormone treatment in GH-
deficient adults. Lancet 1989; 1:1221-5.

19 - Crist DM, Peake GT, Egan PA, Waters DL. Body composition response to exogenous GH during training in
highly conditioned adults. J Appl Physiol 1988; 65:579-84.

20 - Salomon F, Cuneo RC, Hesp R, Sonksen PH. The effects of treatment with recombinant human growth
hormone on body composition and metabolism in adults with growth hormone deficiency. N Engl J Med
1989; 321:1797- 803.

21 - Jones AJS, O’Connor JV. Chemical characterization of methionyl human growth hormone. In: Hormone
drugs: proceedings of the FDA–USP Workshop on Drug and Reference Standards for Insulins, Somatropins,
and Thyroid- axis Hormones, Bethesda, Maryland, May 19–21, 1982.

22 - Holl RW, Hartman ML, Veldhuis JD, et al. Thirty-second sampling of plasma growth hormone in man:
correlation with sleep stages. J Clin Endocrinol Metab 1991;72:854–61.

23 - Micic D, et al. Preserved Growth Hormone (GH) Secretion in Aged and Very Old Subjects after Testing
with the Combined Stimulus GH-Releasing Hormone plus GH-Releasing Hexapeptide-6. J Clin Endocrinol
Metab. 1998 Jul;83(7):2569-72

24 - Frohman LA, Downs TR, Williams TC, Heimer EP, Pan YCE, and Felix AM. Rapid enzymatic degradation of
growth hormone-releasing hormone by plasma in vitro and in vivo to a biologically inactive, N-terminally
cleaved product. J Clin Invest 78: 906–913, 1986.

25 - Iordanova VK, Wen SY, Moreau IA, Smith SY, Frohman LA, and Castaigne JP. Every other day
subcutaneous administration of CJC-1295, a drug affinity complex (DAC)-growth hormone releasing factor
(GRF) analogue, increases body weight and bone mineral content in dogs (Abstract). 87th Annual Meeting of
The Endocrine Society, 2005, p. P1–78.

26 - Jette L, Leger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, Paradis V, van Wyk P, Pham K, and
Bridon DP. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF
receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog.
Endocrinology 146: 3052–3058, 2005.

27 - Peters JRT. All About Albumin. Biochemistry, Genetics and Medical Applications. San Diego, CA:
Academic, 1996.

28 - Hoffman, Andrew R., et al. Efficacy of a Long-Acting Growth Hormone (GH) Preparation in Patients with
Adult GH Deficiency. J Clin Endocrinol Metab 90(12):6431–6440

29 - Teichman SL, Neale A, Lawrence B, Cagnon C, Castaigne JP, and Frohman LA. Prolonged stimulation of
growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-
releasing hormone, in healthy adults. J Clin Endocrinol Metab 91: 799–805, 2006.

30 – Wen, S. et al. Immunogenicity AND Immunotoxicity Assessments of Two Drug Affinity Complexe
Compounds in Cynomogus Monkeys. Toxicologist, Report 170, 2005.

Basic Guide: Growth Hormone Secretagogues

Growth Hormone Secretagogues

In the 1980's three classes of compounds where studied to determine their effect on growth hormone
release. These three compounds were:

Growth Hormone Releasing Hormone (natural hormone) Growth Hormone Releasing Peptides (synthetic
molecules often termed "GH-Secretagogues") Opiates (Dermorphin & Benzomorphan) Individually each class
of compound when administered in laboratory rats was found to induce growth hormone release. However
when they were all combined growth hormone release dramatically increased.

Growth Hormone Releasing Hormone (GHRH) + Growth Hormone Releasing Peptide (GHRP) was found to
induce a large synergistic secretion of growth hormone (GH).

However when the Opiate was combined with GHRH & GHRP the synergy was huge amounting to a release of
GH more than double that achieved by the GHRH/GHRP combo alone.

When all three classes of compounds were examined it was discovered that each compound released GH by
a mechanism different and distinct from that of the others. Furthermore it was found that these three modes
of action accomplished growth hormone release in ways complementing and not interfering with each other.
Unfortunately opiates have several drawbacks. Not withstanding their illegality chronic use is both toxic and
addicting with undesirable alterations in normal physiology.

Fortunately we are left with two tools with which we can maximize a synergistic release of growth hormone.
These tools have no toxicity and promote desirable alterations in normal physiology.

Growth Hormone Releasing Hormone (GHRH) in the form of its long-lasting analog (CJC-1295) was discussed
in the previous article. It is therefore left to this article to discuss Growth Hormone Releasing Peptides
(GHRPs) and the human studies that demonstrate synergy between these two compounds (GHRP + GHRH).

NOTE: The information presented in this section was drawn generally from Refs: 1-11

Growth Hormone Releasing Peptides (GHRPs) - A Quick Look

What are they?

Growth Hormone Releasing Peptides (GHRPs) are synthetic forms of the natural hormone Ghrelin. These
simple short-chained amino acid peptide strings possess most of the positive characteristics of Ghrelin (such
as effecting GH secretion) and few of the negative properties (such as Ghrelin's lipogenic behavior (i.e.
conversion of glucose to fatty acids)).

GHRPs belong to a broader class of compounds all of which share the common trait of being able to bind to
the Growth Hormone Secretagogue Receptor (GHS-R) and effect GH release. These compounds include the
synthetic peptides (GHRP-6, GHRP-1, GHRP-2, Hexarelin, Ipamorelin) and smaller synthetic non-peptide
molecular compounds such as MK-0677 as well as the natural ligand Ghrelin. This broad class which includes
all of the above but not Growth Hormone Releasing Hormone (GHRH) is termed Growth Hormone
Secretagogues (GHSs).

These Growth Hormone Secretagogues (GHSs) exert their effect on increasing GH output in multiple ways.

First they INDIRECTLY increase growth hormone (GH) secretion by inducing Growth Hormone Releasing
Hormone (GHRH) release from the hypothalamus in the brain. GHRH once released makes its way to the
Growth Hormone Releasing Hormone Receptors (GHRH-R) in cells within the pituitary (a gland just below the
brain) where it binds and exerts its direct influence in signaling GH release.

Second these GHS also make there way to those same pituitary cells where they themselves bind to a Growth
Hormone Secretagogue Receptor (GHS-R) and exert a DIRECT influence in signaling GH release. This signaling
uses a different mode of action distinct from that of GHRH. As a consequence both bound GHRH & bound
GHS can exert their positive influence concurrently resulting in synergistic growth hormone (GH) release.

Third they INDIRECTLY increase GH secretion by reducing release of Somatostatin (the GH inhibiting
hormone) from the hypothalamus and DIRECTLY by reducing the magnitude of Somatostatin's inhibiting
action once it binds to its receptor on the pituitary cells.
In essence Growth Hormone Secretagogues (GHS) turn up the positive signal to release GHRH, turn down the
negative signal to release the inhibiting hormone Somatostatin, speak directly to the growth hormone
releasing pituitary cells themselves to encourage them to release GH and speak directly to the growth
hormone releasing pituitary cells themselves to encourage them to ignore Somatostatin's message to stop
releasing GH.

Oral GHS

Based on the effectiveness of GHRPs smaller non-peptide molecules were created in an effort to mimic the
GH releasing effects of GHRPs with the desire to develop a compound with high oral bioavailability. As a
result MK-0677 was eventually created as a non-peptide compound with sustainedGH release and higher oral
bioavailability. Unfortunately desensitization was found to occur fairly rapidly. In addition the dose for the
orally administered MK-0677 is measured in several milligrams while the effective dose for the injectable
GHRPs is measured in micrograms makingGHRPs more cost effective. Research is ongoing on non-peptide
GHSs, particularly with Ipamorelin derivatives so perhaps an oral GHS devoid of desensitization will
eventually be developed.

My own thought is that these molecular compounds appear to be small enough to be used in a transdermal
formula. Also it would be nice to have these orally/transdermally active compounds available to use on a
limited basis perhaps making usage when traveling convenient.

NOTE: The information presented in this section was drawn generally from Ref: 12

Growth Hormone Releasing Peptides - A Longer Look

What are they?

In 1980 the first highly potent GH-Releasing peptide was developed and named GHRP-6. This peptide was
found to illicit a strong GH release response and so became the first member of a class of growth hormone
releasing peptides more broadly called GH secretagogues. StructurallyGHRP-6 is composed of the amino
acids L-Histidine, D-Tryptophan, L-Alanine, L-Tryptophan, D-Phenylalanine and L-Lysine. The "L" form of an
amino acid is the naturally occurring form and often in the nomenclature the "L" is dropped. The "D" form
does not occur in nature and is the isomeric form (i.e. mirror image) of the naturally occurring "L" form.

GHRP-6 is composed of both natural and isomeric forms of those aforementioned six amino acids. Its
structure is represented as:

His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

Investigators subsequently modified the structure of GHRP-6 and identified more potent peptides. For
example, activity was enhanced by replacing D-Trp with D-2-(2-napthyl)alanine and His with D-Alanine to
create GHRP-2 whose structure is represented as:
D-Ala-D-2 Nal-Ala-Trp-D-Phe-Lys-NH2

In 1982, after a long search the natural hormone "Growth Hormone Releasing Hormone" (GHRH) was finally
isolated and identified. As a result the interest in Growth Hormone Secretagogues (at that point limited to
the three peptides) faded. Eventually researchers discovered that those GH-Releasing Peptides (specifically
GHRP-6 & GHRP-2) followed a mode of action which bound them to and was mediated through receptors
different from those for GHRH. In addition researches discovered that these GH-Releasing Peptides acted
synergistically with the natural hormone Growth Hormone Releasing Hormone (GHRH) in vivo (in both
laboratory animals & humans) to produce large releases of Growth Hormone.

Taken together these two discoveries made it clear that GHRPs were not simply surrogates of GHRH. GHRP-6
and its analogues were artificial activators of a separate newly discovered receptor termed the "Growth
Hormone Secretagogue Receptor" (GHS-R). Eventually the natural hormone Ghrelin was discovered as the
endogenous ligand that binds to the GHS-R. Together the natural hormone Ghrelin, and all the synthetic
compounds (both peptides & smaller molecules) such as GHRP-6 were termed "Growth Hormone
Secretagogues" (GHSs).

This nomenclature continues in the literature to this day however increasingly new terminology is used. For
instance the "Ghrelin Receptor" is synonymous with "GHS-R" and "Ghrelin mimetics" are synonymous with all
the synthetic compounds that are capable of binding to the GHS-R. This paper uses the more established
nomenclature throughout.

NOTE: The information presented in this section was drawn generally from Refs: All of the Bower's studies

Pituitary Actions of GHSs

All GHSs act directly on the pituitary. They do so by binding to and activating their specific receptor (GHS-R).
Once this occurs GH secretion is commanded to rise. GHRH does the same thing. It acts directly on the
pituitary and binds to and activates its specific receptor (GHRH-R). Once this occurs GH secretion is
commanded to rise.

However GHSs and GHRH operate through a different "mode of action" or intracellular signaling system
within the cell that eventually activates GHsecretion. These modes of action are contrasted as follows.

GHRH when it binds to its receptor (GHRH-R) on the cellular membrane of a somatotrope cell activates the
cAMP–PKA (cAMP-dependent proteinkinase) pathway (in essence a secondary messenger), and by a poorly
understood mechanism causes a persistent rise in intracellular Calcium (Ca2+) ions by opening Ca2+ channels
(simply ports on the cell membrane that open and close to either permit or deny entry) on the cellular
membrane and letting into the cell Ca2+ from the outside. The rise in calcium concentration within the cell
signals in conjunction with other signaling processes the instruction to the somatotrope cell to release
Growth Hormone.
It should be noted that Somatostatin (the GH inhibiting hormone) once bound to its receptor brings about a
decrease in GH in part by inhibiting cAMP formation. As a consequence of limiting this messenger the
signaling cascade is weakened resulting in less Calcium (Ca2+) ions entering the cell and thus inhibition of GH
release.

GHSs however do not rely on cAMP as a messenger. GHSs once bound to their respective receptor initiate a
process that leads to an inhibition of Potassium (K+) ion channels. This action results in a sustained
depolarization of the cellular membrane. The result is identical to that affected byGHRH, namely the Calcium
ion level rises via voltage-activated channels leading to the signal to secrete GH. But the mode of action relies
on the use of depolarization of the cellular membrane and inhibiting Potassium ion channels rather then
GHRH's cAMP-mediated opening of Calcium ion channels.

In addition to allowing Ca2+ into the cell, GHSs may also cause a rise in intracellular Ca2+ by redistribution
from internal stores of Ca2+ within the cell. This process is mediated by the generation of inositol
trisphosphate whose main functions are to mobilize Ca2+ from storage organelles and to regulate cell
proliferation.

This brief description is an over simplification. The important point is that GHRH and GHS act through their
own receptors and distinct intermediate pathways.

This is not the only difference. Although the image herein depicts one pituitary somatotrope with both types
of receptors activated (GHRH-R &GHS-R) this may not give a completely accurate picture. GHRH and GHS
appear to act on different somatotrope subpopulations. GHRP has been shown to increase the number of
somatotropes releasing GH, without altering the amount of hormone released by each individual cell. On the
other hand, GHRH stimulates both the number of cells secreting GH and the amount of GH secreted per cell.

From these limited discoveries we can begin to understand how GHRH and GHSs compliment each other's GH
releasing actions rather then duplicate one another.

It should be noted that Somatostatin (the GH inhibiting hormone) has been shown primarily to decrease the
number of cells secreting GH without affecting the amount of GH secreted per cell.

To sum up in very general terms GHS increases, while Somatostatin decreases, the number of active GH
secreting somatotropes, probably because these two factors act by depolarizing and hyperpolarizing cells,
respectively (i.e. GHSs turns the cell into a Calcium ion sponge &Somatostatin turns the cell into a squeegee,
squeezing out and repelling Calcium ions).

On the other hand GHRH does both, but acts primarily by stimulating the amount of secreted GH within the
active somatotropes.

NOTE: The information presented in this section was drawn generally from Refs: 13-17
Hypothalamic Actions of GHS

In vitro (in a laboratory dish) the amount of GH release from GHRH and GHSs is additive. GHSs cause a rise of
2...GHRH causes a rise of 1...put them together and the GH rise is merely the sum 3.

But something different happens when you put these two compounds into living breathing mammals. In vivo
(in body) the GH rise that occurs from the combination of GHRH and GHSs is more then the sum of their
individual contributions. There is substantial synergy such that 1 + 2 = 6.

This occurs as a result of GHSs actions within the Hypothalamus (region of the brain) rather then its direct
pituitary actions. There are GHSreceptors (GHS-R) in the hypothalamus; perhaps even subtype receptors.
When GHSs bind to these receptors they behave like a hypothalamic neurohormone and as such exhibit a
dual action.

They stimulate endogenous GHRH release and concurrently suppress endogenous Somatostatin release. How
they do this is a complex process with much still unknown. Basically they incite electrical activation of arcuate
neurons (within the hypothalamus). About seventy-five percent of the cells excited by GHRP-6 project
outside the blood brain barrier (hypothalamus) into the median eminence (boundary between hypothalamus
& the portal system which connects to the pituitary which lies just below the brain) and are neurosecretory
involved in the regulation of pituitary function.

The activation of these neurons by GHRP-6 is extremely long lasting (longer than 1 hour) and reaches the
peak rapidly (within 5 to 10 minutes). Non-peptide GHSs respond slower perhaps for the reason that they
penetrate the blood brain barrier slower than GHRP-6.

GHRP-6s excitation of neuronal activity beyond those neurons that regulate GHRH & Somatostatin (i.e. the
remaining 25%) may account for some of the impact GHRPs have on non-GH releasing activity.

The important point is to recognize that GHSs have an impact on GHRH release and Somatostatin suppression
at the hypothalamus which appears to be responsible for the now well-recognized synergistic effect on GH
release from concurrent administration of GHRH & GHRPs in vivo.

Furthermore it should now be firmly understood that GH release is regulated by the following trinity - GHRH,
Somatostatin and GHSs.

NOTE: The information presented in this section was drawn generally from Refs: 13-5, 9, 18

GHS Potency (i.e. efficacy) & Dosing in Humans

When administered at clinical research dosages, all GHSs (both peptides and non-peptides) release
significantly larger amounts of GH (i.e. are more efficacious) than GHRH. This is not to be confused with the
term potency which takes into account the molecular weight of a compound and thus measures GH output
on a "per mol" basis. By this measure GHRH is more potent.
However if the desire is to administer these compounds and effect GH release then the only relevant
standard is absolute amount of GH release and in that regard GHSs release more GH than GHRH. The
following standards determined through clinical study will specifically clarify this concept.

In humans the maximal i.v. dose for GHRH has been found to be 1 mcg per kg of bodyweight. That is a level
that saturates the receptors and beyond which there is no further benefit, until that dosage has dissipated.

In humans the maximal i.v. dose for GHSs such as hexarelin has been found to be 2 to 3 mcg per kg of
bodyweight. In normal humans (i.e. those without disease or clinical malady) GH release is increased as the
GHS dose increases up to the aforementioned maximal dose. Even very small amounts have been shown to
have positive effects.

Unlike GHRH, GHSs are resistant to well-known inhibitors of GH secretion. Studies demonstrate that
hexarelin-mediated GH secretion is reduced but not blocked by a rise in circulating free fatty acids or by a
glucose load, nor by an infusion of Somatostatin nor drugs that enhance hypothalamic Somatostatin
secretion.

GHRH is influenced by metabolic and hormonal factors that consequently make GHRH a very unpredictable
GH stimulator, with large variations between individuals and a diversity of peaking times.

In contrast GHSs are not greatly influenced by metabolic and hormonal factors, the absence of which makes
GHSs a very predictable GHstimulator. GHSs are potent and efficacious, their actions synchronized and
reproducible, with no non-responders.

GHSs have been repeatedly demonstrated in studies to be very strong GH releasers in healthy young males.
In addition GHSs have been shown in studies to be very strong GH releasers in females at all stages of the
menstrual cycle. This again is important to note because GHSs are not greatly affected by changes in various
hormone levels, be they thyroid hormone, estrogen, etc.

There may be an age-related reduction in the GH-releasing capability of GHSs. The studies have not yet been
able to come to a consensus. However, the synergistic effect of GHRH and GHS on GH secretion is not
reduced as humans age throughout the entire lifespan. This holds true even for the very old (Those in their
90's).

There are no reported side-effects with GHS usage. However both the peptidyl and non-peptidyl compounds
have been found to induce slight increases (still within what is deemed the normal range) in prolactin and in
adrenocorticotrophin(ACTH)/cortisol, and in a few studies dehydroepiandrosterone (DHEA). Low to moderate
dose (1 mcg/kg) administration of GHRP-6 has been found to result in very large GH release with no
significant effects on cortisol or prolactin. Of the peptides, Hexarelin appears to induce the highest level of
these hormones (prolactin & cortisol). Ipamorelin a newer GHS has no effect on these hormones no matter
what the dose.
NOTE: The information presented in this section was drawn generally from Refs: 19-31

Why you need both GHRH analog (CJC-1295) and GHRP

GHS Down Regulation

A single dose of a GHS in vivo brings about an immediate down-regulation of responsiveness to subsequent
administration. This desensitization appears to abate and sensitivity fully restored within a few hours.

However continual infusion of large amounts of GHS brings about a substantial initial release of GH, followed,
after several hours, by long-term down-regulation of GH secretion.

The only published comparison of the results of differing modes of GHS delivery (twice daily injections vs.
continuous infusion) in vivo demonstrated a dramatic dissipation of anabolism following infusions of high-
dose GHS. However a pronounced anabolic effect was maintained with the same dose of GHS administered
by intermittent injection.

From the results of this study graphed out above it is evident that with GHSs the optimal dosing pattern is
administration by injection with sufficient intervals between dosing so as to maintain sensitivity.

The effectiveness is greatly diminished, perhaps to the point of having no benefit if GHSs duration of action
becomes prolonged and sustained.GHSs unlike GHRH are best used to amplify those very import GH pulses
while GHRH is effective at raising the total level of GH.

If we understand desensitization than we will easily understand why the oral GHS, MK-0677 in recent studies
failed to demonstrate a "maintained acceleration of statural growth in children with GH-deficiency". MK-
0677 was developed to be a long lasting orally active analogue of GHRP-6. MK-0677 is to GHRP-6 what CJC-
1295 is to GHRH (i.e. long-lasting).

The problem is that while long-lasting analogues of GHRH do not result in desensitization and pronounced
down-regulation, long-lasting analogues of GHRP-6 do desensitize and consequently lose effectiveness.

CJC-1295 brings about persistent and chronically elevated levels of GH while GHRP-6 if injected a couple of
times a day amplifies the very important GH pulses. The two compounds greatly compliment each other. In
the previous article on GHRH & CJC-1295 we discussed the importance of pulsation which has been shown to
be necessary for growth. The other important component of anabolism is chronic GH elevation.

Continuously elevated levels of GH increase IGF-I levels more than intermittent increases in GH. The
intermittent nature of GH release brought on by GHSs' mode of action does create a rise in IGF-I levels but
the anabolic effect may not be pronounced.

It has been repeatedly demonstrated and is now recognized that in children the growth response to
injections of IGF-I is far less than the growth response to injections of GH. This is in accordance with most
animal studies, which demonstrate that treatment with IGF-I does "not produce the full anabolic and growth-
promoting effects of GH treatment".

Protocols that elevate GH while maintaining and amplifying the pulses seem to be effective at producing
anabolism. The combination of CJC-1295 and GHRP-6 do just that.

NOTE: The information presented in this section was drawn generally from Refs: 32-37

GHRH (and analogs) + GHSs = a lot of synergistic growth hormone release

There is not a lot of deviation in the published studies on the effect of these peptides and the saturation dose
needed to bring about the effect in normal people (who often act as a control group).

We need only to examine the results of the normal test subjects from three oft-cited studies that established
the relevant protocol.

In the first study "Inhibition of growth hormone release after the combined administration of GHRH and
GHRP-6 in patients with Cushing's syndrome", Alfonso Leal-Cerro..., Clinical Endocrinology 1994, 41 (5) , 649–
654, three different peptide/peptide combinations were used.

GHRH was administered alone at 100mcg. This resulted in area under the curve (AUC) measured for 120
minutes of GH secretion of 1420 ± 330.

GHRP-6 was administered alone at 100mcg. This resulted in area under the curve (AUC) measured for 120
minutes of GH secretion of 2278 ± 290.

GHRH plus GHRP-6 was administered together at 100mcg each. This resulted in area under the curve (AUC)
measured for 120 minutes of GHsecretion of 7332 ± 592.

As a single dose these results show that GHRP-6 is about twice as effective as GHRH.

The synergy between GHRH & GHRP-6 is clearly evident as co-administration resulted in twice the benefit of
the additive values of single doses of the two peptides.

The second study is the one that established the saturation dose for these peptides often used in other
studies. "Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts
synergistically with GH-releasing hormone ", CY Bowers..., J. Clin. Endocrinol. Metab., Apr 1990; 70: 975-982.

In that study GHRH at a dose of 1.0 microgram/kg was administered alone and then together with various
doses of GHRP-6 (0.1, 0.3, and 1.0 microgram/kg). They found that the submaximal dosages of 0.1 and 0.3
microgram/kg GHRP-6 plus 1 microgram/kg GHRH did have the effect of stimulating GH release
synergistically.
However the larger dose of 1 mcg/kg of GHRP-6 was found to be the saturation dose when used in
combination w/ 1 mcg/kg of GHRH.

It is also noteworthy that serum prolactin and cortisol levels rose about 2-fold above base levels only at the 1
microgram/kg dose of GHRP-6 and not at the submaximal dosages.

The final study, "Preserved Growth Hormone (GH) Secretion in Aged and Very Old Subjects after Testing with
the Combined Stimulus GH-Releasing Hormone plus GH-Releasing Hexapeptide-6", Micic D..., J Clin
Endocrinol Metab. 1998 Jul;83(7):2569-72 is fascinating for several reasons.

By reference to citation it is noted that "GHRH plus GHRP-6 (both at saturating dose) is nowadays considered
the most potent stimulus of GHsecretion in man being able to restore the GH secretion in states associated
with chronic blockade of somatotroph activity (as in obesity)...it elicits a near-normal GH discharge in obesity,
in patients with hypothyroidism and in patients with type 2 diabetes mellitus."

This particular study examined the effects of combined administration of GHRH, immediately followed by
GHRP-6 in a group of very old subjects (age higher than 75 yr), as compared with both normal adults (less
than 40 yr) and aged subjects (age 46–65 yr). The dosing levels used were 90mcg of GHRH followed by
1mcg/kg of GHRP-6.

All the subjects had a positive GH secretory response to the combined administration with no differences
observed between men and women. However the group comprising the very old had the highest level of GH
release followed by the group comprising the aged subjects with the "less than 40 yr group" experiencing a
substantial rise but not as high as the other two groups.

The study concluded that the lack of side-effects & safety of the protocol and the discovered lack of age-
related decline in the "GHRH-GHRP-6-mediated GH release opens the possibility of using it as a therapeutical
tool to revert some deleterious manifestations of aging in man."

In CONCLUSION, Growth Hormone (GH) is regulated by a trinity composed of Growth Hormone Releasing
Hormone (GHRH), Growth Hormone Secretagogues (GHS) and Somatostatin. GHRH and GHSs individually
have a positive impact on GH secretion. These two compounds operate through distinct modes of action
which complement each other and when administered together result in synergistic GH secretion.

Growth Hormone Releasing Peptides (GHRPs), a subclass of GHSs are effective across all age groups in
amplifying GH pulses. Pulsation is a necessary component of growth generation in mammals. GHRH when co-
administered with GHRPs has the effect of further increasing the amplitude and "area under the curve" of a
GH pulse. The result is a GH pulse many multiples more effective then that achieved by an unaided GH pulse.

In addition to pulsation, overall growth is better accomplished when total levels of GH are elevated without
hindering pulsation. Elevated GH levels appear to be a necessary component of growth generation as well.
 One of the reasons this is so appears to be that chronically elevated GH levels result in more pronounced
sustained levels of IGF-1 then that achieved through intermittent GH elevations.

Persistent levels of GHRH do not result in desensitization. Elevated levels of GHRH result in sustained GH
release. A long-lasting version of GHRH, CJC-1295 has demonstrated the ability to sustain elevated GH levels
in humans.

GHRP-6 is perhaps the most well studied of all GHSs. In physiological doses there are virtually no side effects.
It has been demonstrated to be effective for all age groups.

Combined administration of CJC-1295 and GHRP-6 is a very effective, well studied method of increasing the
total amount of GH secreted within the body. By adjusting the dosing of these compounds and accounting for
such factors as age one may choose to achieve a "youthful" restoration, an above normal elevation or a
substantially above normal elevation of both GH levels and pulsatile release.

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Growth Hormone Administration vs. CJC-1295/GHRP-6 + GHRH

Units of Measurement

Growth Hormone (GH) like other biologically active substances is measured in International Units
(abbreviated as IU) which are based on the measured biological activity for that substance the establishment
of which is determined by international agreement. International Units are specific to each substance and so
one IU of one substance has no equivalence to one IU of another substance.

While it is fairly straightforward to compare the amount of GH among various dosing administrations (a two
(2) iu dose is twice the amount of a four (4) iu dose) and it is easy to ask the manufacture the weight of each
iu (Nutropin reveals that 1 iu of their GH is equal to 333 mcg while Lilly's Humatrope trials define 1 iu as 370
mcg (2.7iu per 1mg)) it is not so simple to compare Growth Hormone to other "Growth Hormone Releasing"
compounds such as CJC-1295 and GHRP-6.

Practically all studies that use Growth Hormone (GH) or Growth Hormone Releasing Hormone (GHRH) or its
analog CJC-1295 or Growth Hormone Releasing Peptides all take blood samples to measure the amount of
GH present in blood plasma at various points in time. The unit of measurement is a standardized unit which
can be used to make comparisons across different compounds.

The studies either report results as "nanograms (ng) per milliliter (ml)" or "micrograms (ug) per liter (L)". For
the reason that ng = 1/1000 ug and ml = 1/1000 L, ng/ml will always equal ug/L. So no matter how the studies
report results comparison is straightforward. In making the cross-comparisons contained herein for simplicity
I have chosen to report results as ng/ml.

In addition the amount of hormone released into plasma (i.e. concentration) is based on units divided by
time. This measurement is called area under the curve (AUC). However some studies will use the hour as the
unit of time while others will use the minute. Therefore comparing AUCs between studies using different
units of time requires a conversion to a common unit of time.

I will make the conversion herein in written form but be careful when you look at graphs.
Therefore this examination will look to several studies involving administration of the compounds of interest
and compare the blood plasma levels of GH and peak concentration as a result of administration of each
tested compound. The result of this cross-study examination will reveal the efficaciousness of various doses
of GH, CJC-1295 and GHRH + GHRP-6 in increasing GH in blood plasma.

Studies used for comparison

Growth Hormone Administration

The primary study used herein is the Lilly Clinical trial using single dose administration of Humatrope in
normal adults to assess pharmacokinetics. The doses used were .05 IU/kg (intravenously) and .27iu/kg
(subcutaneously and intramuscular). In an 80kg adult that equates to 4iu and about 22iu. In our comparison
we will only look at the 22iu subcutaneous and intramuscular dose.

CJC-1295 Administration

In "Prolonged Stimulation of Growth Hormone (GH) and Insulin-Like Growth Factor I Secretion by CJC-1295, a
Long-Acting Analog of GH-Releasing Hormone, in Healthy Adults", Sam L. Teichman, et al. Journal of Clinical
Endocrinology & Metabolism 91(3):799-805, sixty-six healthy normal men and women aged 21-61 were
administered various doses of CJC-1295 (long-lasting GHRH analog). The CJC-1295 was administered in a
single dose and again in some groups 7 days later and other groups 14 days later. For the reason that we are
only examining a week's worth of data only the initial dose is of interest. Blood samples were collected
before dosing and then at 15, 30, and 60 minutes and 2, 3, 4, 6, 8, 10, 12, and 24 hours afterdosing; and then
every 8 hours on days 2–3, then daily on days 4, 5, 6, 7.

The doses administered were: 30mcg/kg; 60mcg/kg; 125mcg/kg; 250mcg/kg

GHRH + GHRP-6 Administration

While we are limited in our choice of GH administration studies and CJC-1295 studies (there are only two, the
results of which are available to the public) we have many available studies measuring the effects of co-
administration of GHRH and GHRPs.

So we will briefly look at the results from two studies to give us an idea of how much GH release is
contributed by the enhanced pulse brought on by this synergistic combination.

They are, "Inhibition of growth hormone release after the combined administration of GHRH and GHRP-6 in
patients with Cushing's syndrome", Alfonso Leal-Cerro, et al., Clinical Endocrinology 1994, 41 (5) , 649–654

and

"Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with
GH-releasing hormone", Bowers, C.Y., et al. J. Clin. Endocrinol. Metab. 70, 975–982.
What's Normal?

Before we look at the studies lets take a brief look at how much growth hormone (GH) is secreted naturally.

The following very comprehensive study measured growth hormone output over twenty-four hours among
healthy normal people of all ages.

Age-Related Changes in Slow Wave Sleep and REM Sleep and Relationship With Growth Hormone and
Cortisol Levels in Healthy Men, Eve Van Cauter, PhD; Rachel Leproult, MS; Laurence Plat, MD, JAMA. 2000;
284:861-868

The youngest category, those under 25 years of age secrete about 2iu of GH per 24 hours, while those in
older categories sectrete 1 iu or less.

Note that Humatrope indicates that absolute bioavailability of an intramuscular or subcutaneous dose is
about 66%. So perhaps 3iu of exogenously administered synthetic GH is a replacement dose equivalent to 2iu
of indogenously secreted GH.

Comparing GH administration to CJC-1295 administration

Total GH Release:

When CJC-1295 was administered at 30mcg/kg; 60mcg/kg; 125mcg/kg and 250mcg/kg the total GH levels
(area under the curve (AUC)) were respectively:

AUC: 758, 969, 977, and 1370 ng/ml per hour

Keep in mind that for a 80kg adult the 30mcg/kg dosing amounts to 2.4mgs of CJC-1295 per week and the
60mcg/kg dosing amounts to 4.8mgs of CJC-1295.

So 2.4 mgs of CJC-1295 produced an AUC of 758 ng/ml per hour.

When synthetic Growth Hormone (Humatrope) was administered at the equivalent of 22iu (in someone
weighing 80+ kg) the following GH levels (area under the curve (AUC)) were reached:

AUC Intramuscular: 495 +/- 106

AUC Subcutaneous: 585 +/- 90

Peak Concentration:

However the GH release pattern results in a much higher mean maximum concentration for the GH
administration than the CJC-1295 administration.

The GH study resulted in peaks of 53 to 63 ng/ml.

The CJC-1295 study resulted in dose respected peaks of 6.6; 9.6; 9.9; 13.3 ng/ml.

Comparing GH administration to GHRP + GHRH administration

Total GH Release:

The Alfonso Leal-Cerro study demonstrated the following GH release:

GHRH by itself dosed at 100mcg resulted in: (AUC) 120 minutes = 1420 ± 330 ng/ml when we convert that to
AUC measued in hours we get about: 25 ng/ml

GHRP-6 by itself dosed at 100mcg resulted in: (AUC) 120 minutes = 2278 ± 290 ng/ml when we convert that
to AUC measued in hours we get about: 40 ng/ml

GHRH + GHRP-6 dosed together at 100mcg each resulted in: (AUC) 120 minutes = 7332 ± 592 ng/ml when we
convert that to AUC measued in hours we get about: 130 ng/ml The Bowers study demonstrated that a small
dose of GHRP (.1mcg/kg) added to a saturation dose of GHRH (1mcg/kg) resulted in the following GH release:

(AUC) 120 minutes = 10,065 ng/ml when we convert that to AUC measued in hours we get about: 170 ng/ml

In comparison to synthetic GH administration we find that:

22iu of synthetic GH results in 495 - 585 ng/ml Saturation doses of GHRH & GHRP results in 130 - 170 ng/ml

These results indicate that 22iu is between 3.8 and 3.4 more efficacious then a single administration of GHRH
& GHRP which means that a single dose of GHRH & GHRP has the potential to produce better then the
equivalent of 5iu of GH in plasma.

A dosing protocol of GHRH + GHRP at saturation dose, administered 3 times per day has the potential to
exceed the equivalent of 15iu.

Note though that using this methodology GHRP-6 at a saturation dose by itself may add the equivalent of 1.4
to 1.8 iu per administration... or 4.2 to 5.4 iu per day if administered three times.

Peak Concentration:

From the graphs it is easy to see that GHRH+GHRP results in short-term peaks of 80 to 130 ng/ml.

While the synthetic GH study resulted in less pronounced peaks of 53 to 63 ng/ml of longer duration.

Systemic IGF-1 levels

Simply stated the synthetic Growth Hormone when administered intramuscularly or subcutaneously in high
enough dose results in a release profile that is not pulsatile. The release profile is an elevation and this
elevation results in higher levels of systemic IGF-1 in circulation then either an intravenous administration of
GH or administration of the pulsatile peptides.
While multiple daily dosings of GHRH/GHRP result in a significant rise in systemic IGF-1 (not graphed out
here) they do not over time result in as substantial an elevation of circulating IGF-1 as synthetic GH
administered non-intravenously.

To understand the difference in GH in plasma profile of synthetic GH administered by intravenous I provide a

copy of the GH study graph identical to the clinical study graph posted above with the addition of the
intravenous dosing of GH. As you can see intravenous dosing of GH results in what could be described as a
pulse because GH is elevated very high and then clears quickly.

So what does a high dose of synthetic GH administered subcutaneously or intramuscularly (but not by IV) do
to systemic levels of IGF-1?

To find out we must switch to a Japanese study which undertook such study.

In Pharmacokinetics and Metabolic Effects of High-Dose Growth Hormone Administration in Healthy Adult
Men, Toshiaki Tanaka, et al., Endocrine Journal 1999, 46 (4), 605-612, fifteen healthy normal Japanese adult
males aged from 20 to 27 years were administered various doses of recombinant GH (Norditropin). The GH
was administered in a single dose at 9:00 a.m. after overnight fasting. Blood samples were collected at 0, 1, 2,
3, 4, 5, 6, 9, 12 and 24 hours after the single injection.

The doses administered were: .075iu/kg; .15iu/kg and .30iu/kg When the average weight of each test subject
is accounted for the doses administered approximated: 5iu; 10iu and 20iu

In the higher dose category the study dosed every day for a week and collected blood samples each day.

IGF-1 levels were measured and can be graphed as follows:

From this graph a few quick things can clearly be understood:

• IGF-1 creation is a slow ongoing process that increases every day that you administer GH until it plateaus
after a week. This should tell you that there is no fear that anything will specifically interfere with GH's ability
to instigate IGF-1 creation. All of the timing protocols which fear that insulin or "this and that" will interfere
with IGF-1 creation are baseless and such "write-ups" that call for timing are flawed. • It is constant GH
elevations that result in ever higher levels of systemic IGF-1 creation

What none of this tells us

This does not tell us what is happening locally. By locally I mean IGF-1 that is not made in the liver and
circulated systemically. Local IGFs are made in small amounts and used exclusively in the tissue of their birth.

Local IGF-1 in muscle has been demonstrated to be responsible for muscle growth and only if muscle-made
IGF-1 is lacking does systemic IGF-1 play a significant (although incomplete) role.
Local IGFs in muscle are increased by growth hormone and testosterone. It is conjectured that pulsatile GH
(such as IV dosing) or the use of GHRH/GHRPs results in high levels of muscle IGFs w/o creating high levels of
systemic circulating IGFs.

SWS & GH release

There are two types of sleep, rapid eye movement (REM) and non-rapid eye movement (NREM). Sleep
proceeds in cycles composed of four types of stages of NREM and a stage of REM usually ordered as: 1 > 2 > 3
> 4 > 3 > 2 > REM

The cycle lasts on average 90 to 110 minutes, with a greater quantity of stages 3 and 4 experienced early in
the night and more REM later in the night.

NREM accounts for 75–80% of total sleep time. Non-REM is comprised of four stages; stages 1 and 2 are
considered 'light sleep', and 3 and 4 'deep sleep' or slow-wave sleep (SWS).

It has been shown that sleep, more specifically slow-wave sleep (SWS), does affect growth hormone levels in
adult men. During eight hours sleep, it has been demonstrated in several studies that the men with a high
percentage of SWS (average 24%) also had high growth hormone secretion, while subjects with a low
percentage of SWS (average 9%) had low growth hormone secretion.

In one very complete study referenced by several others, it was demonstrated that “GH secretory rates and
peripheral GH concentrations were maximally correlated with sleep stage, with lags of 4.5 and 16 min,
respectively, suggesting that maximal GH release occurs within minutes of the onset of stage 3 or 4 sleep”.

Furthermore “sleep-related augmentation of GH secretion… usually occurs around midnight and the GH
levels at that time are, as a rule, at their highest during the 24-hour period. Partially, this phenomenon is
time-entrained and partially related to sleep itself. It is associated with a slow wave sleep, and the maximal
GH levels occur within minutes of the onset of slow wave sleep” -Holl RW, Hartman ML, Veldhuis JD, et al.
Thirty-second sampling of plasma growth hormone in man: correlation with sleep stages. J Clin Endocrinol
Metab 1991;72:854–61.

The origin of nocturnal GH release in humans is still unknown. Most likely hypothalamic GHRH release is a
major contributing component, but an additional role of another factor, presumably augmenting GHRH
responsiveness of the somatotrophs, is likely. However the precise explanatory mechanisms are still not fully
identified.

It is worth reiterating though that nocturnal release of GH makes up only a fraction of the total daily GH
release in women, but the bulk of GH output in men.
Modified GRF(1-29) is different then GRF(1-29)

NOTE that native GRF(1-29) is native GHRH or GRF(1–44) with the inactive final 15 amino acids removed.

It is very important to use ONLY modified GRF(1-29) w/ the four amino acid substitutions as discussed before
and NOT unmodified GRF(1-29) Enhanced stability and potency of novel growth hormone-releasing factor
(GRF) analogues derived from rodent and human GRF sequences, Robert M. Campbell, Peptides Volume 15,
Issue 3, 1994, Pages 489-495

Native human GRF(1–44)-NH2 (hGRF44) is subject to biological inactivation by both enzymatic and chemical
routes. In plasma, hGRF44 is rapidly degraded via dipeptidylpeptidase IV (DPP-IV) cleavage between residues
Ala [at the 2nd position] and Asp [at the 3rd position]. The hGRF44 is also subject to chemical rearrangement
[at the 8th position] and oxidation [at the 27th position] in aqueous environments, greatly reducing its
bioactivity.

It is therefore advantageous to develop long-acting GRF analogues using specific amino acid replacements at
the amino-terminus [2nd position] (to prevent enzymatic degradation): residue 8 (to reduce isomerization)
and residue 27 (to prevent oxidation). Inclusion of Ala [at the 15th position] substitution for Gly, previously
demonstrated to enhance receptor binding affinity, would be predicted to improve GRF analogue potency.

In vitro, these analogues were approximately threefold more potent than hGRF44, whereas in vivo they were
eleven- to thirteenfold more potent. As the in vitro results reflect only receptor affinity and signal
transduction, the increment in potency observed in vivo is likely due to the increased biological half-life of
these analogues (i.e., the result of decreased enzymatic and chemical decomposition such that more
bioactive peptide is available per unit time). So these changes are made to reduce enzymatic cleavage, amino
rearrangement and oxidation in plasma.

In addition "Ala [position] 15-substitution (for Gly) displayed 4–5 times higher affinity for the GRF receptor
relative to hGRF(1–44)-NH2...and hence potency." - GRF analogs and fragments: Correlation between
receptor binding, activity and structure, Robert M. Campbel, Peptides Volume 12, Issue 3, May-June 1991,
Pages 569-574

So the above highlighted amino acids need to be modified to:

2nd position - D-Ala 8th position - Gln 15th position - Ala 27th position - Leu

How GHRPs are cardio-protective

The growth hormone secretagogues (GHS) are a family of synthetic compounds originally selected for their
potent and specific effects on GH release. Nonetheless, it has been reported by us and other researchers that
the GHS have also many extraendocrine actions, including those on energy metabolism and cardiovascular
function. Ghrelin, the endogenous GHS, specifically binds to the GHS-R1a, a receptor that has been proposed
to mediate the biological activities of endogenous and synthetic GHS.

The activation of the GHS-R1a is not enough to explain the results that we have previously reported on the
ability of hexarelin, a synthetic full agonist of the GHS-R1a, to protect the rat heart from the damage induced
by the ischemia-reperfusion procedure. In fact, the GHS-R1a is not expressed in the myocardium, and ghrelin
is much less effective than hexarelin in protecting the heart from ischemia-reperfusion damage.

Moreover, it has also been demonstrated that in the cardiovascular system hexarelin and other GHS can also
bind to the CD36, a scavenger receptor.

Interestingly, a large similitude exists between the cardioprotective effects of hexarelin and those of some
angiotensin-converting enzyme (ACE)-inhibitors. For this reason, we have decided to ascertain whether
hexarelin, ghrelin and other synthetic GHS can modify the catalytic activity of serum and tissue ACE in rats
and humans.

Briefly, 10 ul of serum or tissue homogenate were incubated in presence of hippuryl-histidyl-leucine, a

substrate of ACE that is cleaved to histidyl-leucine. The cleavage of the substrate was quantified by
measuring the fluorescence at 365/495 nm (excitation/emission) in presence of orthophthaldialdehyde.
Enalapril was chosen as reference ACE-inhibitor.

Hexarelin (1 to 100 uM) dose-dependently blunted ACE activity up to about 50% in rat and human plasma
and rat lung, heart and kidney. Enalapril (0.1 to 5 uM) dose-dependently inhibited ACE activity in serum and
tissues up to 85%. Ghrelin (1 to 100 uM) did not significantly modify serum and tissue ACE activity at all the
concentrations tested, whereas other synthetic GHS-R1a ligands demonstrated a dose-dependent inhibition
of ACE activity ranging from 10 to 85%.

We conclude that the protective actions of certain GHS on the cardiovascular system might be mediated, at
least in part, by the capability of these compounds to modulate the ACE activity in the general circulation and
locally in tissues. Source: Characterization of a Novel Extraendocrine Action of the Growth Hormone
Secretagogues: Inhibition of Angiotensin-Converting Enzyme (ACE) Activity, A Torsello, M Ravelli, E Bresciani,
I Bulgarelli, L Tamiazzo, S Caporali, V Locatelli,

Dept of Experimental Med, Univ of Milano-Bicocca, Monza, Italy; Interdepartmental Ctr for Bioinformatics
Proteomics, Univ of Milano-Bicocca, Monza, Italy

Ghrelin (assumed GHS) increases GH signalling in muscle

I have always maintained that GH signaling activity in muscle or autocrine/paracrine IGFs in muscle are more
important then circulating systemic levels.

Well here is support for Ghrelin (assumed the mimetics of GHRPs as well) inducing these important changes.
Ghrelin infusion stimulated endogenous GH secretion, which peaked at t = 60 min ...Western blots performed
on skeletal muscle biopsies revealed distinct STAT5 phosphorylation in all six subjects 30 min after the
endogenous GH burst ...

This investigation is also the first to document that ghrelin-induced endogenous GH release translates into
Janus kinase/STAT signaling in skeletal muscle. - Ghrelin Infusion in Humans Induces Acute Insulin Resistance
and Lipolysis Independent of Growth Hormone Signaling, Esben Thyssen, Diabetes, December 1, 2008;
57(12): 3205 - 3210

Hormonal Set-Points

Here is evidence that there are set-points for hormones which can change based on environmental factors. It
is very interesting that these environmental events can shift hormonal parameters that exhibit themselves
throughout the post-shift life period.

It is a deep but possible conjecture that we could shift hormonal set-points in general as a therapy for those
with low hormonal levels perhaps by triggering a "famine state" or prolonged fast.

Exposure to the Dutch Famine of 1944 -1945 and Shifts in Hormonal Set Points: Parathyroid Hormone, Paulus
A. H. van Noord, J. Nutr. 135:3037S-3060S, December 2005

BACKGROUND: Exposure to the 1944–1945 Dutch famine was shown to be associated with increased levels
of androgens, estrogens, and insulin-like growth factor later in life, hormones under control of the pituitary
luteinizing hormone/follicle stimulating hormone and growth hormone axes. Moreover, exposed women
were at increased risk of breast cancer.

A neurodevelopmental set-point-shift hypothesis, proposed to consolidate these findings, predicts a

mechanism of shifting in hormonal set points. In the present study, we tested whether famine exposure
affects parathyroid hormone (PTH).

STUDY DESIGN: We used data from a study on osteoporosis nested within the DOM breast cancer screening
cohorts including 212 women born in 1911 to 1925 whose hormones were measured in 1980. During a
subsequent screening round 2 y later, 156 women provided information about exposure to the Dutch Famine
of 1944–1945, thus enabling secondary analyses.

RESULTS: A clear univariate increase in postmenopausal PTH levels was found among women who indicated
exposure to the Dutch famine. Odds ratio by extreme PTH tertiles was 1.5 (95% CI: 0.6, 3.4) for moderately
exposed women and 2.3 (95% CI: 1.1, 5.2) for severely exposed women. In a regression analysis of famine
exposure on PTH levels, after controlling for levels of phosphorus, calcium, calcitonin, alkaline phosphatase,
and estrone; having been pregnant; parity; age at famine; age at blood donation; smoking; hormone
replacement therapy use at time of blood collection; height; weight; and socioeconomic status, the
independent significant contribution of PTH remained.
CONCLUSIONS: The results corroborate the hormonal set-point hypothesis and seem to extend effects of
famine exposure to hormones such as PTH, which plays a role in early bone growth as well as in osteoporosis
later in life. Though PTH is not under hypothalamic or pituitary control, it is partially under ganglion control.
Embryologically, the parathyroids and the adenohypophysis share a common origin from pharyngeal
endodermal pouches.

GHRH binds to GHS-receptor & potentiates GHRP's GH releasing action!

We have spent a lot of time in this thread discussing how GHRPs (such as GHRP-6, GHRP-2, Hexarelin &
Ipamorelin) potentiate GHRH's GH releasing effect. We talk of synergy, note GHRPs somatostatin inhibition at
the hypothalumus & pituitary and note that GHRPs use a different method then GHRH in changing calcium
concentrations within somatotrophs (GH releasing cells in the pituitary) that lead to GH secretion.

But now we learn that GHRH also enhances GHRP's effect on GH release by binding to the GHS-receptor
(obviously in addition to binding to their own GHRH receptors) and increasing the binding strength for GHRPs
when they in turn bind. In other words GHRH will partially bind to a GHS-receptor and still allow GHRPs to
bind as well. In fact this arrangement likely permits a double stack of two GHRP ligands thus modulating
(increasing) GHRPs action.

The study uses Ghrelin but the peptides should behave identically. However the non-peptide mimetics may
not.

From the CONCLUSION of Growth hormone-releasing hormone as an agonist of the ghrelin receptor GHS-R1a
,Felipe F. Casanuevaa, PNAS December 23, 2008 vol. 105 no. 51

In the present study, we provide the first evidence that GHRH specifically binds to the ghrelin receptor GHS-
R1a, increasing the binding capacity of its natural ligand. This binding activates the signaling route of inositol
phosphate, leading to an intracellular calcium rise, and finally leads to a GHRH-mediated ghrelin receptor
endocytosis. Furthermore, GHRH augments the maximal response to ghrelin in respect to inositol phosphates
turnover through Gq-associated signal transduction that increases the potency of ghrelin, at least on
intracellular calcium rise. ...

Thus, GHRH is able to bind to the ghrelin receptor and does not compete for binding against ghrelin. Instead,
GHRH increases the affinity of ghrelin, displaying positive binding cooperativity. Furthermore, GHRH
increased the maximal response to ghrelin with respect to inositol phosphates turnover through Gq-
associated signal transduction. This is in accordance with the concept of GHRH being an allosteric modulator
(28, 29). This enhancer function is further supported by the fact that GHRH decreased the EC50 for ghrelin, at
least as measured in the calcium assay. ...

Finally, and quite remarkably, GHRH activated the endocytosis of the ghrelin receptor. The GHRH/GHSR1a
complex progressively disappears from the plasma membrane after 20 minutes exposure to GHRH and
 accumulates in the perinuclear region after 60 minutes. This observation fits in well with the kinetics of
receptor endocytosis described for ghrelin in the present and previous works (27). ...

With regard to molecular mechanisms, it is not possible from the present data to establish a model of GHRH
action on the ghrelin receptor. A homodimeric model was recently proposed for the ghrelin receptor, in
which, because of negative cooperativity, the binding of ghrelin occurs only in one subunit, preventing
another ghrelin molecule from binding to the other subunit (32). On the basis of this model, we suggest that
GHRH might be able to bind in a multivalent form. When GHRH is present alone, it might bind to one subunit
of the dimeric receptor interacting with the orthosteric site (main ghrelin binding site) that determines the
agonist properties. However, when ghrelin is also present, GHRH occupies an ‘‘allosteric site,’’ acting as co-
agonist that stabilizes the ghrelin binding. This implies that GHRH allows two ghrelin molecules to bind at the
same time in the two subunits, which might explain the increase in ghrelin binding capacity observed in the
present study.

A Couple of quick notes:

1. Beware taking MTII with CJC-1295/GHRP-6 seems to prolong and intensify nausea. (Sample of two at the
moment... one of them being me.)

2. Beware GHRP-6 (assume all GHRPs) has been shown conclusively to increase gastic motility & "accelerate
gastric emptying of solids ...through activation of GHS receptors, possibly located on local cholinergic enteric
nerves" (Sample various effects from different people) *

3. Beware that as part of the gastric response, "GHRP-6 enhances neural contractile responses, partially via
interaction with the motilin receptor on noncholinergic nerves with tachykinins as mediator, and partially via
another receptor that may be a GHS-R subtype on cholinergic nerves that corelease tachykinins." (Sample at
least two reports, occurs from time to time) **

4. Exogenic GH when administered every 3 hours does not inhibit pulsation.

The reason this is interesting is that it may be possible to dose say 2iu of synthetic GH every 3 hours with
mod GRF(1-29)/GHRP-6 taken say 10 minutes prior. This could be done up to six times a day.

Alternatively 2iu of GH could be alternated with mod GRF(1-29)/GHRP-6.

The key has to be strict adherence to a schedule or else synthetic GH will inhibit natural GH.

It is just interesting to think about.

• - Gastric motor effects of peptide and non-peptide ghrelin agonists in mice in vivo and in vitro, T Kitazawa,
Gut 2005 54;1078-1084
** - Interaction of the Growth Hormone-Releasing Peptides Ghrelin and Growth Hormone-Releasing Peptide-
6 with the Motilin Receptor in the Rabbit Gastric Antrum, Inge Depoortere, The Journal Of Pharmacology And
Experimental Therapeutics Vol. 305, No. 2

GHRH & GHRP-2 and GH mRNA & GH-R mRNA

The following is the majority of the discussion from, EXPERIMENTAL STUDY - Effect of GHRH and GHRP-2
treatment in vitro on GH secretion and levels of GH, pituitary transcription factor-1, GHRH-receptor, GH-
secretagogue-receptor and somatostatin receptor mRNAs in ovine pituitary cells, Ming Yan, Maria
Hernandez, Ruwei Xu and Chen Chen, European Journal of Endocrinology (2004) 150 235–242

Its a long read, but I posted it in full because it references relevant in vivo studies as well as their own findings
to give us a picture of precisely how GHRH & GHRP-2 effect GH mRNA levels. The timing is interesting...

Note that Sermorelin's half-life comes up a little short....as perhaps 10 minutes is needed.

Solution? - maybe inject Sermorelin & GHRP-6 together, wait 6 minutes and inject another bit of Sermorelin.

Solution? - modify Sermorelin at the 2nd position (swap alanine for D-alanine)

The relevant timing points are highlighted below. As we would expect the combined GHRH (serum made
GHRH longer-lasting) + GHRP-2 had the largest impact.

Of interest, GH-receptor mRNA is increased by GHRH immediately as is the GH ligand so it seems that
synthesis of GH-receptor triggers early GH release. This point is very interesting to me.

Discussion ... Pituitary GH secretion is, to a large extent, controlled by three regulatory hormones: GHRH, GHS
and SRIF. Each binds to G-protein-coupled membrane receptors through which intracellular signalling
systems are activated (1). GHRH and GHRP administration potently increases GH secretion and this is not
altered by gender, adiposity or age (9). However, peripheral circulating GHRH levels are not usually linked to
an increase in GH levels as evidenced in patients with hypothalamic GHRH-secreting tumors (33). The key cell
type in the regulation of GH levels is the pituitary somatotrope, which determines the amount of GH secreted
in response to hypothalamic GHRH stimulation. Combined GHRH and GHRP treatment plays an important
role clinically, however, the data on the mechanism of GHRH/GHRH-R and GHRP/GHS-R action are
controversial (19–21). The differences may relate to the duration of GHRH and GHRP treatment and cell
culture conditions as well as animal age.

In this study, we investigated the mechanism of action of GHRH/GHRP using primary cultures of ovine
pituitary cells treated with GHRH and GHRP-2 in vitro. The present study carefully investigated the
concentration and duration of GHRH and GHRP treatment using 0.5, 1, 1.5 and 2 h time points and serum-
free incubation conditions for cell culture to clarify the mechanism of GHRH/GHRH-R and GHRP/GHS-R
action. Treatments with 10nM GHRH and 100nM GHRP-2 for 0.5, 1, 1.5 and 2 h were chosen in this study to
investigate short- to mid-term changes in somatotropes. GHRH at 1.0 mg/kg (i.v.) in vivo maximally
stimulated GH secretion at 15–45 min, with GH levels returning to baseline by 90–120 min after GHRH
injection in humans (34). GHRP-2, GHRP-6, hexarelin or non-peptidyl GHRP mimetic compound (L-692, 429)
treatment rapidly increases serum GH concentrations within 5–15 min, with the peak GH concentration
usually observed 15–30 min after intravenous injection in humans (35, 36). The presence of serum in the
culture medium maintains basal levels of the GHRH receptor and is important in long-term GHRH treatment
(20). However, the biological half-life of GHRH 1–44 is about 3–6 min in vivo (37) as GHRH is rapidly
inactivated by a plasma dipeptidyl aminopeptidase, producing a more stable metabolite, GHRH 3–44, which is
about 1000 times less potent than the parent compound (37). The culture of ovine pituitary cells in serum-
free culture conditions, as employed in this study, overcomes the quick degradation of GHRH and allows
subsequent stimulatory GHRH and GHRP treatments to be performed under defined conditions (38).

GHRH and GHRP treatment for 15 and 30 min rapidly stimulates maximal GH release (34–36).Furthermore,
GHRH treatment for as little as 10 min rapidly increased GH transcription rate by 200–300% in primary
cultured pituitary cells (39, 40). To analyse the transcription regulation of GH, we examined GH mRNA levels
in response to GHRH and GHRP-2. Our results show that treatment with GHRH, GHRP-2 and combinations of
GHRH and GHRP-2 increased GH mRNA expression and GH release 0.5, 1.0, 1.5 and 2 h after treatment, in a
time-dependent manner. The level of GH mRNA 0.5, 1, 1.5 and 2 h after treatment was greatest in the
combined GHRH and GHRP- 2 treatment group rather than in the GHRH or GHRP-2 alone treatment groups.
Our results are consistent with early reports that 10nM GHRH treatment of rat pituitary cells in serum-free
medium increased GH mRNA expression by 1.8- and almost 2.0-fold at 0.5 and 1 h respectively (40). This
demonstrates that the effects of GHRH, GHRP-2 and combinations of GHRH and GHRP-2 on GH mRNA
expression are rapid and occur at GH gene transcription level (40).

GHRH and GHRP bind to their specific receptors on the membranes of somatotropes (37). GHRH stimulates
GH synthesis by increasing the transcription rate of the GH gene and consequently GH release (40, 41). GHRP-
2 enhances pituitary GH gene expression and directly stimulates GH release (42). Our results show that the
duration of GHRH or GHRP-2 treatment influences the effects on the corresponding receptor mRNA
expression and GH release. GHRH and GHRP treatment for 1.5 h reduces their own receptor mRNA levels.
These results are consistent with previous reports which suggest that GHRH in the short-term suppresses its
own receptor expression (8, 20). Surprisingly, in this experiment, the short-term GHRH or GHRP treatment
(0.5 h) significantly increased the expression of ligand-specific receptor mRNAs, and also increased GH
release from ovine pituitary cells. This suggests that GHRH-R or GHS-R mRNA expression may contribute to
the increase in GH secretion. GHRH treatment does not significantly influence the mRNA level of GHS-R, nor
does GHRP-2 change GHRH-R expression with short-term treatment. The results supported our previous
report suggesting that GHRP-2 does not act through the GHRH receptor (6). It is worth mentioning that
another study indicated that GHRH, at any dose tested, did not affect GHS-R levels in vitro (8).
GH expression is mainly controlled by Pit-1, a member of the homobox POU (representing a
homeodomainprotein family of which the founder members are Pit-1, Oct 1/2 and Unc-86) family of DNA-
binding proteins, and GHRH and GHRP-2 elicit a time-dependent activation of Pit-1 expression by anterior
pituitary cells (1, 35). Our results indicate that with combined GHRH and GHRP-2 treatment, Pit-1 mRNA
expression is increased to 150, 121 and 168% at 0.5, 1.5 and 2 h after treatment respectively. GHRH
enhances the levels of Pit-1 mRNA expression 0.5, 1, 1.5 and 2 h after treatment. GHRP-2 also significantly
increases the levels of Pit-1 mRNA 0.5 and 2 h after treatment. GHRH and GHRP-2 may activate Pit-1
transcription and stimulates GH expression in pituitary cells through mediation of protein kinase C (PKC),
mitogen-activated protein (MAP) kinase and PKA activation (1, 13, 14, 43).

Somatostatin binds to a family of specific receptors and inhibits adenylyl cyclase via Gi proteins, and inhibits
GH release but not its biosynthesis (44). In addition, somatostatin may potentially play (dual) inhibitory and
stimulatory roles in controlling GH secretion by acting on two distinct somatotrope cell populations in the
porcine pituitary (45). Five somatostatin receptor subtypes have been cloned and characterized and their
expression is regulated in a subtype and tissue-specific manner (46–48). The results of GHRH action on sst
receptor synthesis shows that, in vivo, a 4 h GHRH infusion and, in vitro, a 4 h 10nM GHRH treatment of rat
pituitary cells increased sst-1 and sst-2 mRNA levels but decreased sst-5 mRNA levels (26). In the current
study, 10 nM GHRH treatment increased sst-1 mRNA expression 0.5 to 2 h after the treatment. Although
GHRH also increased sst-2 mRNA expression this was not statistically significant. This suggests that the acute
direct regulatory action of GHRH on the synthesis of sst-1 and sst-2 receptor subtypes may be time-
dependent. GHRH increased sst-1 mRNA expression may be partially due to GHRH-induced increases in Pit-1
mRNA, which activates pituitary sst-1 mRNA expression (14, 49). In contrast, 100nM GHRP-2 reduced sst-1
and sst-2 mRNA expression 0.5 to 2 h after treatment. GHRP has been suggested to act as a functional SRIF
antagonist (11). Inhibition of the SRIF receptors including sst-1 and sst-2 by GHRP-2 supports this view.

In summary, the results of this study indicate that GHRH and GHRP-2 are important mediators regulating GH,
GHRH-R, GHS-R, Pit-1, sst-1 and sst-2 mRNA expression, and GH synthesis. Effects on somatotropes manifest
as either a priming or an inhibitory modification of the cells, leading to increased or decreased GH secretion.
Moreover, the results demonstrate that GHRH and GHRP regulate their receptor synthesis and GH release in
a time-dependent manner. This study represents an essential step forward in understanding the influence of
GHRH and GHRP on somatotropes. Application of this understanding may aid the development of new GHSs
with high efficacy.

Selected References

37 Frohman LA & Kineman RD. Growth hormone-releasing hormone and pituitary somatotrope proliferation.
Minerva Endocrinology 2002 27 277–285.

38 Gick GG, Zeytin FN, Brazeau P, Ling NC, Esch FS & Bancroft C. Growth hormone-releasing factor regulates
growth hormone mRNA in primary cultures of rat pituitary cells. PNAS 1984 81 1553–1555.
39 Barinaga M, Yamonoto G, Rivier C, Vale W, Evans R & Rosenfeld MG. Transcription regulation of growth
hormone gene expression by growth hormone-releasing factor. Nature 1983 306 84–85.

40 Barinaga M, Bilezikjian LM, Vale WW, Rosenfeld MG & Evans RM. Independent effects of growth hormone
releasing factor on growth hormone release and gene transcription. Nature 1985 314 279–281.

8 Kineman RD, Kamegai J & Frohman LA. Growth hormone (GH)- releasing hormone (GHRH) and the GH
secretagogue (GHS), L692,585, differentially modulate rat pituitary GHS receptor and GHRH receptor
messenger ribonucleic acid levels. Endocrinology 1999 140 3581–3586.

20 Lasko CM, Korytko AI, Wehrenberg WB & Cuttler L. Differential GH-releasing hormone regulation of GHRH
receptor mRNA expression in the rat pituitary. American Journal of Physiology 2001 280 E626–631.

Insulin, how it works and why GH isn't anabolic w/o it

I am tired of seeing the same wrong explanations on why insulin & growth hormone are anabolic so lets take
a look. I don't feel like writing an article so I'll just borrow from a couple of sources.

Insulin physiology

It is often stated that the primary benefit of insulin in bodybuilding is that it increases the uptake of glucose
into muscle and further that this movement of glucose is insulin dependent. But that is not exactly true. It
may not be widely known but it is clearly established that insulin is NOT needed for glucose uptake and
utilisation in man and therefore glucose uptake is NOT insulin dependent.

There is a sufficient population of glucose transporters in all cell membranes at all times to ensure enough
glucose uptake to satisfy the cell’s respiration, even in the absence of insulin. Insulin can and does increase
the number of these transporters in some cells but glucose uptake is never truly insulin dependent.

Stimulatory & Inhibiting actions

Through stimulating the translocation or movement of 'Glut 4' glucose transporters from the cytoplasm of
muscle and adipose tissue to the cell membrane insulin increases the rate of glucose uptake to values greater
than the uptake that takes place in the basal state without insulin.

When insulin is administered to people with diabetes who are fasting, blood glucose concentration falls. It is
generally assumed that this is because insulin increases glucose uptake into tissues, particularly muscle. In
fact this is NOT the case and is another error arising from extrapolating from in vitro rat data. It has been
shown quite unequivocally that insulin at concentrations that are within the normal physiological range
lowers blood glucose through inhibiting hepatic glucose production without stimulating peripheral glucose
uptake. As hepatic glucose output is 'switched off' by the inhibiting action of insulin, glucose concentration
falls and glucose uptake actually decreases. Contrary to most textbooks and previous teaching, glucose
uptake is therefore actually increased in uncontrolled diabetes and decreased by insulin administration.
When insulin is given to patients with uncontrolled diabetes it switches off a number of metabolic processes
(lipolysis, proteolysis, ketogenesis and gluconeogenesis) by a similar inhibiting action. The result is that free
fatty acid (FFA) concentrations fall effectively to zero within minutes and ketogenesis inevitably stops
through lack of substrate. It takes a while for the ketones to clear from the circulation, as the 'body load' is
massive as they are water and fat soluble and distribute within body water and body fat. Since both ketones
and FFA compete with glucose as energy substrate at the point of entry of substrates into the Krebs
cycle,glucose metabolism increases inevitably as FFA and ketone levels fall (despite the concomitant fall in
plasma glucose concentration).

Thus insulin increases glucose metabolism more through reducing FFA and ketone levels than it does through
recruiting more glucose transporters into the muscle cell membrane.

NOTE: The above was taken from:

Mechanism of action of insulin in diabetic patients: a dose-related effect on glucose production and
utilisation, Brown P, Tompkins C, Juul S & Sonksen PH, British Medical Journal 1978 1239–1242.

Anabolic effect

Through facilitating glucose entry into cells in amounts greater than needed for cellular respiration insulin will
stimulate glycogen formation.

It is possible to increase muscle bulk and performance not only through increasing muscle glycogen stores on
a "chronic" basis but also to increase muscle bulk through inhibition of muscle protein breakdown. Just as
insulin has an inhibiting action in inhibiting glucose breakdown in muscle glycogen, it also has an equally
important inhibiting action in inhibitingprotein breakdown.

The evidence now indicates that insulin does NOT stimulate protein synthesis directly (this process is under
the control of growth hormone (GH) and insulin-like growth factor-I (IGF-I)). It has long been known that
insulin-treated patients with diabetes have an increase in lean body mass when compared with matched
controls. This results from insulin's inhibition ofprotein breakdown in muscle tissue.

Growth Hormone Anabolic Actions

GH’s major action is to stimulate protein synthesis. It is at least as powerful as testosterone in this effect and,
as they both operate through distinct pathways, their individual effects are additive or possibly even
synergistic. In addition to stimulating protein synthesis, GH simultaneously mobilises fat by a direct lipolytic
action. Together, these two effects are responsible for the 'partitioning' action of GH whereby it diverts
nutritional calories toprotein synthesis, possibly through using the energy derived from its lipolytic action. It
most likely stimulates protein synthesis through mobilisation of amino acid transporters in a manner
analogous to insulin and glucose transporters.
IGF-I also acts directly to stimulate protein synthesis but it has a weaker lipolytic action. GH, IGF-I and insulin
thus act in concert to stimulate protein synthesis.

GH and IGF-I act in a promoting manner to stimulate protein synthesis while insulin acts in its characteristic
inhibiting manner to inhibit protein breakdown. Thus they are synergistic in their powerful anabolic action.

Insulin is essential for the anabolic action of GH. GH administration in the absence of adequate insulin
reserves (as during fasting or in Type 1 diabetes) is in fact catabolic and its lipolytic and ketogenic properties
can induce diabetic ketoacidosis. Thus GH and insulin are closely linked in normal physiology and it is of great
interest to see that athletes have discovered ways in which this normal physiological dependence can be
exploited to enhance performance.

NOTE: The above was "lifted" with little change from parts of:

HORMONES AND SPORT: Insulin, growth hormone and sport, P H Sonksen, Journal of Endocrinology (2001)
170, 13–25

Boosting Insulin Naturally

I understand not wanting to use exogenously administered insulin. Does this mean you would lose out on
insulin's contribution to GH induced anabolism?

No...you can achieve what would amount to a couple iu of Hum-R by using glucose & leucine. The two work
synergistically to spike insulin.

About 3.5 grams of Leucine was sufficient to double the insulin response to 25grams of glucose. See below:

Leucine, when ingested with glucose, synergistically stimulates insulin secretion and lowers blood glucose,
Dionysia Kalogeropoulou, Metabolism Clinical and Experimental 57 (2008) 1747–1752

Thereafter, they received 25 g glucose or 1 mmol/kg lean body mass leucine or 1 mmol/kg lean body mass
leucine plus 25 g glucose in random order. Serum leucine, glucose, insulin, glucagon, and alpha-amino
nitrogen concentrations were measured at various times during a 2.5-hour period after ingestion of the test
meal. The amount of leucine provided was equivalent to that present in a high-protein meal, that is, that
approximately present in a 350-g steak. After leucine ingestion, the leucine concentration increased 7-fold;
and the alpha-amino nitrogen concentration increased by 16%. Ingested leucine did not affect the serum
glucose concentration. When leucine was ingested with glucose, it reduced the 2.5-hour glucose area
response by 50%. Leucine, when ingested alone, increased the serum insulin area response modestly.
However, it increased the insulin area response to glucose by an additional 66%; that is, it almost doubled the
response. Ingested leucine stimulated an increase in glucagon. Ingested glucose decreased it. When ingested
together, the net effect was essentially no change in glucagon area. In summary, leucine at a dose equivalent
to that present in a highprotein meal, had little effect on serum glucose or insulin concentrations but did
increase the glucagon concentration. When leucine was ingested with glucose, it attenuated the serum
glucose response and strongly stimulated additional insulin secretion. Leucine also attenuated the decrease
in glucagon expected when glucose alone is ingested. The data suggest that a rise in glucose concentration is
necessary for leucine to stimulate significant insulin secretion. This in turn reduces the glucose response to
ingested glucose.

Here is the Insulin Cheat Sheet I put together in September

The following was a nice little concise summation of the effect insulin has on GH, GHRs and intracellular
events, put together about 6 months back. It was designed to be a pointer to the primary studies that
demonstrate each point.

It might be of use to someone so I post it here today:

INSULIN CODEX - I

Many factors are known to regulate the responsiveness of the growth hormone receptor (GHR) to growth
hormone (GH). The most important are insulin, thyroid [SEE: THYROID HORMONES CODEX] and sex
hormones [SEE: ESTROGEN CODEX & TESTOSTEONE CODEX].

The growth-promoting action of GH is mediated by IGF-I which is produced mainly in the liver, but also in
extrahepatic tissues. There is strong evidence that the anabolic action of GH requires the presence of insulin
and adequate nutrition. This is exemplified in type 1 diabetes where IGF-I levels are low and longitudinal
growth is impaired despite high serum levels of GH [1, 2]. These abnormalities are corrected by insulin
treatment [3, 4].

Insulin's effect on GHR expression

The effects of insulin on GHR expression and function are tissue specific.

In cultures of rat hepatoma cells, insulin increases GHRs [5]. In animal studies, insulin deficiency results in a
decrease of GH binding and GHR expression in liver [6, 7], which can be reversed by insulin administration [6,
8]. In extra-hepatic tissues such as bone and kidney, there is evidence that insulin down-regulates GHRs [9, 6–
8].

It is well established that surface membrane receptors are dynamically regulated, with cell surface
abundance representing the net balance of "recycling of internalised receptors" and translocation of newly
synthesized receptors to the cell membrane.

There is recent evidence that the surface translocation of GH receptors is inhibited by insulin.

Insulin dose-dependently stimulates liver GHR synthesis and GH binding, however increasing insulin
concentrations reduce GHR surface translocation, which overcomes the effect on receptor synthesis [5].
These findings show that the mechanism by which insulin regulates tissue responsiveness to GH is complex
and in part mediated by effects on GHR expression and surface translocation.

Decrease in receptor surface availability with high dose insulin may represent rapid mechanism for insulin
regulation of the GHR function.

In human studies, there is also evidence that insulin modulates the expression of GHRs. This is based on
measurement of circulatory levels of GHBP. As GHBP is derived from proteolytic cleavage of the extracellular
domain of the GH receptor, change in GHBP levels may reflect GH receptor status [10].

Thus when insulin levels are low, high levels of GH does not translate into a rise in circulating IGF-I [11-17]. In
type I diabetes, GHBP levels are low and associates with low IGF-I levels [18]. These investigations have also
observed a significant positive correlation between levels of GHBP and total insulin dose, suggesting that GHR
status in humans is dependent on adequate insulinisation [18].

Insulin's effect on GH receptor signaling

There is strong evidence that insulin modulates GHR signaling in addition to the effects on receptor
expression and surface translocation.

In rat hepatoma cells, low dose insulin administration results in GH-induced stimulation of JAK2
phosphorylation however high dose insulin treatment results in inhibitory effect [5, 19].

The effect of insulin on GHR function appears to be mediated by the PI-3 kinase and MAPK/ERK pathways [5,
20, 21]. It has been shown that insulin increases GH signaling by enhancing GH-induced activation of
MAPK/ERK pathway through post signalling cross-talk [21].

In human muscle, in vivo, ERK1/2 phosphorylation was increased by insulin, but insulin per se did not induce
phosphorylation of Stat5. [22]

Overall Summation

Insulin regulates GHR expression, translocation and GHR function. The regulation of GH receptor expression
is complex and tissue dependent. Insulin stimulates hepatic GHR synthesis and GH binding but down-
regulates GHR expression in kidney and bone tissue.

In liver, high concentrations of insulin reduce GHR surface translocation, in such a way as to regulate receptor
surface availability.

The effects of insulin on GHR function are mediated by stimulation of GH-induced JAK2 phosphorylation, PI-3
kinase and MAPK/ERK pathways.

SOURCES: 1 - Horner JM, Kemp SF, Hintz RL. Growth hormone and somatomedin in insulin-dependent
diabetes mellitus. J Clin Endocrinol Metab. 1981;53:1148–53.
2 - Tan K, Baxter RC. Serum insulin-like growth factor I levels in adult diabetic patients: the effect of age. J Clin
Endocrinol Metab. 1986;63:651–5.

3 - Vigneri R, Squatrito S, Pezzino V, Filetti S, Branca S, Polosa P. Growth hormone levels in diabetes.
Correlation with the clinical control of the disease. Diabetes. 1976;25:167–72.

4 - Amiel SA, Sherwin RS, Hintz RL, Gertner JM, Press CM, Tamborlane WV. Effect of diabetes and its control
on insulin-like growth factors in the young subject with type I diabetes. Diabetes. 1984;33:1175–9.

5 - Leung KC, Doyle N, Ballesteros M, Waters MJ, Ho KK. Insulin regulation of human hepatic growth hormone
receptors: divergent effects on biosynthesis and surface translocation. J Clin Endocrinol Metab.
2000;85:4712–20.

6 - Baxter RC, Bryson JM, Turtle JR. Somatogenic receptors of rat liver: regulation by insulin. Endocrinology.
1980;107:1176– 81.

7 - Menon RK, Stephan DA, Rao RH, Shen-Orr Z, Downs LS Jr, Roberts CT Jr, et al. Tissue-specific regulation of
the growth hormone receptor gene in streptozocin-induced diabetes in the rat. J Endocrinol. 1994;142:453–
62.

8 - Maes M, Ketelslegers JM, Underwood LE. Low plasma somatomedin-C in streptozotocin-induced diabetes
mellitus. Correlation with changes in somatogenic and lactogenic liver binding sites. Diabetes. 1983;32:1060–
9.

9 - Flyvbjerg A, Bennett WF, Rasch R, Kopchick JJ, Scarlett JA. Inhibitory effect of a growth hormone receptor
antagonist (G120K-PEG) on renal enlargement, glomerular hypertrophy, and urinary albumin excretion in
experimental diabetes in mice. Diabetes. 1999;48:377–82.

10 - Baumann G. Growth hormone binding protein 2001. J Pediatr Endocrinol Metab. 2001;14:355–75.

11 - Ho KY, Veldhuis JD, Johnson ML, Furlanetto R, Evans WS, Alberti KG, et al. Fasting enhances growth
hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. J Clin Invest.
1988;81:968–75.

12 - Hartman ML, Veldhuis JD, Johnson ML, Lee MM, Alberti KG, Samojlik E, et al. Augmented growth
hormone (GH) secretory burst frequency and amplitude mediate enhanced GH secretion during a two-day
fast in normal men. J Clin Endocrinol Metab. 1992;74:757–65.

13 - Baxter RC, Bryson JM, Turtle JR. The effect of fasting on liver receptors for prolactin and growth
hormone. Metabolism. 1981;30:1086–90.

14 - Maes M, Underwood LE, Ketelslegers JM. Low serum somatomedin-C in protein deficiency: relationship
with changes in liver somatogenic and lactogenic binding sites. Mol Cell Endocrinol. 1984;37:301–9.
15 - Thissen JP, Triest S, Maes M, Underwood LE, Ketelslegers JM. The decreased plasma concentration of
insulin-like growth factor-I in protein-restricted rats is not due to decreased numbers of growth hormone
receptors on isolated hepatocytes. J Endocrinol. 1990;124:159–65.

16 - Ohashi S, Kaji H, Abe H, Chihara K. Effect of fasting and growth hormone (GH) administration on GH
receptor (GHR) messenger ribonucleic acid (mRNA) and GH-bindingprotein (GHBP) mRNA levels in male rats.
Life Sci. 1995;57:1655–66.

17 - Maccario M, Aimaretti G, Grottoli S, Gauna C, Tassone F, Corneli G, et al. Effects of 36 hour fasting on
GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects
and hypopituitary patients with severe GH deficiency. Int J Obes Relat Metab Disord. 2001;25:1233–9.

18 - Kratzsch J, Keliner K, Zilkens T, Schmidt-Gayk H, Selisko T, Scholz GH. Growth hormone-binding protein
related immunoreactivity is regulated by the degree of insulinopenia in diabetes mellitus. Clin Endocrinol
(Oxf). 1996;44:673–8.

19 - Ji S, Guan R, Frank SJ, Messina JL. Insulin inhibits growth hormone signaling via the growth hormone
receptor/JAK2/ STAT5B pathway. J Biol Chem. 1999;274:13434–42.

20 - Bennett WL, Keeton AB, Ji S, Xu J, Messina JL. Insulin regulation of growth hormone receptor gene
expression: involvement of both the PI-3 kinase and MEK/ERK signaling pathways. Endocrine. 2007;32:219–
26.

21 - Xu J, Keeton AB, Franklin JL, Li X, Venable DY, Frank SJ, et al. Insulin enhances growth hormone induction
of the MEK/ERK signaling pathway. J Biol Chem. 2006;281:982–92.

22 - Growth Hormone Signaling in Vivo in Human Muscle and Adipose Tissue: Impact of Insulin, Substrate
Background, and Growth Hormone Receptor Blockade, Charlotte Nielsen, et al., The Journal of Clinical
Endocrinology & Metabolism July 2008 Vol. 93, No. 7 2842-2850

Protein Metabolism - The complementary role of various hormones in inducing Anabolism

Too many people have very little idea how the following factors work together in increasing proteinsynthesis
and preventing protein breakdown. If they truly understood these things would they give up seeking THE
magic bullet? I doubt it... Would they stop seeking out self-proclaimed gurus who in my opinion fail miserably
in understanding these things themselves.

• Insulin • Growth Hormone • Amino Acid Pool • Exercise • Blood Flow • IGF-1 • IGF-1/IGFBP-3 • Androgens
• Thyroid Hormones

What follows are basically my notes structured in such a way as to be highly readable, massively informative
and well referenced for further research should someone be so inclined.
I didn't really intend to post this for public consumption so forgive the format. I ask that you not cut and
paste this post onto other forums. Basically it is here for anyone who reads this thread and no one else.

The following post was derived both generally and specifically from the following studies. Additional studies
are provided as references for selective material herein.

An abundant supply of amino acids enhances the metabolic effect of exercise on muscle protein, Gianni
Biolo, Am. J. Physiol. 273 (Endocrinol. Metab. 36): El22-E129, 1997.

Acute Growth Hormone Effects on Amino Acid and Lipid Metabolism, K. C. Copeland,Journal of Clinical
Endocrinology and Metabolism Vol. 78, No. 5 1994

Effects of Insulin-Like Growth Factor-1/Binding protein-3 Complex on Muscle Atrophy in Rats, Martin M.
Zdanowicz, 2003 by the Society for Experimental Biology and Medicine

Hormonal regulation of human protein metabolism, Pierpaolo De Feo, Eur J Endocrinol 1996:135:7-18

Physiologic Hyperinsulinemia Stimulates protein Synthesis and Enhances Transport of Selected Amino Acids
in Human Skeletal Muscle, Gianni Biolo, J. Clin. Invest. vol. 95, 811 - 819

Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with
aging, Micah J. Drummond, J Appl Physiol 104: 1452-1461, 2008

Compartmental model of leucine kinetics in humans, Claudio Cobelli, Am. J. Physiol. 261 (Endocrinol. Metab.
24): E539-E550, 1991

Dose-response curves of effects of insulin on leucine kinetics in humans, Paolo Tessari, Am. J. Physiol. 251
(Endocrinol. Metab. 14): E334-E342, 1986.

Growth hormone decreases muscle glutamine production and stimulates proteinsynthesis in hypercatabolic
patients, Gianni Biolo, Am J Physiol Endocrinol Metab 279:323-332, 2000

Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans,
Gianni Biolo, Am. J. Physiol. 268 (Endocrinol. Metab. 31): E514-E520, 1995.

Insulin action on protein metabolism in acromegalic patients, Alberto Battezzati, Am J Physiol Endocrinol
Metab 284:823-829, 2003

Leucine and phenylalanine kinetics during mixed meal ingestion a multiple tracer approach, Gianni Biolo, Am.
J. Physiol. 262 (Endocrinol. Metab. 25): E455-E463,1992.

protein synthesis and breakdown in skin and muscle a leg model of amino acid kinetics, Gianni Biolo, Am. J.
Physiol. 267 (Endocrinol. Metab. 30): E467-E474, 1994.
Transmembrane transport and intracellular kinetics of amino acids in human skeletal muscle, Gianni Biolo,
Am. J. Physiol. 268 (Endocrinol. Metab. 31): E75-E84, 1995.

Insulin

There is indirect evidence that post-prandial [after a meal] hyperinsulinemia induces protein anabolism,
other than through the suppression of whole-body proteolysis [i.e. protein breakdown/ catabolism], also by
facilitating the incorporation of dietary amino acids into new proteins. In fact, when post-prandial
hyperinsulinemia and hyperaminoacidemia [high insulin & high amino acids] are reproduced in normal
subjects by a combined intravenous infusion of insulin and amino acids, the estimates of whole-bodyprotein
synthesis increase more than after amino acids alone (20).

[Insulin + Amino Acids = greater increase in entire body proteinsynthesis] The stimulatory effect of
hyperinsulinemia on whole-body protein synthesis cannot be demonstrated when insulin alone is infused
(20-25). In this case, by reducing the rate of protein breakdown, hyperinsulinemia decreased the intracellular
concentrations of most amino acids (26), limiting their utilization for proteinsynthesis (27).

[In other words the store of amino acids (often called the intracellular amino acid pool) is replenished in two
ways. One by eating/ingestion of protein & the other by the breakdown of protein in muscle (i.e.protein
degradation). This latter, protein degradation reduces proteinto its constituent parts (amino acids) which will
be transported outside the cell & either be further removed or remain in the amino acid pool (which resides
between muscle cells) and is available for reuse in muscle for the next round of transport into muscle & new
proteinsynthesis. Insulin reduces protein breakdown so the amino acid pools are not replenished.] Branched-
chain amino acids are particularly sensitive to hyperinsulinemia (28) and it has been shown the insulin-
induced suppression of plasma isoleucine concentration (29), i.e. of a single essential amino acid, is sufficient
to decrease wholebody protein synthesis.

[So in essence protein synthesis requires all the essential amino acids. If one is missing no protein synthesis
will occur.]

The results of recent studies demonstrate that the effects of insulin on whole-body protein kinetics represent
the mean results of differential effects of the hormone on the rates of protein breakdown and synthesis of
individual proteins. For instance, despite the rate of whole-body proteolysis being decreased by insulin (20-
25), the rate of muscle protein proteolysis is not affected by local hyperinsulinemia (30). Such a differential
effect can be explained by the fact that insulin decreases the proteolytic activity of lysosomes but does not
control the ubiquitin system (31) that is responsible for the bulk of muscle proteolysis (31).

[So insulin decreases protein breakdown/degradation throughout the entire body but does not inhibit
protein breakdown specifically in muscle.] References:
 20 - Castellino P, Luzi L, Simonson DC. Haymond M. DeFronzo RA. Effect of insulin and plasma amino acid
concentrations of leucine metabolism in man: role of substrate availability on estimates of whole body
protein synthesis. J Clin Invest 1987: 80:1784-9 3

21 - Fukagawa NK. Minaker KL. Rowe JW. Goodman MN. Matthews DE. Bier DM, et al. Insulin-mediated
reduction of whole body protein breakdown: dose-response effects on leucine metabo¬ lism in
postabsorptive men. J Clin Invest 1985:76:2306-11

22 - Tessari P, Trevisan R, Inchiostro S, Biolo G, Nosadini R, De Kreutzenberg SV, et al. Dose-response curves
of effects of insulin on leucine kinetics in humans. Am J Physiol 1986;251:E334-42

23 - Tessari P. Nosadini R. Trevisan R. De Kreutzenberg SV. Inchiostro S. Duner E. et al. Defective suppression
by insulin of leucine-carbon appearance and oxidation in type 1, insulin dependent diabets mellitus: evidence
for insulin resistance involving glucose amino acid metabolism. J Clin Invest 1986:77:1797-804

24 - Luzi L, Castellino P. Simonson DC, Petrides AS, DeFronzo RA. Leucine metabolism in IDDM: role of insulin
and substrate availability. Diabetes 1990:39:38-48

25 - De Feo P. Volpi E, Lucidi P, Cruciani G. Reboldi G. Siepi D, et al. Physiological increments in plasma insulin
concentrations have selective and different effects on synthesis of hepatic proteins in normal humans.
Diabetes 1993:42:995-1002

26 - Alvestrand A, DeFronzo RA, Smith D, Wahren J. Influence of hyperinsulinaemia on intracellular amino

acid levels and amino acid exchange across splanchnic and leg tissues in uraemia. Clin Sci 1988;74:155-63

27 - De Feo P. Haymond MW. Effect of insulin on protein metabolism in humans: methodological and
interpretative questions. Diab Nutr Metab 1991:4:241-9

28 - Fukagawa NK. Minaker KL. Young VR. Rowe JW. Insulin dosedependent reductions in plasma amino acids
in man. Am J Physiol 1986;250:E13-7

29 - Lecavalier L, De Feo P. Haymond MW. Isolated hypoisoleucinemia impairs whole body but not hepatic
protein synthesis in humans. Am J Physiol 1991;261:E578-86

1. Biolo G, Declan Fleming RY. Wolfe RR. Physiologic hyper¬ insulinemia stimulates proteinsynthesis and
enhances trans¬ port of selected amino acids in human skeletal muscle. J Clin Invest 1995:95:811-9

Insulin increases the amount of protein deposited in muscle by directly increasing the rate of
proteinsynthesis (40-60% as measured by lysine & phenylalanine dissapearance from intracellular pools).
Insulin does not increase (or regulate) transmember amino acid transport. Therefore transportation of amino
acids is not a primary mediator of insulin anabolic actions in muscle.

[So Insulin's primary modes of action are reduction of whole-bodyprotein breakdown as discussed already &
in muscle an increase in the rate of protein synthesis. Now it draws on the intracellular pool of amino acids to
effect this increased synthesis. It is possible to run out of amino acids from that pool. Insulin can suck the
reservoir dry so to speak.

In addition insulin in general (there is an exception) does not increase the rate of transportation of amino
acids across the cell membrane into the cell. That remains normal. But the benefit of insulin in muscle is that
it increases protein synthesis. However other things are needed besides insulin to effect anabolism.] Insulin
draws on an existing intracellular pool of amino acids. When amino acid concentrations are maintained at
levels higher than normal during systemic insulin administration insulin increased muscleprotein synthesis
(40).

[So anabolism occurs when both insulin increased protein synthesis occurs and amino acid levels are
maintained higher then normal. The primary way to effect this is to increase amino acid/protein ingestion.]
40. - Bennett, W. M., A. A. Connacher, C. M. Scringeour, R. T. Jung, and M. J. Rennie. 1990. Euglycemic
hyperinsulinemia augments amino acid uptake by human leg tissues during hyperaminoacidemia. Am. J.
PhysioL 259:E185-E194

Insulin does not significantly modify protein breakdown in muscle. It has been shown that, during adequate
amino acid supply, the most important degradative system in muscle is an ATP-independent system that
requires the presence of a specialized protein, termed ubiquitin. This system is not sensitive to insulin.
Concerning protein breakdown Insulin apparently plays a role only in the regulation of the lysosome activity.
These intracellular organelles are not involved in the myofibrillar protein degradation in normal conditions,
but only in the presence of low insulin levels or decreased amino acid availability).

[So again insulin will increase protein synthesis in muscle but will not inhibit protein breakdown. So in general
anabolism will occur if moreprotein synthesis then protein breakdown occurs.]

Following protein degradation, the amino acids from the degradation event are either transported outward
(or in the case of leucine oxidized) or are redirected back into protein synthesis. Phenylalanine & leucine have
been shown to be redirected back into protein synthesis while lysine may not.

Insulin induces hyperpolarization in the skeletal muscle cells by directly activating the sodium ion (Na+) and
potassium ion (K+) -ATPase pump. Those amino acids which are strongly "attracted" to the electrochemical
characteristics of the cell membrane are more readily taken up into muscle from the intracellular pool of
amino acids. Alanine & lysine are two amino acids that have this attraction and are more readily drawn into
muscle by insulin.

[When protein in muscle is broken down and its constituents removed back to the amino acid pool, those
amino acids may be removed from muscle pools entirely, may be reused for new synthesis or for some amino
acids oxidized or used for energy. It would not benefit anabolism to lose the important amino acid leucine to
oxidation.
 Insulin which in general doesn't increase transport of amino acids from pool into cells, does so for a few
amino acids which use NA+ & K+ channels, namely alanine & lysine.]

The branched-chain amino acids (leucine, valine, and isoleucine) and the aromatic (phenylalanine and
tyrosine) are preferably transported through system L . This sodium-independent system is unable to
generate high transmembrane gradients for its substrates. It has been shown that the kinetic characteristics
of system L are not influenced by insulin.

[So insulin which has no effect on this mode of transport does not increase the uptake of some very
important amino acids.] Blood flow has been found to increase local amino acid delivery to muscle and
secondarily increase amino acid transport. This effect may be responsible for increase in leucine uptake.

[This is an extremely important way in which amino acids are drawn to muscle and into cells. Time and again
the important amino acid leucine has been shown to make its way into cells via increase in blood flow.]
Alanine synthesis (which is a function of pyruvate) also increases in the presence of insulin because insulin
increases glucose uptake & intracellular pyruvate in muscle.

[Certain amino acids can be synthesized from the breakdown of other amino acids. Alanine is one of them.
Alanine is often used for energy and so protein synthesis rate or anabolism may depend on the availability of
alanine not yet oxidized. The fact that insulin increases alanine synthesis is a desirable effect.] The anabolic
effect of insulin on muscle may have become self-limited because of an intracellular depletion of precursor
amino acids for protein synthesis, unless amino acid transport is independently stimulated by other factors,
i.e., amino acid administration.

[Again an external source of amino acids is needed to make insulin anabolic in muscle.]

1. Kettlehut IC. Wing SS. Goldberg AL. Endocrine regulation of protein breakdown in skeletal muscle. Diab
Metab Rev 1988;4:751-72 - - -

Growth Hormone

Growth hormone promotes protein anabolism with mechanisms different from insulin. It does not affect the
rates of whole-body proteolysis but decreases those of amino acid oxidation (51, 52). The sparing effect on
amino acid oxidation results in a greater rate of their incorporation into proteins (51-53), with a net
proteinanabolic effect.

1. Horber FF. Haymond MW. Human growth hormone prevents the protein catabolic side effects of prednisone
in humans. J Clin Invest 1990:86:265-72

2. Copeland KC. Nair KS. Acute growth hormone effects on amino acid and lipid metabolism. J Clin Endocrinol
Metab 1994: 78:1040-7
3. Yarasheski KE. Campbell JA. Smith K, Rennie MJ, Holloszy JO, Bier DM. Effect of growth hormone and
resistance exercise on muscle growth in young men. Am J Physiol 1992;262:E261-7 [So Growth Hormone
decreases amino acid oxidation (or break down for energy). This should have the effect of preserving key
amino acids in that very important amino acid pool. This means that muscleprotein synthesis or even
increased muscle protein synthesis induced by insulin will be more prolonged because there will be a larger
pool of raw material (aminos) to draw from.]

Growth hormone decreases muscle glutamine production

In agreement with previous observations in animals (20, 23), this study shows that rhGH infusion in
traumatized patients accelerates the rates of transmembrane transport of the essential amino acids leucine
and phenylalanine. This effect was independent of changes of leg blood flow and arterial amino acid
concentrations. This rhGH-mediated increased ability of transmembrane systems to transport essential
amino acids confirms previous observations in vitro (20, 23) and represents a novel observation in vivo.

[So while insulin increases transport of a few aminos (alanine & lysine), GH increases amino acid transport for
leucine and phenylalanine. This would mean that GH would increase transport of the other aromatic amino
acid tyrosine and the other branch-chain amino acids valine and isolecine]

Besides stimulating protein synthesis, growth hormone suppressed the rate of catabolism of the branched-
chain amino acids leucine, isoleucine, and valine. This effect has been reported by several other authors using
isotopic tracers of leucine at the whole body level (8, 12).

[So growth hormone unlike insulin suppresses the breakdown and loss of branch-chain amino acids &
probably all amino acids. Thus GH provides more raw material for insulin-induced higher rate of
proteinsynthesis.]

glutamine and alanine constitute the major carriers of nitrogen among body tissues (2).In skeletal muscle,
these amino acids are constantly being synthesized and released into the bloodstream (2). In severe trauma,
alanine release from muscle is greatly accelerated, whereas glutamine release was found to be increased or
unchanged (5). Our results indicate that rhGH administration selectively decreases the rates of synthesis and
release of glutamine, whereas alanine synthesis did not change during the hormone administration.

[Growth hormone has a negative effect on glutamine synthesis.] In our patients, whole body skeletal muscle
released 19 g of glutamine per day into the bloodstream before rhGH administration. After rhGH
administration, glutamine release from skeletal muscle decreased by 50%, whereas at the whole body level,
glutamine clearance tended to decrease by 15%.

[So glutamine which is very important to the immune system & is urgently needed in times or severe trauma
is not really made available. This in part may be the reason why death occurs in critically ill patients given
 GH.] The obvious solution for this potential side effect of growth hormone treatment in critically ill patients is
to simultaneously administer exogenous glutamine to offset the decreased availability of the endogenous
amino acid.

[This also is a lesson for those seeking muscle anabolism while using GH. Less glutamine is synthesized and
thus available in the presence of GH. Thus supplementation with glutamine should increase the potential for
anabolism.]

Amino Acid Pool

From a dynamic point of view, such muscle hypertrophy results from changes in the rates of proteinsynthesis
and/or breakdown. In addition, an acceleration of the rates of amino acid transport into muscle cells may
contribute to muscle anabolism by increasing amino acid availability for protein synthesis. Studies suggest
that muscle protein accretion occurs in the recovery phase after exercise rather than during the actual
exercise period. The leucine tracer incorporation technique has shown that the rate of muscle protein
synthesis in humans is increased after exercise (7) and remains elevated for > 24 h (7).

In these studies, muscle protein breakdown was not ddirectly measured. However, the increase in
proteinsynthesis was so large that if it were not accompanied by a concomitant increment in protein
breakdown, exercise training would result in a greater increase in muscle size than actually occurs.

1. Chesley, A., J. D. MacDougall, M. A. Tarnopolsky, S. A. Atkinson, and K. Smith. Changes in human muscle
protein synthesis after resistance exercise. J. AppZ. Physiol. 73: 1383- 1388,1992.

Exercise

We found that, after exercise, the rates of muscle protein turnover and amino acid transport were increased.
protein synthesis and breakdown increased simultaneously but to a different extent. Synthesis increased by -
lOO%, whereas breakdown increased by only - 50%. Consequently, protein balance (synthesis minus
breakdown) improved after exercise (becoming not significantly different from zero) but did not shift to a
positive value. These results suggest that physical exercise can restrain net muscleprotein catabolism but
does not directly promote net protein deposition in the postabsorptive state. Thus exercise probably needs
to interact with other factors, such as feeding, to promote muscle anabolism.

[Although this paragraph is not completely clear, having read the studies I can say that the take home
message is that exercise reduces catabolism. Exercise increase both breakdown & synthesis ofprotein but
that exercise alone will not tilt things toward anabolism. Amino acid availability is required.] The notion that
increased amino acid availability can directly regulate protein synthesis is further supported by the fact that
the rate of synthesis was enhanced during amino acid infusion or in catabolic patients, in whom a large
primary increase of breakdown occurs. In the present study therefore the acceleration of protein breakdown
and amino acid transport may have contributed to the increase inprotein synthesis. Because of the increase
 in amino acid transport, the changes in protein degradation have been more than offset by the increased rate
of synthesis.

We found that, after exercise, the absolute rate of protein breakdown was accelerated. This catabolic
response almost counteracted the increase in protein synthesis.

[So exercise + amino acids = anabolism]

Our study suggests that this mechanism may also be important for amino acid and protein metabolism. Thus
physical exercise may not have a direct regulatory effect on the membrane transport systems, but its effect
may be due to the increased amino acid delivery to muscle tissue secondary to the increased blood flow.

Anabolism vs Catabolism

The intracellular availability of amino acids may not be the sole acute regulator of muscle proteinsynthesis,
inasmuch as hormones and other factors may have direct effects. Nonetheless it seems clear that the rates of
breakdown and inward amino acid transport are important factors. The importance of variations in inward
transport can be appreciated when the difference between the anabolic response to exercise is compared
with the catabolic response to critical illness. In both circumstances, the rate of breakdown is increased, but
in the case of critical illness, inward transport is relatively impaired, rather than stimulated. As a
consequence, muscle synthesis is not stimulated to the same extent as breakdown, with net catabolism
resulting. Thus the increase in inward transport after exercise appears to be an important response that
enables synthesis to increase to a greater extent than breakdown.

Side Note (skin more important then muscle)

Thus the stability of muscle mass throughout the day is maintained by alternating phases of catabolism
during fasting and anabolism after feeding. This process is necessary to supply liver and gut with amino acids
for protein synthesis in the fasting state. Our data suggest that the same mechanism is not involved in the
skin, because, after - 20 h of fasting, we did not observe any net loss of essential amino acids from this tissue.
From these results, it appears that maintenance of skin mass is a high metabolic priority, and this may occur,
at least in part, at the expense of muscle tissue.

Blood flow

Over the last decade, evidence has accumulated supporting the hypothesis that blood flow is a major
regulator of glucose uptake in skeletal muscle (1).

1. Baron, A. D., H. Steinberg, G. Brechtel, and A. Johnson. Skeletal muscle blood flow independently modulates
insulinmediated glucose uptake. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E248-E253,1994.
 The results of our study suggest that variations in blood flow may also affect muscle protein metabolism by
increasing transport of free amino acids into cells, which in turn stimulates protein synthesis. This notion is
supported by the high correlation between blood flow and FSR.

In summary, the results of our study demonstrate that net protein synthesis during amino acid
administration can be doubled by previous performance of heavy resistance exercise. Moreover, the data
suggest a link between the stimulation of protein synthesis after exercise and an acceleration in amino acid
transport. The greater rate of transport after exercise may be due to the increase in blood flow.

An abundant supply of amino acids enhances the metabolic effect of exercise on muscle protein, Gianni
Biolo, Am. J. Physiol. 273 (Endocrinol. Metab. 36): El22-E129, 1997. [So Exercise + increased bloodflow +
amino acids = increased amino acid transport. Of course this leads to the understanding that aminos need to
be in the blood prior to the increased blood flow of exercise.]

IGF-1

The data available in humans indicate that IGF-I has a mechanism of action similar to insulin on
proteinmetabolism (62-65) because IGF-I administration also reduces the rates of whole-body protein
breakdown and synthesis. When compared on a molar basis, the action of IGF-I is ~ 14 times less potent than
that of insulin (65),

IGF-I might affect protein metabolism only in selected tissues through a paracrine action on whether IGF-I,
due to its longer half-life could influence whole-body protein metabolism when plasma GH concentrations
decline; and the role played by IGF-I binding proteins in the modulation of the endocrine action of IGF-I
onprotein metabolism needs to be established.

1. Turkalj I. Keller U. Ninnis R, Vosmeer S, Stauffacher W. Effect of increasing doses of recombinant human
insulin-like growth factor I on glucose, lipid and leucine metabolism in man. J Clin Endocrinol Metab
1992;75:1186-91

2. Mauras . Horber FF, Haymond MW. Low dose recombinant human insulin-like growth factor-1 fails to affect
protein anabolism but inhibits islet cell secretion in humans. J Clin Endocrinol Metab 1992;75:1192-7

3. Elhay D. McAloon-Dyke M. Fukagawa NK, Sclater AL, Wong GA. Shannon RP. et al. Effects of recombinant
human IGF-1 on glucose and leucine kinetics in men. Am J Physiol 1993:265: E831-8

4. Giordano M, Castellino P. Carrol CA, DeFronzo RA. Comparison of the effects of human recombinant insulin-
like growth factor 1 and insulin on plasma amino acid concentrations and leucine kinetics in humans.
Diabetologia 1995:38: 732-8
 IGF-1/IGF-1 Binding protein 3 complex

The major beneficial effect of IGF-1/BP3 in this study appeared to be reduced muscle proteolysis. IGF-1/BP3
significantly reduced net protein degradation rates in muscles from HLS rats. Preservation of muscle weight
and protein content paralleled this reduced muscle proteolysis. In a previous study with highly catabolic
muscle from dystrophic hamsters, we reported a 27% decrease in muscle protein degradation rates with
rhIGF-1 (29); here with IGF-1/BP3, we report a near 40% decrease. A key component of muscle proteolytic
pathways, namely calpain-mediated myofibrillar degradation, was also reduced in rhIGF-1-treated dystrophic
mice (30)

Effects of Insulin-Like Growth Factor-1/Binding protein-3 Complex on Muscle Atrophy in Rats Martin M.
Zdanowicz, Experimental Biology and Medicine 228:891-897 (2003) [So there is an action that GH alone nor
insulin effects, namely the reduction in protein degradation/breakdown in muscle. Of course GH increases
the amount of IGF-1/IGF-1 Binding protein 3 complex.]

In humans, IGF-I administration promoted protein anabolism both by stimulating protein synthesis and by
inhibiting protein degradation both in muscle and at the whole body level (10, 11).

1. Elahi D, McAloon-Dyke M, Fukagawa NK, Sclater AL, Wong GA, Shannon RP, Minaker KL, Miles JM,
Rubenstein AH, Vandepol CJ, Guler H-P, Good WR, Seaman JJ, and Wolfe RR. Effects of recombinant human
IGF-I on glucose and leucine kinetics in men. Am J Physiol Endocrinol Metab 265: E831–E838, 1993.

2. Fryburg DA. Insulin-like growth factor I exerts growth hormone- and insulin-like actions on human muscle
protein metabolism. Am J Physiol Endocrinol Metab 267: E331–E336, 1994.

[So IGF-1 administration both stimulates protein synthesis and inhibitsprotein degradation in muscle & the
entire body. However the reduction in protein degradation in muscle is unique to this hormone as this is not
a benefit of GH's sole actions, of insulin's actions or of androgen action.]

Androgens

Pharmacological doses of androgens increase lean body mass in normal men (77) and muscle sized in trained
athletes (78). The mechanisms responsible for the anabolic effects of testosterone have been explained by
Griggs et al. (79). In a group of healthy volunteers, a 12-week administration of a pharmacological dose of
testosterone enanthate increased mixed muscle protein synthesis (muscle biopsy during the infusion of
labeled leucine) by 27% did not significantly affect leucine estimates of the whole-body protein breakdown...

...androgens promote protein anabolism by sparing amino acids from oxidation and increasing their
incorporation into proteins, especially muscle proteins.
 Thus, part of the effects attributed to androgens, namely the suppression of leucine oxidation (51, 52) and
the stimulation of whole-body (51-53) and muscle (57- 59) protein synthesis, might be mediated by GH.

[So androgens supress amino acid oxidation and increase proteinsynthesis ...either alone or as a synergistic or
complementary action of GH.]

Thyroid hormones (catabolic NOT anabolic)

In contrast, both rates of whole-body protein breakdown and synthesis are increased by the administration
of T3 and T4 to normal subjects (110). Under these circumstances net protein catabolism occurs because the
stimulation of protein synthesis is overcome by a greater stimulation of amino acid oxidation (110).

1. Tauveron I, Charrier S, Champredon C, Bonnet Y, Berry C, Bayle G, et al. Response of leucine metabolism to
hyperinsulinemia under amino acid replacement in experimental hyperthyroidism. Am J Physiol
1995;269:E499-507 [Thyroid hormones are catabolic because they stimulate breakdown to a greater extent
then synthesis.] The data on the role played by normal thyroid hormone concentration in the physiological
regulation of everyday protein metabolism in normal humans are very limited. In growing rats it has been
suggested that thyroid hormones contribute to the increase in protein synthesis induced by meal absorption
(113). This does not appear to be the case in humans, according to the evidence that meal-induced changes
inprotein kinetics occur in the absence of significant changes in the plasma concentrations of T3 and T4 (114).

2. Jepson MM, Bates PC, Millward DJ. The role of insulin and thyroid hormones in the regulation of msucle
growth and protein turnover in response to dietary protein. Br J Nutr 1988;59:397-415

3. Pacy PJ, Price GM, Halliday D, Quevedo MR, Millward DJ. Nitrogen homeostasis in man: the diurnal responses
of protein synthesis and degradation and amino acid oxidation to diets with increasing protein intakes. Clin
Sci 1994:86:103-18 [Thyroid hormones do not appear to contribute to protein synthesis following meals in
humans. In rats yes... In other words these hormones in normal humans do not add to the protein synthesis
that meals induce.]

Basal concentrations of thyroid hormones have differential effects on individual protein kinetics and they
play a role in the physiological regulation of protein metabolism of selectively modulating the synthetic or the
catabolic rates of target proteins.

[Base levels of thyroid hormones play a general role in modulating both catabolism and synthesis of proteins.
Other then restroing abnormalities there doesn't appear to be predictable benefit to manipulating thyroid
hormone levels if anabolism is the goal.]

Catabolism
Cortisol, Glucagon, Thyroid hormones

Thus, whole-body and muscle protein catabolism induced by triple hormonal infusions appear to be
mediated by a similar mechanism. The hormones, through the stimulation of protein breakdown, increase
the intracellular availability of amino acids; the net catabolic effect results from the fact that hormonal action
promotes the oxidative disposal of these amino acids more than their utilization for the synthesis of new
proteins.

[These hormones, especially if they are present together promoteprotein breakdown and rather then making
the amino acid pool available for resynthesis, they increase loss by stimulating oxidation.]

EOD Calorie Restriction = Longevity?

EasyEJL your mind is just wasted when it is mixed in with all the "fluff" posts at AM. You mentioned
something that to my mind is an awesome area of research with tremendous potential to make people less
susceptible to cancer, better cardiovascular profiles, better memory & less damage to brain, lower oxidative
stress, much better insulin sensitivity, prolonged life, ...just on and on...there are a lot of studies going back
to the 1940's that demonstrate these positive effect...

I became very interested in every other day calorie restriction when I experimented for years with it on
myself and found that if I alternated between:

a day of very low calories (say between 1000 & 1400) w/ food intake primarily at the beginning and end of
the day & cardio exercise(s) in the earlier portion of the day followed by no food intake for several hours...

and a day where I ate at about maintenence w/ a higher intake of carbs around a session of weightlifing.

I could readily lose fat & retain muscle. In fact I always made minor but consistent strength gains and felt
mentally sharp & had energy during the fasted portion of low cal day.

I have been researching a pattern of eating involving a day of eating less then 20% of maintenance calories
(or a complete fast) followed by eating freely (but not excessively). I have very little doubt that this pattern is
as beneficial as calorie restriction diets in promoting longevity. But has the advantage of preserving body
mass.

It is interesting that on fasted days there is no depletion of glycogen from muscle, circulating levels do go
down but stores are drawn from the liver. I conjecture that during periods of no energy intake the body
preserves muscle as best it can (at least in the 24 hour period) so that the homo sapien can use his strength
to obtain more energy. *

What is interesting is that the following non-fasted day when energy intake is occurring the body is more
insulin sensitive. In fact over time w/ this pattern of eating the body can become up to 7 times more insulin
sensitive.
 The area that I am attempting to reconcile is whether the use of GHRH/GHRP-6 to restore youthful GH levels
(and a little higher IGF-1 levels) undermines the longevity benefits of alternate day calorie restriction?

Resveratrol I suspect is not the answer to longevity in humans even though it mimics many of the
transcriptional aspects of calorie restriction. It has been shown not to extend lifespan in normal mice. **

Eating at 60% of maintenance every day is not desirable, but EOD calorie restriction might be the answer to
health and longevity while maintaining the body in a fit muscular state.

• - "With the present fasting protocol and maintenance of habitual daily physical activity in the fasting periods,
we had expected to detect a decrease in IMTG content in the skeletal muscle. The fact that this was not seen
and that muscle glycogen content was unchanged could suggest that skeletal muscle is not immediately
involved in recognition of acute energy oscillations." -Effect of intermittent fasting and refeeding on insulin
action in healthy men, Nils Halberg, J Appl Physiol 99: 2128-2136, 2005

** - Resveratrol delays age-related deterioration and mimics transcriptional aspects of dietary restriction
without extending life span, Pearson KJ , Cell Metab. 2008 Aug;8(2):157-68.

STUDY: Effect of intermittent fasting and refeeding on insulin action in healthy men

Eight healthy young Caucasian men, body mass index 25.7 +- 0.4 kg/m2

Throughout the intervention, the subjects were instructed to uphold their normal exercise habits, to maintain
their usual macronutrient mixing of their meals, and to eat sufficient quantities of food on the nonfasting
days to ensure that their body weight was stable.

The fast period was 20 hours. Each fasting period started at 2200 and ended at 1800 the following day (for
protocol see Fig. 1). During the fasting periods the subjects were allowed to drink water and were instructed
to maintain habitual activities.

CONCLUSION:

In conclusion, the findings that intermittent fasting increases insulin sensitivity on the whole body level as
well as in adipose tissue support the view that cycles of feast and famine are important as an initiator of
thrifty genes leading to improvements in metabolic function (6). We suggest that a fastinginduced increase in
circulating adiponectin is at least partly responsible for this finding. The change in adiponectin, together with
changes in plasma leptin with fasting, underlines the important role of the adipose tissue in recognizing the
oscillation in energy stores. Finally, the data indicate that intermittent fasting and physical training may
increase insulin action via different mechanisms because muscle energy stores did not change with the
present fasting intervention.
Caprylic Acid (MCTs) - reduce expression of lipogenic genes

Thank you for posting that up BT. MCTs, specifically caprylic acid (octonate) does much more than that.
Permit me to introduce you to one of my secrets. Very few people know and understand what follows. Best
explained by the study Modulation of adipocyte lipogenesis by octanoate: involvement of reactive oxygen
species, Wen Guo, Weisheng Xie and Jianrong Han, Nutrition & Metabolism 2006, 3:30

Background:

Medium-chain fatty acids (MCFA) belong to a unique type of fatty acids that is metabolized differently from
either long-chain fatty acids or carbohydrates. Dietary Medium-chain triglycerides (MCT) inhibit body fat
mass growth in both animals and human. Early studies suggest that this effect might be caused by rapid
absorption of MCT-derived MCFA and their ß-oxidation in the liver, which reduces the circulating fatty acids
available to the adipocytes [11]. This model is supported by the evidence that MCFA enters the ß-oxidation
pathway in liver mitochondria independent of carnitine palmitoyl transferase I (CPT-I) [12].

[The afore-mentioned was presented by you BT & your wonderful illustrations]

However, it does not explain the findings that dietary MCT inhibits lipogenesis in adipocytes [13,14].

Furthermore, MCFA are recovered in the adipose tissue fatty acids up to 30 mole % in both animals and
humans adapted to MCT diets [6,15-17]. These findings imply that a substantial influx of MCFA into the
adipocytes occurs in vivo, which might affect adipose tissue function more than previously appreciated.

[MCTs in significant quantity do make there way into fat cells and do what?]

Indeed, we found that a reduction in fat mass was associated with reduced expression of lipogenic genes and
adipocyte transcription factors in MCT-fed animals [6]. This effect was reproduced in cultured adipocytes
treated with octanoate [18]. When added to differentiating rodent preadipocytes, MCFA also inhibits fat
accumulation and reduces expression of adipocyte specific proteins [19,20]. In this study, we provide new
evidence that octanoate suppresses lipogenesis, at least in part, by inactivating the key adipocyte
transcription factor, peroxisome proliferator-activated receptor y (PPARy). Furthermore, our data revealed,
for the first time, an involvement of reactive oxygen species (ROS) as a possible intermediate component that
might regulate the anti-lipogenic effects.

[Wow!]

[What is so Wow?]

Discussion:
Fatty acid oxidation is normally activated only under fasting conditions when circulating levels of insulin and
glucose are low. Conversely, lipogenesis is down-regulated by fasting. The mechanistic link between these
two events, however, has not been established.

In this work, we provided the first evidence that medium-chain octanoate can be ß-oxidized in adipocytes
independent of CPT-I regulation. Hence, supplement of octanoate maintains active ß- oxidation in the
presence of insulin and glucose. This is correlated with inhibition of lipogenesis and reduction of lipogenic
gene expression. In other words, octanoate induces a metabolic state in adipocytes mimicking a fasting
condition without actual hormone/nutrient deprivation. Our results also demonstrated that ROS might be
involved as a mediator for octanoate in lowering PPARy activity, the master control of lipogenic gene
expression.

As extensively reviewed previously, PPARy is a prototypical member of the nuclear receptor superfamily
which integrates the control of energy, lipid and glucose, homerostasis [50-54]. PPARy binds a variety of small
lipophilic compounds derived from metabolism and nutrition. These ligands, in turn, determine cofactor
recruitment and regulate the transcription of a variety of metabolic genes. Recent literature highlights the
development of partial agonists of PPARy to block adipogenesis and reduce fat mass development [54-59]. In
one of our previous studies, we proposed that octanoate might act as a partial agonist for PPARy because it
can potentially bind to PPARy as does the long-chain fatty acids [29,60], hence competitively blocking the
binding of the latter or other endogenous ligands. This model was supported, but not proved, by the findings
that the anti-adipogenic [19] and antilipogenic (this work) effects of octanoate was efficiently blocked by
selected synthetic PPARy agonists.

The current findings that octanoate induced ROS generation in adipocytes suggest that octanoate might also
modulate PPARy activity indirectly via the ROS signaling pathways. It has been well established that ROS
activates the stress-responsive protein kinases [61,62], which either directly or indirectly inhibit PPARy
activity [47-49,62-67]. In our preliminary studies, we found that octanoate also induced sustained activation
of Erk1/2 and JNK/SAPK (data not shown). How these kinase pathways are involved in the regulation of
PPARy activity and lipogenesis in our cell system and, more importantly, in primary adipocytes, are currently
under investigation.

Inhibition of adipocyte lipogenesis can be a useful tool for the prevention of obesity. In this regard, our
studies contribute to the scientific basis for the application of MCT in dietary weight management. On the
other hand, a complete inhibition of fat mass growth is disastrous since adipocytes play important roles in
physiological functions of mammals. Compared to the pharmaceutical inhibitors of lipogenesis [68,69], the
effects of octanoate can be considered as moderate and yet might be more desirable for physiological
regulation of body fat mass without adversely affecting normal fat tissue functions. According to recent
surveys, a majority of the middle age population is moderately over-weighed (BMI 23–27), and a slight
increase in BMI in this range is associated with a greater risk for metabolic syndrome [70,71]. It will be of
 important social and economical values if MCT can be used for body weight regulation in this sub-population,
as demonstrated by a recent clinical trial [5].

Conclusion:

This study demonstrated that octanoate had a direct inhibitory effect on fat storage in adipocytes under
conditions that normally favor lipogenesis. This was related to its unique ß-oxidation mechanism which links
to elevated cellular ROS levels and subsequent inactivation of PPARy. The exact mechanism by which PPARy
is inactivated, in particular, how ROS is involved in this process, still remains to be elucidated. Furthermore,
ROS is known to have diverse and complex molecular targets, which might directly or indirectly influence the
activities of additional adipocyte transcription factors or modify selected lipogenic proteins [44,71].
Elucidation of these mechanisms will be helpful for the application of MCT for dietary intervention to prevent
obesity and may reveal possible pharmaceutical targets to modulate fat metabolism.

From the RESULTS an important practical tip [l-carnitine & MCTs (Caprylic Acid) should not be used together
& MCTs (Caprylic Acid) are more effective then l-carnitine in the presence of insulin]

As shown in Figure 3A, ß-oxidation of octanoate was slightly inhibited (~18%) by insulin, a hormone that
promotes the generation of the natural inhibitor of CPT-I [37], and Etomoxir, a pharmaceutical inhibitor of
CPT-I. On the other hand, l-carnitine, an activator of CPT-I, caused a ~60% inhibition of octanoate oxidation. A
combination of l-carnitine and exogenous oleate further enhanced the inhibition (> 85%). In contrast, ß-
oxidation of oleate was increased by l-carnitine more than 2 fold but inhibited by insulin by about 60% (Fig.
3B), consistent with the literature [37]. These results indicate that in adipocytes, octanoate was mainly
oxidized independent of CPT-I (> 80%). A small fraction (< 20%), that was sensitive to insulin and etomoxir,
might be activated in the cytosol and hence depend on CPT-I to enter the mitochondria. The observation that
l-carnitine inhibited, rather than promoted, ß-oxidation of octanoate suggests that activation of CPT-I largely
increased the transport of endogenous fatty acids into the ß-oxidation pathway which compete with
octanoate for the enzymes downstream from CPT-1. This competition was further enhanced in the presence
of added oleate.

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Fish Oil (DHA) increases metabolism (fat loss)

I thought you might be interested in this because almost no nutritionists or people involved in bodybuilding
know this.

But in the world of aging and longevity research there is the knowledge that the lipid make up of the cellular
membrane influences cellular metabolism. High DHA content in phospholipids of the cellular membrane is
associated with high metabolic activity and this leads into the "membrane pacemaker" theory of metabolism.

This theory proposes that highly polyunsaturated acyl chains impart physical properties to cellular membrane
bilayers that enhance and speed up the molecular activity of membrane proteins and consequently the
metabolic activity of cells, tissues and the whole animal.

There is a positive correlation in the animal kingdom between body size and cellular metabolism with smaller
animals possessing cellular membranes with higher DHA content and thus higher cellular metabolisms. Larger
animals, humans for instance have cellular membranes with a lot less DHA and thus slower cellular
metabolism.

All of this is correlated to lifespan. Highly polyunsaturated acyl chains (primarily DHA) are very susceptible to
peroxidative damage. This kind of damage shortens lifespan.

The brain however is not correlated to any of this and in humans posses high DHA content in the cellular
membrane & thus higher metabolism. It is thought that evolution probably weeded out those sluggish
thought creatures that had slower brain cell metabolism.
How does it work? Well the physical properties of polyunsaturates primarily DHA are such that these lipid
chains are flexible and active compared to unsaturated lipids. Because of the active or rapid movement of
DHA lipids they exert lateral pressure on neighboring molecules in the cellular membrane. This creates
greater activity in membrane enzymes, Na+/K+-ATPase molecules and thus ion channels become
approximtely 25% more active. A large part of cellular energy goes into operating those channels.

Similar sorts of activity occur in the mitochondrial membrane proteins.

A good & recent review of all of this is The links between membrane composition, metabolic rate and
lifespan, A.J. Hulbert, Comparative Biochemistry and Physiology, Part A 150 (2008) 196–203

Now we know from source material such as Evolutionary Aspects of Diet, the Omega-6/Omega-3 Ratio, and
Gene Expression by Artemis P. Simopoulos found in the book Phytochemicals: Nutrient-Gene Interactions,
Mark S. Meskin (Editor), CRC; 1 edition (February 22, Phytochemicals: Nutrient-Gene Interactions, Mark S.
Meskin (Editor), CRC; 1 edition (February 22, 2006) that:

"... the polyunsaturated fatty acid (PUFA) composition of cell membranes is to a great extent dependent on
the dietary intake."

So if you ingest a large quantity of Omega 3 fatty acids which contain high DHA content you will alter the
makeup of the cellular membrane such that it is composed of more DHA which will increase cellular
metabolism.

This is great for dieting but increases the potential oxidative damage. Enough to effective lifespan? Probably
not. But it should increase energy expenditure and thus be beneficial on a diet.

CREATING A BACKBONE AROUND WHICH TO LOSE FAT

Glucose is an indispensable metabolic fuel for the brain. For the reason that the brain is unable to synthesize
glucose or store more than a few minutes supply as glycogen, it is critically dependent on a continuous supply
of glucose from the circulation. "At normal (or elevated) arterial glucose concentrations, the rate of blood-to-
brain glucose transport exceeds the rate of brain glucose metabolism. However, as arterial glucose levels fall
below the physiological range, blood-to-brain glucose transport becomes limiting to brain glucose
metabolism, and ultimately survival." - Hypoglycemia in Diabetes, Philip E. Cryer,Diabetes Care 26:1902-1912,
2003

So what happens at various blood glucose levels?

For practical purposes we can say that the body desires to maintain a stable glucose level in blood plasma of
around 90 ng/dL. Blood glucose levels above that threshold are viewed as excess energy and this engenders a
storage response via the pancreatic secretion of insulin. The hormone insulin removes glucose from blood
plasma until levels return to 90ng/dL at which point insulin ceases to be active.
Below that insulin triggering blood glucose threshold of 90ng/dL, down to about 70ng/dL, there is insufficient
circulating energy and therefore the hormone glucagon is released to catabolize stored energy and make it
available to the brain and body. Physical activity or energy demanding activity without the presence of
circulating glucose or concurrent intake of food requires stored energy. Activity is the catalyst that drives the
blood glucose level below 90ng/dL.

Below 70ng/dL of glucose in blood plasma the body becomes concerned and because the brain is a critical
organ and needs glucose, this threshold is considered critical. The hormone epinephrine (adrenaline) is
released at this stage in order to trigger a quick release of stored energy to get blood glucose levels back to
normal.

The body when it is in this emergency state will burn anything for fuel and muscle can be catabolized. It is
best to avoid this state.

When you diet you can not lose fat in the presence of the hormone insulin. You want to have the hormone
glucagon active and this requires that your blood glucose levels be between 70ng/dL and 90ng/dL. Glucagon
acts to free up stored energy by signaling the adipocytes to activate Hormone-sensitive lipase which converts
triglycerides into free fatty acids.

Hormone-sensitive lipase is a vital component of fat mobilization and is a positively active force in the
presence of glucagon and inhibited in the presence of insulin.

Fatty acids have very low solubility in the blood however serum albumin, binds free fatty acids, and thereby
increases their effective solubility by a factor of about 1000. Serum albumin transports fatty acids to organs
such as muscle and liver for oxidation and this happens when blood sugar is low.

So what is the minimal amount of glucose needed to trigger insulin & why again is insulin bad?

From the textbook Biochemical and Physiological Aspects of Human Nutrition, Stipanuk et al. ed. 2000

Insulin ...is secreted in response to changes in circulating glucose; a change of as little as2mg/100ml of
plasma can be detected by the pancreas. Insulin release can also be stimulated in response to certain amino
acids in the circulation. Other important signals for insulin secretion include gut hormones and nervous
stimulation. - p395

In adipose tissue insulin increases fatty acid uptake and triacylglycerol storage via increases in lipoprotein
lipase activity, and at the same time decreases lipolysis by decreasing hormone-sensitive lipase activity. The
latter may be one of insulin's strongest actions because it occurs at very low insulin levels and effectively
lowers the levels of free fatty acids in the circulation thereby decreasing there utilization as fuel. - p396

Is there way to minimize glucose's influence?

Again from the textbook Biochemical and Physiological Aspects of Human Nutrition, Stipanuk et al. ed. 2000
Soluable viscous polysaccharides [certain fibers] can delay and even interfere with the absorption of
nutrients...

Positive benefits of delayed nutrient absorption include an improvement of glucose tolerance and a lowering
of serum cholesterol levels. Delayed absorption of carbohydrates results in a lower postprandial (following a
meal) glucose level. In general the more viscous the fiber the greater the effect on blood glucose. This is
similar to the effect seen with eating several small meals rather than one large meal. When glucose is
absorbed in small amounts over an extended period, such as seen with viscous fibers, the insulin response is
attenuated (Pick, et al. (1996) Oat bran concentrate bread products improve long term control of diabetes: A
pilot study J. Am Diet Assoc 96:1254-1261) ...

Viscosity of the polysaccharides and their ability to form gels in the stomach appear to slow gastric emptying.
This in turn results in a more uniform presentation of the meal to the small intestine for absorption. [Poorly
soluble fibers that do not form gels such as wheat and cellulose have little effect...unlike those that do which
include guar gum, pectin, psyllium, oat bran.] - p146. 147

A Practical Experiment

For two days I used my glucose monitor to check my blood glucose after ingestion of coffee. • Black coffee w/
no additives = zero rise in glucose • Black coffee w/ Stevia = a 2 point rise in glucose • Black coffee w/
Splenda = a 5 - 8 point rise in glucose. • Coffee w/ Splenda & generic Coffee Mate creamer = 15+ point rise in
glucose • Coffee w/ Splenda & 2% Lactose free Milk = 17+ point rise in glucose

So for me the caffeine in a cup of coffee does not effect blood glucose BUT the additives sure as heck do!

How do you reduce the rise in blood glucose w/ these additives (besides the obvious)? ....add FIBER.

So ingesting 2 grams of Psyllium Husk powder just prior to drinking Coffee w/ Splenda & Coffee Mate
creamer resulted in only a 4 point rise in blood glucose. WOW!

So how does Growth Hormone fit in to all of this?

First recognize that there will be periods of time post meal where blood glucose and thus insulin will be
elevated. There is no fat loss during this time and Growth Hormone will not be effective during these periods.

With this recognition it makes sense to reduce the amplitude and area under the curve (in graph-type
language) of insulin spikes. Meals should be constructed with both the glycemic index of foods in mind and
the total glycemic load of the meal. Fiber should be used to reduce blood glucose levels.

With this recognition it makes sense to maximize the time period when glucagon is active. That requires
insulin to return to baseline quickly after a meal and a sufficient period of time between meals to allow
glucagon to have an effective impact. Activity between meals as well as the presence of GH will have positive
impacts on fat loss.
The reason it is necessary to write about everything in this post is so that you understand how easy it is to
waste Growth Hormones fat loss potential and what one must do to maximize GH's fat loss power.

Too often someone will use GH and admit that their diet wasn't very good. That negates much of GH's
positive impact on fat loss.

I also wanted to put GH into a proper context which sadly is often lacking in people who hope for better body
attainment. The things I have barely touched on are of utmost importance and make up the backbone of a
sound fat loss protocol.

GH can be a very useful adjunct to a properly constructed protocol which focuses on food intake with proper
hormonal impact and sustained activity level.

Use of GH

From other posts we understand that GH has a dual role to play in a diet. It can increase the rate of fat loss
and it can help inhibit the breakdown of muscle. So you want to administer GH in smaller amounts, you want
to have off periods (i.e. time when GH is not active) so that the intracellular pathways can reset and you want
to maximize the frequency of administration.

So we need to understand the impact of GH dose on levels of GH in plasma to set a schedule. We can
extrapolate from the chart from the GH study posted above. Assuming a linear relationship (since 7.5ius were
active for 12 hours & 15ius for 24 hours) we can assume that a dose of 2ius of synthetic GH administration
will elevate GH in plasma for 3.2 hours.

If we need about 4 hours off (we can probably round down to 3.8 hours) we can dose 2ius of GH every 7
hours. For ease of fitting a dosing schedule into our lives we can round up to 8 hours and say that we can
dose 2ius three times a day spaced out by 7-8 hours.

Since GH isn't effective for fat loss in the presence of insulin we probably want the meals that have the
biggest impact on blood glucose and thus insulin to be ingested during the time GH is not active. After that
meal is digested and insulin rises and then falls back to 90ng/dL we can administer GH and be confident it will
have a positive impact on our overall fat loss protocol.

Further Note on GH & Insulin

In plain language, GH in certain circumstances increases glucose uptake identical to that of insulin into both
muscle and adipose tissue. This involves translocations of glut 4 and to a lesser extent glut 1 from an
intracellular pool to the plasma membrane. BUT in order for this to happen there must be an absence of GH
for prolonged periods of time. It appears that this rarely occurs because the base level of GH is still too high
to create this effect. *
 Of more importance is the "likely" effect of GH on glucose transport into adipose tissue. GH, dose
dependently reduces glucose transport (diabetogenic effect). The addition of GH to adipocytes in vitro and
dose dependently in vivo reduces the rate of glucose uptake in a way that we could characterize as the
opposite of the insulin effect.

"The data reported here not only confirm the earlier findings but also further demonstrate the importance of
GH in vivo for the restriction of basal glucose transport in adipocytes. ... The data give evidence for the
importance of GH in vivo, in balance with insulin, for the control of the activity of the glucose carrier in
adipose tissue." - Glucose transport in adipocytes and its control by growth hormone in vivo, Schoenle et al.
242 (6): E368. (1982)

So there is a good possibility that although GH in the presence of insulin will not lead to substantial fat lossvia
lipolysis, it will inhibit the uptake of glucose into adipose tissue. This leads us to the generalization that
concurrent administration of GH & insulin will skew nutrient partitioning in favor of muscle tissue and away
from adipose tissue.

One further note of interest though is this glucose uptake inhibiting effect of GH leads to a restoration of
sensitivity to insulin in that tissue.

• - Cellular mechanism of the insulin-like effect' of growth hormone in adipocytes Rapid translocation of the
HepG2-type and adipocyte/muscle glucose transporters, Tanner, J. W. et al, Biochem. J. (1992) 282, 99-106

Age-Related Changes in Slow Wave Sleep and Relationship With Growth Hormone Levels

I've tried to emphasize that Slow Wave Sleep (SW) and Growth Hormone (GH) are not merely positively
correlated but are intricately bound together such that a change in one leads to a change in the other. That is
why from the start I have attempted to underscore that a pre-bed dose of Growth Hormone Releasing
Hormone (GHRH) & Growth Hormone Releasing Peptide 6 (GHRP-6) will increase that vital period of sleep
known as Slow Wave Sleep which has restorative benefits beyond amplified GH release.

The following study is fascinating for all of us because it reveals that somatopause begins dramatically
between age 25 and 35. The following study published in the prestigious Journal of the AmericanMedical
Association is well worth examining.

The chronology of aging of GH secretion follows a pattern remarkably similar to that of SW sleep. Thus, in
men, the so-called "somatopause" occurs early in adulthood, between age 25 and 35 years, an age range that
corresponds to the human life expectancy before the development of modern civilization and is essentially
completed by the end of the fourth decade.

Our analyses further indicate that reduced amounts of SW sleep, independent of age, are partly responsible
for reduced GH secretion in midlife and late life. That this correlative evidence reflects a common mechanism
underlying SW sleep generation and GH release rather than an indirect association is supported by 2 studies
that have shown that pharmacological enhancement of SW sleep results in increased GH release. - Age-
Related Changes in Slow Wave Sleep and REM Sleep and Relationship With Growth Hormone and Cortisol
Levels in Healthy Men, Eve Van Cauter, PhD; Rachel Leproult, MS; Laurence Plat, MD,JAMA. 2000;284:861-
868

The objective of the study was, to determine the chronology of age-related changes in sleep duration and
quality (sleep stages) in healthy men and whether concomitant alterations occur in GH and cortisol levels.

They combined data from a series of studies conducted between 1985 and 1999 at 4 laboratories which
examined 149 healthy men, aged 16 to 83 years, with a mean (SD) body mass index of 24.1 (2.3) kg/m2,
without sleep complaints or histories of endocrine, psychiatric, or sleep disorders.

They created twenty-four–hour profiles of plasma GH and cortisol levels and polygraphic sleep recordings
and found the following results:

The mean (SEM) percentage of deep slow wave sleep decreased from 18.9% (1.3%) during early adulthood
(age 16-25 years) to 3.4% (1.0%) during midlife (age 36-50 years) and was replaced by lighter sleep (stages 1
and 2) without significant increases in sleep fragmentation or decreases in rapid eye movement (REM) sleep.

The transition from midlife to late life (age 71-83 years) involved no further significant decrease in slow wave
sleep but an increase in time awake of 28 minutes per decade at the expense of decreases in both light non-
REM sleep (-24 minutes per decade; P<.001) and REM sleep (-10 minutes per decade; P<.001).

The decline in slow wave sleep from early adulthood to midlife was paralleled by a major decline in GH
secretion (-372 µg per decade; P<.001). From midlife to late life, GH secretion further declined at a slower
rate (-43 µg per decade; P<.02).

Independently of age, the amount of GH secretion was significantly associated with slow wave sleep (P<.001).

Increasing age was associated with an elevation of evening cortisol levels (+19.3 nmol/L per decade; P<.001)
that became significant only after age 50 years, when sleep became more fragmented and REM sleep
declined. A trend for an association between lower amounts of REM sleep and higher evening cortisol
concentrations independent of age was detected (P<.10).

For a deeper read I include the following Introduction & Comments which elaborate on the significance of the
results. I strongly encourage any one interested in anti-aging to read it so that they can adopt the appropriate
compensatory strategies.

INTRODUCTION

Decreased subjective sleep quality is one of the most common health complaints of older adults.1 The most
consistent alterations associated with normal aging include increased number and duration of awakenings
and decreased amounts of deep slow wave (SW) sleep (ie, stages 3 and 4 of non–rapid eye movement (non-
REM) sleep).2-4 REM sleep appears to be relatively better preserved during aging.3-7 The age at which
changes in amount and distribution of sleep stages appear is unclear because the majority of studies have
been based on comparisons of young vs older adults. Several investigators have noticed that there are
marked decreases in SW sleep in early adulthood in men but not in women.8-11

Sleep is a major modulator of endocrine function, particularly of pituitary-dependent hormonal release.

Growth hormone (GH) secretion is stimulated during sleep and, in men, 60% to 70% of daily GH secretion
occurs during early sleep, in association with SW sleep.12 Whether decrements in SW sleep contribute to the
well-known decrease in GH secretion in normal aging is not known.13-15

In contrast to the enhanced activity of the GH axis during sleep, the hypothalamic-pituitary-adrenal (HPA)
axis is acutely inhibited during early SW sleep.16-20 Furthermore, even partial sleep deprivation results in an
elevation of cortisol levels the following evening.21 Thus, both decreased SW sleep and sleep loss resulting
from increased sleep fragmentation could contribute to elevating cortisol levels. An elevation of evening
cortisol levels is a hallmark of aging14-15,22 that is thought to reflect an impairment of the negative
feedback control of the HPA axis and could underlie a constellation of metabolic and cognitive alterations.23-
25

The present study defines the chronology of age-related changes in sleep duration and quality (ie, amounts of
sleep stages), GH secretion, and cortisol levels in healthy men and examines whether decrements in sleep
quality are associated with alterations of GH and cortisol levels.

...

COMMENT

The present analysis demonstrates that, in healthy men, aging affects SW sleep and GH release with a similar
chronology characterized by major decrements from early adulthood to midlife. In contrast, the impact of
age on REM sleep, sleep fragmentation, and HPA function does not become apparent until later in life. The
analysis further suggests that age-related alterations in the somatotropic and corticotropic axes may partially
reflect decreased sleep quality.

Human sleep is under the dual control of circadian rhythmicity and of a homeostatic processrelating the
depth of sleep to the duration of prior wakefulness.44 This homeostatic process involves a putative neural
sleep factor that increases during waking and decays exponentially during sleep. Slow wave sleep is primarily
controlled by the homeostatic process. Circadian rhythmicity is an oscillation with a near 24-hour period
generated by a pacemaker located in the hypothalamic suprachiasmatic nucleus. Circadian rhythmicity plays
an important role in sleep timing, sleep consolidation, and the distribution of REM sleep.45 The present data
indicate that an alteration in sleep-wake homeostasis is an early biological marker of aging in adult men. In
contrast, components of sleep that are under the control of the circadian pacemaker appear to be relatively
well preserved until late in life.
The chronology of aging of GH secretion follows a pattern remarkably similar to that of SW sleep. Thus, in
men, the so-called "somatopause" occurs early in adulthood, between age 25 and 35 years, an age range that
corresponds to the human life expectancy before the development of modern civilization and is essentially
completed by the end of the fourth decade. Our analyses further indicate that reduced amounts of SW sleep,
independent of age, are partly responsible for reduced GH secretion in midlife and late life. That this
correlative evidence reflects a common mechanism underlying SW sleep generation and GH release rather
than an indirect association is supported by 2 studies that have shown that pharmacological enhancement of
SW sleep results in increased GH release.46-47 Also supporting a causal relationship between decreased
sleep quality and reduced nocturnal GH secretion are studies inpatients with sleep apnea showing a marked
increase in GH release following treatment with positive airway pressure.48-49 The reverse interaction
between sleep and GH, ie, a deleterious impact of reduced somatotropic function on sleep, is also possible
since studies in both normal and pathological conditions have shown that GH-releasing factor and GH
influence sleep quality.12, 50 In the present study of nonobese men, the finding of a negative impact of BMI
on both GH secretion during waking and amount of SW sleep is consistent with the hypothesis that inhibition
of the GH axis may adversely affect sleep regulation.

While the clinical implications of decreased SW sleep are still unclear, the relative GH deficiency of the elderly
is associated with increased fat tissue and abdominal obesity, reduced muscle mass and strength, and
reduced exercise capacity.51-53 Multiple trials are currently examining the clinical usefulness and safety of
replacement therapy with recombinant GH, the other hormones of the GH axis, and synthetic GH
secretagogues in elderly adults without pathological GH deficiency. While the benefits of such interventions
are still unproven, the present findings suggest that they should target a younger age range than currently
envisioned, ie, individuals in early midlife rather than those older than 65 years,when peripheral tissues have
been continuously exposed to very low levels of GH for at least 2 decades. Furthermore, since
pharmacological enhancement of SW sleep in young adults has been shown to result in a simultaneous and
proportional increase in GH release 46-47 and ongoing studies in our laboratory indicate that similar effects
can be obtained in older subjects,drugs that reliably stimulate SW sleep may represent a novel class of GH
secretagogues.

The present data demonstrate that the amount of REM sleep is reduced by approximately 50% in late life vs
young adulthood. However, reduced amounts of REM sleep and significant sleep fragmentation do not occur
until after age 50 years. The impact of aging on cortisol levels followed the same chronology. Aging was
associated with an elevation of evening cortisol levels, reflecting an impaired ability to achieve evening
quiescence following morning stimulation. Studies in both animals and humans have indicated that
deleterious effects of HPA hyperactivity are more pronounced at the time of the trough of the rhythm than at
the time of the peak.25, 54 Thus, modest elevations in evening cortisol levels could facilitate the
development of central and peripheral disturbances associated with glucocorticoid excess, such as memory
 deficits and insulin resistance,24-25 and further promote sleep fragmentation. Indeed, elevated cortisol
levels may promote awakenings.55-56

Elevated evening cortisol levels in late life probably reflect an impairment of the negative feedback control of
the HPA axis in aging. Our analyses suggest that there is a relationship between this alteration of HPA
function and decreased amounts of REM sleep that is independent of age. The data generally support the
concept that decreased sleep quality contributes to the allostatic load, ie, the wear and tear resulting from
overactivity of stress-responsive systems.57

The present study focused on the effects of aging on the relationship between sleep and the somatotopic
and corticotropic axes in men because the predominant GH secretion occurs during sleep in men but not in
women11 and because there is evidence to suggest that the marked decreases in SW sleep in early
adulthood occur in men but not in women.8-11 Whether conclusions similar to those obtained for men hold
for women will require a separate evaluation as sex differences in sleep quality as well as 24-hour profiles of
GH and cortisol secretion have been well documented in both young and older adults.11-12,22

In conclusion, in healthy men, the distinct changes in sleep quality that characterize the transitions from early
adulthood to midlife, on the one hand, and from midlife to old age, on the other hand, are each associated
with specific alterations in hormonal systems that are essential for metabolic regulation. Strategies to
prevent or limit decrements of sleep quality in midlife and late life may therefore represent an indirect form
of hormonal therapy with possible beneficial health consequences.

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Growth Hormone Receptor structure, post-biogenesis behavior and degradation

The following was originally created primarily for my benefit and serves as a basic summary of Growth
Hormone Receptor structure, post-biogenesis behavior and degradation.

It is not intended for a wider audience and is not a Datbtrue copyrighted article. It represents the current
state of knowledge in the aforementioned area (October, 2008) and was derived primarily from an
unpublished paper by Stuart J. Frank & Serge Y. Fuchs on growth hormone receptor abundance and function
and from Growth hormone receptor; mechanism of action, Andrew J. Brooks, Jong Wei Wooh, Kathryn A.
Tunny, Michael J. Waters, The International Journal of Biochemistry & Cell Biology 40 (2008) 1984–1989

These unrefined notes are for educational use only.

GHR Structure

The growth hormone receptor (GHR) is a member of the cytokine receptor superfamily. Cytokines is a general
category encompassing signaling proteins and glycoproteins (often cellular membrane proteins) that similar
to hormones and neurotransmitters facilitate cellular communication. [12,13] It is a type I cytokine receptor
as is the prolactin receptor, which in essence means it is connected to Janus kinase (JAK) which acts as its
primary mediator of signaling events.

Physically the GHR is composed of 620 residues (a residue is an individual amino acid in a peptide chain). 350
of these residues reside inside the cell and make up what is known as the intracellular domain. 246 of these
residues reside outside the cell and make up what is known as the extracellular domain. The remaining 24
residues reside in the membrane of the cell and make up what is known as the transcellular domain. [13-16]

The GHR extracellular domain consists of two fibronectin type III beta sandwich domains connected by a
short flexible linker.

The intracellular domain comprises Box 1 and Box 2 motifs which bind the tyrosine kinase, Janus kinase 2
(JAK2) and several tyrosine residues that act as substrates for phoshorylation by JAK2 and thus become
binding sites for SH2 domain proteins.

A Kinase is a type of enzyme that transfers phosphate groups from high-energy donor molecules, such as
ATP, to specific target molecules (substrates) in a process called "phosphorylation".

Since cytokine receptors such as GHR possess no catalytic kinase activity, they rely on the Janus kinase family
of tyrosine kinases to phosphorylate and activate downstream proteins involved in their signal transduction
pathways.

Phosphorylation of a substrate by tyrosine kinases acts as a switch to trigger binding to an SH2 domain-
containing protein. STAT & PI3K proteins possess an SH2 "docking" protein and once bound begin to exert
their respective effects.

The growth hormone (GH) molecule intiates this phosphorylation process by binding to one of the two GHR
domains via its site of stongest attraction. For the 22kDa form of GH it would be site 1. Once bound via GH
site 1 to one of the two GHR domains the GH molecule binds to the second GHR domain via the GH molecule
location known as site 2.

Note that the result of the GH molecule binding with the two receptor domains does not have the effect of
connecting the two receptor domains for they were already connected by a short flexible linker. Rather the
binding of the GH molecule to the GHR causes a repositioning of the intracellular domains, resulting in the
activation of associated tyrosine kinases and thus signal transduction. [17]

JAK2
The GHR does not possess built-in tyrosine kinase activity and relies on associated kinases for signal
transduction. The Janus kinase JAK2 provides a major component of signal transduction by GH. JAK2
associates with the GHR intracellular domain proline rich Box 1 motif via its amino terminal (JH5-7) FERM
domain. JAK2 phosphorylates tyrosine residues on the associated GHR intracellular domain which provide
docking sites for Src homology 2 (SH2) domain proteins, in particular STAT5a and 5b. The STATs 1, 3, 5a, and
5b are subsequently phosphorylated by JAK2, homo- or heterodimerise, translocate to the nucleus, bind to
STAT responsive elements and activate transcription. [18]

In the GHR unliganded state (unbound by the Gh molecule) it is thought that the JAK2 pseudokinase JH2
domain interacts with and autoinhibits the JH1 kinase domain resulting in an inactive JAK2. GH binding
causes structural reorientation of the receptor GH domains , which results in a structural re-orientation of
JAK2 and disruption of the ability of pseudokinase JH2 domains to inhibit the JH1 kinase domain, leading to
JAK2 activation. There are several mechanisms for the termination of the JAK2 mediated signal which involve
phosphatases, suppressors of cytokine signalling (SOCS) proteins that block signalling via their SH2 domains
and receptor downregulation. [19]

In essence GH binding to the GHR triggers activation of JAK2 which causes the GHR and JAK2 tyrosine
phosphorylation which induces signaling systems. The primary signaling systems are:

STATs (most notably STAT5b) ERKs PI3-kinase [23-25]

GH-induced STAT5b activation requires receptor tyrosine phosphorylation and promotes gene transcription
(eg., IGF-1, acid-labile subunit (ALS) of the IGF binding protein complex, SOCS proteins, hepatic P450
enzymes, and serine protease inhibitor[26–36]).

Unlike STAT5b, GH-induced ERK and PI3K activation does not require the entire GHR cytoplasmic domain, but
only JAK2 coupling [23,37,38 ,39-41]. ERK activity is critical for GH-induced c-fos transcription [42], enhances
GH-stimulated proliferation [43], and mediates crosstalk with EGF signaling [44-46]. GH-induced PI3K activity
is implicated in antiapoptosis and/or proliferation and likely contributes to GH-induced ERK, p70 S6 kinase,
and phosphodiesterase activity [42,43,47-50].

GH sensitivity is substantially affected by the abundance of GHR available for ligand engagement at particular
target cells and tissues. Surface GHR availability is regulated at several levels, including transcriptional, post-
transcriptional, and post-translational.

For a thorough review of transcriptional and post-transcriptional events see references 51 & 52.

GHR regulation at the post-translational will be reviewed herein.

Movement of newly synthesized GHR to the cell surface

GHR is synthesized as a non-glycosylated precursor that is transported from the endoplasmic reticulum (ER)
to the Gogli apparatus. GHR dimerizes in the ER early in the process of biogenesis thus accounting for the
receptor dimers detected at the cell surface even in the absence of GH engagement. [53, 60,61] In the
process of transport through the Golgi, the GHR acquires carbohydrate in a characteristic fashion, in which
high-mannose sugars added in the ER are ultimately removed during the transition from the early to late
Golgi to yield the mature glycosylated GHR that populates the cell surface.

JAK2 apparently associates with GHR early in the biosynthetic pathway and not only acts as a GHR chaperone
as it makes its way to the surface but fosters GHR maturation [59,62]

Studies suggest that in cells that lack JAK2 the nascent precursor GHR is a target for endoplasmic reticulum
associated degradation (ERAD) and represent the first example of ERAD-associated cleavage of a cytokine
receptor family member that stems from a lack of its cognate JAK. ERAD is a process whereby proteins that
fail to fold properly or otherwise fail quality control mechanisms in the ER undergo retrotranslocation and
proteasomal degradation in the cytosol [67–69]. JAK2, by virtue of its association with the GHR, rather than
via its kinase activity, apparently "chaperones" the dimerized precursor so as to avoid quality control and
proceed with efficient processing to mature GHR in the secretory pathway.

How does JAK2 exert this chaperone effect? Multiple possibilities exist, including the notion that a receptor
region that might otherwise be seen as defective or unfolded to the quality control apparatus is hidden by
JAK2 binding. In a similar fashion, JAK2 binding might allosterically (i.e. shape change) alter a GHR site outside
of the region that interacts with JAK2 to make that site appear less defective.

In essence JAK2 association affects endoplasmic reticulum to cell surface GHR trafficking. In cells harboring
GHR and JAK2 molecules that can associate, GHR moves from the ER to the Golgi, matures, and reaches the
cell surface efficiently. In cells lacking JAK2 or with GHR molecules that cannot associate with JAK2 (by virtue
of mutation of the receptor Box 1 region), GHR primarily undergoes endoplasmic reticulum-associated
degradation (ERAD) while a small amount inefficiently matures and traffics to the cell surface (without
association with JAK2).

Proteolysis (degradation) of the GHR

Over the last decade, it has become appreciated that GHR, like some other surface receptors, is a target for
regulated sequential proteolysis, the first step of which (alpha-secretase cleavage) occurs in the proximal
extracellular domain stem region 8–9 residues (depending on species) outside the plasma membrane
[65,80,81]. This alpha- secretase cleavage results in loss of full-length GHR, appearance of a cell-associated
transmembrane domain (TMD)/intracellular domain (ICD)-containing receptor fragment (the "remnant"), and
a soluble GHR extracellular domain (ECD) (called GH binding protein (GHBP)[82,83]).

GHR alpha- secretase cleavage is constitutive, but can be further induced in various cell types by a
proteinkinase C activator (the phorbol ester, PMA), platelet-derived growth factor (PDGF), or serum
[65,80,81,84– 87]. This cleavage is catalyzed mainly by the extracellular domain of the transmembrane
metalloprotease, TACE (tumor necrosis factor-alpha converting enzyme; ADAM-17) [66,88].

Importantly, inducible alpha- secretase cleavage likely regulates GH sensitivity; that is, GH-induced signaling
is dampened after cells are exposed to stimuli that promote GHR alpha-secretase cleavage, but not in the
presence of metalloprotease inhibitors or if noncleavable receptor mutants are expressed, suggesting that
metalloproteolysis modulates GH responsiveness in part by regulating surface GHR levels [65,83,84].

Further, recent in vivo experiments indicate that administration of bacterial endotoxin leads to
downregulation of hepatic GHR abundance and hepatic insensitivity to GH at least in part by inducing
receptor proteolysis, suggesting that this may constitute a physiologically-relevant mechanism of regulation
of GH action [89]. Notably, GH itself does not promote GHR alpha-secretase cleavage; indeed, GH inhibits
subsequent GHR proteolysis, apparently by altering GHR conformation, rather than by causing signaling [66].

Recent studies have shown that the alpha-secretase-generated GHR TMD/ICD remnant is further cleaved by
an enzyme activity termed gamma-secretase within the TMD, which liberates the ICD, a protein termed the
"GHR stub" [87]. gamma-secretase consists of four molecules, including presenilin, which forms the aspartyl
protease core and facilitates a process known as regulated intramembrane proteolysis (RIP) [90].

In essence inducible alpha-secretase cleavage generates remnant, which is converted to stub by gamma-
secretase. The stub is labile and can accumulate in either the cytosol or the nucleus; proteasome inhibition
prevents stub degradation.

In summary GHR undergoes sequential TACE and gamma-secretase cleavage. Surface GHR undergoes
constitutive and inducible cleavage in the extracellular domain stem region by TACE in a process called
"alpha-secretase" cleavage. This yields the shed GHBP and the GHR remnant. Remnant is then cleaved by
gamma-secretase within the membrane to yield the GHR stub (soluble intracellular domain), which localizes
to the nucleus, where it may affect gene expression.

Surface GHR stability

Once at the cell surface, the GHR could, in principle, achieve several fates. If engaged by GH, signaling is
triggered and the receptor undergoes ligand-dependent downregulation. However, in the natural milieu, GH
is released from the pituitary gland in a pulsatile fashion such that GH levels are quite low in periods between
pulses. Thus, it is critical to understand factors that govern GHR abundance independent of GH. It is believed
that mature GHRs are cleared from the cell surface by constitutive or inducible proteolytic shedding
(discussed above) and by constitutive downregulation (discussed below).

JAK2 affects the fate of the cell surface GHR and in cells lacking JAK2, the ratio of mature (cell
surface):precursor GHR was substantially reduced in comparison to JAK2-replete cells [25,62]. This finding is
partly explained by the chaperone effect of JAK2 during GHR biogenesis [63]. However, notable JAK2-
dependent differences in the constitutive fate of mature GHRs are found as well [62]. In the context of a
stable reconstitution system, the half-life (t1/2) of the receptor was estimated by anti-GHR immunoblotting
after 0–4 h of treatment with cycloheximide (CHX) to inhibit new protein synthesis. The results of such a
"CHX chase" assay indicated that the precursor GHR abundance dropped precipitously and to a similar degree
with increasing duration of CHX treatment both in cells that did or did not express JAK2. For the mature
receptor, however, there was a dramatic effect of JAK2. As measured by this assay, the GHR t1/2 increased
from roughly 1 hr in cells that lack JAK2 to roughly 4 h in cells expressing JAK2 [62].

Thus, in the absence of GH, it appears that, in addition to its role in shepherding the GHR through the
secretory pathway and lessening the degree to which it is targeted for ERAD, JAK2 also extends the receptor's
presence at or near the cell surface, presumably by interfering with constitutively active cellular machinery
that functions to internalize and downregulate the receptor.

In summary JAK2 association affects the constitutive (GH-independent) fate of surface GHR. In cells harboring
GHR and JAK2 molecules that can associate, surface GHR is downregulated at a low constitutive rate and its
half-life is long. In cells that lack JAK2 or have GHR and JAK2 molecules that cannot associate, GHR undergoes
enhanced constitutive downregulation and exhibits a short half-life.

GH-induced GHR downregulation

Like many surface receptors, GHR undergoes important trafficking events in response to binding of its ligand.
The net effect is substantial GH-induced receptor downregulation, which serves to limit or alter the
receptor's signaling capacity and perhaps thereby further emphasize the physiologic effects of pulsatile GH
release from the pituitary gland. Work as early as the 1970s–1980s and since that time suggested that GH-
induced GHR downregulation proceeds via clathrin coated pit-mediated endocytosis and lysosomal
degradation [91,98–100].

GH ultimately causes its receptor to be degraded in lysosomes. However GH-induced receptor ubiquitination
(inactivation by an attaching ubiquitin) depends on both JAK2 activity and the ability of the receptor to be
tyrosine phosphorylated.

Several binding partners have been shown to associate via their SH2 domains with the tyrosine
phosphorylated intracellular domain [107–111, 114]. One of them, the protein tyrosine phosphatase, SHP-2,
may contribute modestly to GH-induced GHR downregulation [108]. More recently, it has been appreciated
that the SOCS family protein CIS (cytokine inducible SH2 domain-containing protein), which interacts with
tyrosine phosphorylated GHR [109,110] and is likely linked to Cullin5-based E3 ubiquitin ligase complex that
can recruit proteins to the proteasome for degradation [112], promotes GH-induced GHR internalization and
thus can desensitize GH signaling [113].

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How GHRPs are cardio-protective

The growth hormone secretagogues (GHS) are a family of synthetic compounds originally selected for their
potent and specific effects on GH release. Nonetheless, it has been reported by us and other researchers that
the GHS have also many extraendocrine actions, including those on energy metabolism and cardiovascular
function. Ghrelin, the endogenous GHS, specifically binds to the GHS-R1a, a receptor that has been proposed
to mediate the biological activities of endogenous and synthetic GHS.

The activation of the GHS-R1a is not enough to explain the results that we have previously reported on the
ability of hexarelin, a synthetic full agonist of the GHS-R1a, to protect the rat heart from the damage induced
by the ischemia-reperfusion procedure. In fact, the GHS-R1a is not expressed in the myocardium, and ghrelin
is much less effective than hexarelin in protecting the heart from ischemia-reperfusion damage.

Moreover, it has also been demonstrated that in the cardiovascular system hexarelin and other GHS can also
bind to the CD36, a scavenger receptor.

Interestingly, a large similitude exists between the cardioprotective effects of hexarelin and those of some
angiotensin-converting enzyme (ACE)-inhibitors. For this reason, we have decided to ascertain whether
hexarelin, ghrelin and other synthetic GHS can modify the catalytic activity of serum and tissue ACE in rats
and humans.

Briefly, 10 ul of serum or tissue homogenate were incubated in presence of hippuryl-histidyl-leucine, a

substrate of ACE that is cleaved to histidyl-leucine. The cleavage of the substrate was quantified by
measuring the fluorescence at 365/495 nm (excitation/emission) in presence of orthophthaldialdehyde.
Enalapril was chosen as reference ACE-inhibitor.

Hexarelin (1 to 100 uM) dose-dependently blunted ACE activity up to about 50% in rat and human plasma
and rat lung, heart and kidney. Enalapril (0.1 to 5 uM) dose-dependently inhibited ACE activity in serum and
tissues up to 85%. Ghrelin (1 to 100 uM) did not significantly modify serum and tissue ACE activity at all the
concentrations tested, whereas other synthetic GHS-R1a ligands demonstrated a dose-dependent inhibition
of ACE activity ranging from 10 to 85%.
We conclude that the protective actions of certain GHS on the cardiovascular system might be mediated, at
least in part, by the capability of these compounds to modulate the ACE activity in the general circulation and
locally in tissues.

Source: Characterization of a Novel Extraendocrine Action of the Growth Hormone Secretagogues: Inhibition
of Angiotensin-Converting Enzyme (ACE) Activity, A Torsello, M Ravelli, E Bresciani, I Bulgarelli, L Tamiazzo, S
Caporali, V Locatelli,

Dept of Experimental Med, Univ of Milano-Bicocca, Monza, Italy; Interdepartmental Ctr for Bioinformatics
Proteomics, Univ of Milano-Bicocca, Monza, Italy

How much GH do we secrete in IUs?

You see people on boards making all sorts of silly claims concerning how many ius we normally secrete.

Did anyone catch the chart I posted in Post #558 which revealed that 24-hour GH secretion in males of ages
16 to 25 was just under 600mcg?

Nutropin reveals that 1 iu of their GH is equal to 333 mcg, so a normal young male secretes about 2iu of GH a
day.

A normal male aged 26 to 35 secretes less than 1 iu of GH with the following age groups secreting less.

Now the comparison isn't entirely accurate (Nutropin weight to how much GH ends up in plasma) but even if
we add 50% to the value we are still talking about a normal male aged mid-twenties to mid-thirties secreting
less than 2iu of GH a day.

So do you think a middle aged male could benefit by a true (meaning accurate as opposed to Chinese generic
product) 1-2iu increase in GH (such that can be created with just GHRP-6 alone)?

From the stand point of healthy restoration to youthful levels, the answer is yes.

For the lazy here is the chart from that post:

Revisiting peptide timing, meals and GH release

This is an interesting study done in cattle. Apparently cattle get one 2 hour feeding a day.

So one hour before the meal GHRH by itself or GHRP-6 by itself worked better then when administered by
itself one hour post-meal. That is what we would expect.

In addition one hour pre-meal the GHRH + GHRP-6 produced a larger pulse of GH together. This we would
also expect.
What is surprising and interesting is that taking GHRP-6 + GHRH together one hour post-meal produced a
pulse of GH basically equivalent to the pre-meal pulse. In other words the synergy of the two peptides over
came the meal refractory effect (where either one administered alone was unable).

Perhaps a similar effect takes place in humans... i.e. even when the stomach is full (1 hour post-meal)
GHRH+GHRP-6 creates an undiminished GH pulse.

ABSTRACT

After a meal, somatotropes are temporarily refractory to growth hormone-releasing hormone (GHRH), the
principal hormone that stimulates secretion of growth hormone (GH). Refractoriness is particularly evident
when free access to feed is restricted to a 2-h period each day. GH-releasing peptide-6 (GHRP-6), a synthetic
peptide, also stimulates secretion of GH from somatotropes. Because GHRH and GHRP-6 act via different
receptors, we hypothesized that GHRP-6 would increase GHRH-induced secretion of GH after feeding.
Initially, we determined that intravenous injection of GHRP-6 at 1, 3 and 10 ug/kg body weight (BW)
stimulated secretion of GH in a dose-dependent manner.

Next, we determined that GHRP-6- and GHRH-induced secretion of GH was lower 1 h after feeding (22.5 and
20 ng/ml respectively) than 1 h before feeding (53.5 and 64.5 ng/ml respectively; pooled (S.E.M.=8.5).

However, a combination of GHRP-6 at 3 ug/kg BW and GHRH at 0.2 ug/kg BW synergistically induced an
equal and massive release of GH before and after feeding that was fivefold greater than GHRH induced
release of GH after feeding.

GF-1, GHRP, Testosterone, Trenbolone & Nandrolone Primer [entire thread...] (What you
should read if you don't want to be a beginner)

I think it's important to start off by visualizing an interesting distinction between peptide hormones such as
insulin and growth hormone and the peptide hormone IGF-1. Insulin and Growth Hormone have their own
specific storage vesicles within specialize cells or tissue where they may sit and await a command for release.
IGF-1 has no such storage compartment. Stated succinctly, Growth Hormone and Insulin are held in storage
compartments before release whereas there is no such storage compartment for IGF-1.

This distinction has the consequence that circulating growth hormone and insulin are low under non-
stimulated conditions. As a result the signal to the body to go on and do something as a command from
growth hormone or insulin derives almost exclusively from controlling the entry rate of those peptide
hormones into circulation. When these peptides can be coaxed from their storage areas into circulation they
have the opportunity to transmit that signal or command to target tissue. As a consequence of having their
own specific storage sites, the signal level that growth hormone is capable of bringing or the signal level that
insulin is capable of bringing is primarily regulated by controlling their entry into circulation. It is not
controlled by their rate of synthesis.
The synthesis of insulin and growth hormone need not be rapid. The concentration of these two hormones
released into circulation is not limited by their rate of synthesis. The body seems to always have plenty at the
ready. Enhancement of growth hormone or insulin synthesis is never something we need be immediately
concerned.

The signaling commands that insulin and growth hormone bring are only effective if target cells express
specific receptors to receive the hormones and capture that signal. So it is rapid changes in hormone
concentration together with receptive tissue that initiates the body to do something.

All of this is distinct from the IGF-1 system. There is no gland or storage vesicle for IGF-1. Without a storage
component housing complete and ready for release IGF-1, it becomes more dependent on various
components to convey it's signaling command. The synthesis rate is important and IGF-1's appearance in
circulation is slow and dependent on it's synthesis rate and on how the body chooses to maintain, discard or
deliver it.

For IGF-1 the circulation becomes the extracellular storage area and it is maintained, discarded or delivered
based on it's attachment to binding proteins or the ternary complex - Acid labile subunit. These binding
proteins and the ternary complex are in a way virtual storage compartments as they maintain IGF-1. The total
serum level of IGF-1 depends on both the synthesis rate and the capacity and stability of the aforementioned
complexes which act as a buffer.

Growth hormone and Insulin are transmitted to target tissue in a pulse through the bloodstream from their
storage units. The bloodstream is merely a means of transmission. For IGF-1 it must rely on the bloodstream
to serve as it's reservoir.

IGF-1 also differs from growth hormone and insulin in that IGF-1 is produced in tissue throughout the body
from muscle to brain (even though the liver remains the primary source). As a consequence IGF-1 is best
thought of as an autocrine or paracrine IGF1 system even though circulating IGF-1 is often characterizes as
endocrine or systemic. In the IGF-1 autocrine/paracrine system local signaling is highly dependent on the
local synthesis and release of IGF acting on the producer cell, or its neighbours, by local diffusion.
Furthermore local production of specific binding proteins may attract circulating IGF-1 and sequester them,
either localizing them to target cells or retaining them in the producer tissue in an extracellular pool from
which that cell population may eventually draw from. Proteases which cut off the IGF-1 from the attached
binding proteins would free IGF-1 and make them available to the cellular receptors. The appearance of
proteases to do this most likely comes from release & activation from damaged cells such as damaged muscle
cells from resistance exercise.

IGF-1 once cut off from the local binding protein could either join a local pool of free IGF-1 for local activity or
escape the local environment and enter circulation. Binding proteins in circulation would reattach to and
buffer the paracrine IGF-1 to prevent the locally generated IGF-1 signaling to spread to other tissues.
Blood tests for circulating IGF-1 do not measure the activity of IGF-1. They are actually measuring the storage
reserve. Whereas blood tests for growth hormone and insulin need to be timed correctly they do not
measure storage but reveal the amount of peptide in route to activity at that point in time.

Endocrine vs paracrine secretory systems. a) The classical endocrine system, with a gland reserve of hormone
and transmission of bursts of hormone release in the bloodstream to stimulate target tissues that selectively
express the relevant hormone receptor. b) The endocrine IGF1 system has no primary gland store, but the
peptide is constitutively produced from many tissues, with liver being a major source. The bloodstream
serves as the IGF reservoir, retaining IGF1 complexed with binding proteins (BPs) and acid labile subunit (ALS)
to prevent rapid elimination. A small proportion of free IGF dissociated from these complexes can bind IGF
receptors in the target tissues. c) IGF1 is also generated locally in many tissues which are also targets for its
action. They also produce binding proteins which may block or enhance IGF1 local action. BP and ALS in the
circulation now serve to capture and buffer any locally produced IGF1 escaping to signal elsewhere.

IGF-1 - Primer part 2 (IGF-1 as a regulator of Skeletal Muscle Hypertrophy and Atrophy)

Let's start simply. Hypertrophy results from an enlargement. It is an increase in the size of something that
exists and in regard to hypertrophy in skeletal muscle it is simply an increase in the size of existing muscle
fibers. Hypertrophy does not refer to an increase in the number of pre-existing muscle fibers. IGF-1 is pro-
hypertrophy meaning it promotes hypertrophy. It can play a role in the rare occurrence of hyperplasia which
is an increase in the number of pre-existing muscle fibers. However most muscle mass increases in everyone
from professional bodybuilders to the weekend hobbiest comes from hypertrophy so much so that
hyperplasia is best left out of the anabolic discussion. Most people like the sound of the word "hyperplasia"
but it is hypertrophy that does all the heavy lifting.

When free IGF-1 or rather the mature form of IGF-1 binds to it's receptor it triggers a series of events within a
cell. This series is called signaling and the path that the signal takes is called a pathway. There are many
components or elements within a cell that are capable of impacting that signal. These elements can play the
role of handing the signal off to another element or they could somehow be an element that takes into
consideration some sort of state... maybe a nutritional state... so they are in a way sensors... and based on
what they sense about some state decide between which fork in the pathway the signal should be
transmitted. Some elements amplify the signal. Some elements may inhibit the signal. Some elements play a
small role while other play a huge role. The ones that play the huge role often receive the signal and based on
that initiate events that will lead to gene transcription. Most elements in a cell aren't even called upon to
play a part in a signaling cascade while some show up repeatedly in many varied contexts. Last but not least
an element may be capable of residing in both the cytoplasm and nucleus and based on where it is currently
residing activates distinct functions. Maybe if it is in the nucleus it is promoting but if it is in the cytoplasm it
is inhibiting the signaling.

Again a pathway is a series of these elements and as a collective they are studied.
IGF-1's pro-hypertrophy activity primarily emanates from its ability to activate the Phosphoinositide 3-kinase
(PI3k)/Akt signaling pathway. The introduction of names for our elements need not confuse. PI3k is an
element and so is Akt. The pathway flows fromIGF-1 binding to it's receptor and triggeringPI3k which
transfers the signaling to Akt. Now there are minor elements between these two but they are the major
elements and so the pathway is named after them.

Akt is a very important element. It can trigger protein synthesis and at the same time block up-regulation of
the key mediators of muscle atrophy - MuRF1 and MAFbx . It triggers protein synthesis more directly by
signaling to mTOR.

It does the latter (prevention of atrophy) by preventing FOXO from moving to the nucleus and this has the
ultimate effect of blocking the up-regulation of those muscle atrophy elements MuRF1 and MAFbx. MuRF1
and MAFbx cause atrophy by "spray painting" parts of proteins so that proteasomes can locate those areas
and degrade the protein.

Under normal growth conditions, FOXOs are inactivated and not required for the survival of cells. Growth
factors (such as insulin & IGF-1) inhibit FOXO activation whereas ROS, DNA-damage, energy stress activate it

The point I appeared to be making is that there are some signals through FOXO that I want and some that I
may not want. There is no inherent good or bad in inhibiting FOXO. Stopping FOXO from excessively
triggering the atrophy of my muscles is good. Stopping FOXO so that things that need to be eliminated aren't
isn't a good thing.

So back to the main topic... MuRF1 is really good at marking the thick muscle fibers for destruction and so by
blocking MuRF1 activation IGF-1 through trigger Akt helps prevent the break down of the thicker parts of
muscle.

IGF-1 may also strongly inhibit the anti-hypertrophy effects of myostatin. Myostatin activates two elements
Smad2 and Smad3. It actually binds to a receptor complex made up of ACTRII and ALK4 or ALK5 and in so
doing activates Smad2 and Smad3. Once activated these two move to the nucleus and from there they are
able to inhibit Akt which ends up inhibiting TORC1. This inhibition feeds back and allows myostatin to activate
even more Smad2. Akt remember does two things. It promotes protein synthesis through mTOR and it
inhibits atrophy. When it does this in myoblast and myotubes this promotes anabolism and muscle mass.
When Myostatin inhibits the activation of Akt in myoblasts and myotubes it hinders anabolism and muscle
mass. To some extent TGFB may also activate SMAD2 & 3.

Now the signaling pathway Akt/mTOR/p70S6 in addition to increasing protein synthesis also mediates both
differentiation in myoblasts and hypertrophy in myotubes.... basically the making and enlarging of muscle. If
left to it's own devices myostatin would cause decreases in the diameters of myotubes.
IGF-1 dominantly blocks the effects of myostatin in myoblasts and myotubes. I didn't make up the word
"dominate" it was used by the authors of Myostatin reduces Akt/TORC1/p70S6K signaling, inhibiting
myoblast differentiation and myotube size, Anne Ulrike Trendelenbur, American Journal of Physiology - Cell
Physiology Published 1 June 2009 Vol. 296 no. 6, C1258-C1270 : .Treatment of human myoblasts with
myostatin for 24h decreased phosphorylation [i.e. activation] of Akt by up to 50%. In addition to inhibiting
Akt, myostatin decreased phosphorylation of p70S6 kinase and the pro-atrophy transcription factor FoxO1,
both of which are normally phosphorylated by Akt.However, Akt, p70S6 kinase, and FoxO1 phosphorylation
were restored by treatment with IGF-1, indicating that IGF-1/Akt signaling is dominant over
myostatin/Smad/Akt inhibition.

The authors also mentioned in partially non-published data that "In addition to restoring Akt
phosphorylation, IGF-1 also partially rescues the differentiation of myostatin-treated myoblasts, as
determined by measuring fusion index, diameters (data not shown), and CK (Creatine kinase) activity."

So IGF-1 gets this signaling pathway going by stimulating PI3k/Akt which leads to the elements that can
induce protein synthesis. It is a serious over simplification but resistance exercise leads to activation of the
PI3k/Akt pathway by directly inducing muscle expression of IGF-1. - DeVol DL,Activation of insulin-like growth
factor gene expression during work-induced skeletal muscle growth, Am J Physiol 259:E89–95 1990 & Yan Z,
Insulin-like growth factor immunoreactivity increases in muscle after acute eccentric contractions, J Appl
Physiol 74:410–414 1993 . This is sufficient to induce hypertrophy in muscle both in vitro - Vandenburgh HH,
Insulin and IGF-I induce pronounced hypertrophy of skeletal myofibers in tissue culture, Am J Physiol
260:C475–484 1991and later in vivo - Musaro A, Localized IGF-1 transgene expression sustains hypertrophy
and regeneration in senescent skeletal muscle, Nature Genet 27:195–200 2001 & Coleman ME,Myogenic
vector expression of insulin-like growth factor I stimulates muscle cell differentiation and myofiber
hypertrophy in transgenic mice, J Biol Chem 270:12109–12116 1995

Activation of Akt is sufficient to induce hypertrophy in vivo. In the study cited for this sentence, acute
activation of Akt for two to three weeks was found to be sufficient to induce a doubling in the size of skeletal
muscle... this increase occurred in the average cross-sectional are of individual muscle fibers brought about
by an increase in the TORC1/p70S6K protein synthesis pathways. - Lai K-MV,Conditional activation of Akt in
adult skeletal muscle induces rapid hypertrophy, Mol Cell Biol 24:9295–9304 2004.

I should note that although IGF-1 activates mTOR and p70S6k downstream of PI3K/Akt activation, amino
acids can activate mTOR directly bringing about a subsequent stimulation of p70S6K activity.

I discuss how important the element eIF2B is to protein synthesis and how GSK3beta blocks eIF2Bs activity.
Well if GSK3beta is inhibited there is also enhanced myotube formation and muscle-specific gene expression
leading to differentiation.
Although all of this may seem to be a bit much for this post I bring it up only to point out that IGF-1 inhibits
GSK3beta which is a different mechanism by which hypertrophy is induced and myoblast differentiation
promoted.

To be continued... but I think I have given a sufficient little primer on IGF-1 and intracellular signaling. IGF-1 is
anabolic and anti-catabolic. It inhibits myostatin and GSK3beta and promotes both protein synthesis and
differentiation.

INFO ON MGF USE

To quickly summarize the difference in function, MGF stimulates muscle stem cells (satellite cells) to reenter
the cell cycle and proliferate, whereas IGF-1 is necessary for the differentiation of newly generated muscle
precursor cells into myoblasts and myofibers.See material from Goldspink posted earlier in this thread at:
Post #158 Mechanical Signals, IGF-I Gene Splicing, and Muscle Adaptation

Growth Hormone bound to its receptor in the liver activates the STAT5b signaling pathway which promotes
movement of that activated signaling protein to the nucleus where it induces transcription of the IGF-1 gene.
From studies in mice and humans, it is evident that GH induces expression of both the endocrine form of IGF-
1, the muscle form of IGF-1 and MGF. 1 Mice deficient in GH (lit/lit mice) respond to administration of GH
with an acute increase in MGF, but not IGF-1, in skeletal muscle, although IGF-1 in liver is increased. 2
However the precise mechanism by which GH has distinct effects on IGF-1 and MGF expression in muscle is
not completely known.

What is known is that in response to stretch overload and the presence of growth hormone combined gene
transcription in muscle and its subsequent "blueprint" assembly" are induced to create mechano growth
factor (MGF also known as IGF-1Ec in humans or IGF-1EB in mice) instead of muscle IGF-1.

How does the behavior of IGF-1 and MGF differ?

"MGF is a non-secreted form of IGF-1 that can be found in the nucleus of cells in culture or in a perinuclear
location in hippocampal cells after ischemia (restriction in blood supply)".

In other words MGF never leaves the cell it was created in. For emphasis I quote from another source:

"...MGF... is not normally secreted."

Geoffrey Goldspink has written "that MGF increases myoblast proliferation via a different signalling pathway"
then IGF-1.

To reiterate & expand upon this concept I quote from another source:
"IGF-1 isoforms differ in the signaling pathways they activate. By over-expressing IGF-1Ea and MGF in muscle,
it has been shown that both isoforms can activate IGF-1R and AKT phosphorylation. In addition, MGF was
shown to induce phosphorylation of ERK, a property not shared with IGF-1Ea."

So IGF-1 and MGF work through different pathways not receptors. There is only one receptor, IGF-1-receptor
(also insulin, IGF-II & hybrid receptors which are not relevant to this discussion). There is no MGF receptor.
The reason why it would be nonsensical to have an MGF receptor is that MGF does not leave the cell.

This contrasts with IGF-1 which is released from the liver into circulation and which is created in muscle and
translocates to the cell surface. Both events result in IGF-1 binding to the IGF-1 receptor.

So what happens in plain language please?

During the process of gene transcription pieces of DNA are transcribed and then spliced together by RNA and
this code is taken to the ribosomes where the peptide is manufactured. In splicing MGF there is a subtle
frame shift such that the right side of the code is a little different then IGF-1. Everything else is identical.

This subtle difference means that when MGF & IGF-1 are manufactured by the riboomes MGF MUST because
of the signal pull that is part of its make up, translocate to the Nucleus of the cell and more specifically the
Nucleolus.

IGF-1 because of its makeup MUST move to the cytoplasm where it forms a pool of IGF-1 which will
transloacte to the cell membrane where it will bind w/ an IGF-1 receptor.

MGF has NO receptor. It does not need it to mediate events. Too many times people think that a lock/key
ligand/receptor is needed to intiate signals. That is not always true especially when proteins move to the
nucleus.

MGF is NEVER found in circulation. It is produced in a muscle cell as described and it will act there always.

IGF-1 however does circulate. It is produced in the liver and secreted into the blood stream. If it is made in
muscle tissue or in local tissue it makes its way to the surface and can bind to a receptor on that cell or
nearby cells. The latter is how muscle made IGF-1 can effect nearby bone growth.

In lab experiments with MGF they usually do one of two things. One they use a viral vector of MGF cDNA to
increase the cDNA of MGF in the cell so that more MGF is made internally. When they do this they get a 25%
increase in muscle in a three week period. If they use the same approach to get IGF-1 to express itself from
within they get less muscle growth (15%) and it takes 4 months.

The second approach is to actually inject MGF into a cell (i.e. penetrate the cell membrane). Unfortunately
for scientists this also invokes a damage repair function in cells so it is difficult to actually attribute all of the
benefits that ensue to MGF.
You follow neither of these approaches when you inject MGF or Peg MGF.

MGF is identical to IGF-1 in chemical makeup on the leftside of the peptide. This allows it to bind with IGF-1
receptors should it ever be injected or find itself outside of the cell. However because of the difference in
right-side structure MGF is incapable of binding to IGF-1 binding proteins (which would prolong its life).

MGF has a very short half-life in blood plasma. If it is pegylated it has a longer half-life. I do not know the
extent to which pegylation reduces binding affinity but it probably does to some extent depending on where
it is pegylated.

Injecting Peg MGF will, if it survives, probably bind to an IGF-1 receptor. If it does so it activates the IGF-1
signaling pathways just as IGF-1 would.

I do not have any data on how strongly MGF will bind to IGF-1 receptors. A pegylated MGF is small enough to
penetrate the vascular wall and travel systemically. It will not be confined to the area injected as IGF-1 bound
to IGF-BindingProtein3 bound to Acid laibile subunit (i.e. the ternary complex) will. Thats why injecting large
amounts of MGF brings vacularization, pumps, glucose uptake, in essence insulin-like activity....because it is
behaving as IGF-1...and doing so in systemic fashion.

Some science (derived from ref:5) followed by both a reiteration and an elaboration on my part.

The IGF-1 gene consists of 6 exons (DNA bases that are transcribed into mRNA and eventually code for amino
acids in the proteins), separated by 5 introns (DNA bases, which are found between exons, but are not
transcribed). Transcription is controlled by alternate use of two upstream promoters and starts at several
transcription start sites located in exons 1 and 2. Together, alternate promoter usage and alternative splicing
at the 5' and 3' ends of the gene generate several distinct mRNAs depending on their exon sequences, which
code for three isoforms of precursor IGF-1.

Note: The notation 5' and 3' refer to the direction of the DNA template in the chromosome and is used to
distinguish between the two untranslated regions (grey).

These isoforms have characteristic N-terminal signal peptide sequences and C-terminal extension (E) peptide
domains. Exons 1 and 2 and part of exon 3 encode the signal peptides. The remainder of exon 3 and exon 4
encode the mature IGF-1 peptide and the proximal part of the E peptide, which are shared by all isoforms.
Splicing of exon 4 to exon 6 generates the predominant transcript IGF-1Ea. Splicing of exon 4 to exon 5
generates IGF- 1Eb, which encodes an isoform with 47 distinct amino acids in the E domain. When part of
exon 5 is spliced to exon 6, the IGF- 1Ec (IGF-1EB in mouse) variant is generated. In this case, a frame-shift
occurs in exon 5 followed by premature transcription stop in exon 6 that results in a stretch of 25 amino acids
unique to this variant.

As a result these templates produce in cellular ribosomes IGF-1 peptide forms that differ in amino acid
structure in the E peptide region. This results in different C-terminal regions for the IGF-1 & MGF peptides.
MGF BECAUSE of its C-terminal sequence, upon "birth" becomes rapidly localized in the nucleus. It is the
carboxy portion which draws either MGF or the altered portion to the nucleus rather than to the cell
membrane.

"We found that the isoform of the human IGF-I precursor encoded by exon 5 [MGF] localized to the nucleus
and strongly to the nucleolus. Precursors containing exon 6 or the upstream portion of exon 5 did not...The
findings are consistent with the presence of a nuclear and nucleolar localization signal situated in the C-
terminal part of the exon 5-encoded domain."

MGF is an autocrine growth factor, and this is THE different signaling pathway...a pathway that does not
involve any receptor. The action of MGF via this pathway is one of promoting myoblast proliferation.

However MGF maintains a dual action. It "activates the muscle stem cell pool through its C-terminal domain
(encoded in exons 5 and 6) as mentioned above AND according to the various studies by Geoffrey Goldspink
"increases anabolic effects as the result of its IGF-I receptor binding domain (encoded in exons 3 and 4),
which all the IGF-I genes possess."

The unaltered portion of MGF is still capable of binding to the IGF-Receptor. The altered carboxy portion
renders MGF incapable of binding to the IGF-1-Binding proteins BUT it possesses the ability to bind to the
IGF-1-Receptor via the unaltered side.

So what if MGF is injected into plasma? Presumably it would bind to the IGF-1-Receptor and initiate the AKT
signaling pathway which will stimulate cell growth signals. In other words MGF stops being MGF and behaves
like IGF-1 in initiating anabolic events. But it has been shown but is not yet fully understood that MGF is
capable of AKT phosphorylation (an IGF-1-IGF-1-receptor mediated event) without ever coming in contact
with the IGF-1-receptor.

This brings up an interesting point. MGF seems to be capable of performing both its unique duties and those
of IGF-1 as well (at times).

What about studies that inject MGF into subjects?

Actually they don't do it that way.

"One of the methods we used to establish the biological action of MGF was to engineer a gene into which its
cDNA was inserted into a vector. To our surprise a single intramuscular injection into a mouse muscle
resulted in a 25% increase in mean muscle fibre cross section area within three weeks." - Goldspink G, Yang
SY. Method of treating muscular disorders, United States Patent. Patent No US 6,221,842 B1, Apr 24, 2001.

This contrasts with, "similar experiments carried out using the systemic or liver type of IGF-I in an adenoviral
vector under the control of a muscle regulatory sequence. This took four months to produce a 15% increase
and is probably due to the anabolic effect of IGF-I, which is common to all the splice variants." - Barton-Davis
E, Shoturma DI, Musaro A, et al. Viral mediated expression of insulin-like growth factor-I blocks the aging-
related loss of skeletal muscle function. Proc Natl Acad Sci USA 1998;95:15603

Testosterone blunts IGF-1 inhibition of GH

Rexanator led me to Testosterone Blunts Feedback Inhibition of Growth Hormone Secretion by

Experimentally Elevated Insulin-Like Growth Factor-I Concentration, Johannes D. Veldhuis, Stacey M.
Anderson, Ali Iranmanesh and Cyril Y. Bowers, The Journal of Clinical Endocrinology & Metabolism Vol. 90,
No. 3 1613-1617, 2005, where they found:

"...supplementation of a high dose of Te in middle-aged and older men attenuates IGF-I feedback-dependent
inhibition of nadir and peak GH secretion."

The results of this study were confirmed in a recent study published this month:

Testosterone Supplementation in Older Men Restrains Insulin-Like Growth Factor’s Dose-Dependent

Feedback Inhibition of Pulsatile Growth Hormone Secretion,Johannes D. Veldhuis, Daniel M. Keenan, Joy N.
Bailey, Adenborduin Adeniji, John M. Miles, Remberto Paulo, Mihaela Cosma and Cacia Soares-Welch,The
Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 1 246-254, 2009

Background: Pulsatile GH secretion declines in older men. The causal mechanisms are unknown. Candidates
include deficient feedforward (stimulation) by endogenous secretagogues and excessive feedback (inhibition)
by GH or IGF-I due to age and/or relative hypoandrogenemia.

Hypothesis: Testosterone (T) supplementation in healthy older men will restrain negative feedback by
systemic concentrations of IGF-I.

Subjects: Twenty-four healthy men (ages, 50 to 75 yr; body mass index, 24 to 30 kg/m2) participated in the
study.

Methods: We performed a prospectively randomized, double-blind, placebo-controlled assessment of the

impact of pharmacological T supplementation on GH responses to randomly ordered separate-day injections
of recombinant human IGF-I doses of 0, 1.0, 1.5, and 2.0 mg/m2.

Analysis: Deconvolution and approximate entropy analyses of pulsatile, basal, and entropic (pattern-
sensitive) modes of GH secretion were conducted.

Results: Recombinant human IGF-I injections 1) elevated mean and peak serum IGF-I concentrations dose-
dependently (both P < 0.001); 2) suppressed pulsatile GH secretion (P = 0.003), burst mass (P = 0.025), burst
number (P = 0.005), interpulse variability (P = 0.032), and basal GH secretion (P = 0.009); and 3) increased
secretory pattern regularity (P = 0.020).T administration did not alter experimentally controlled IGF-I
concentrations, but it elevated mean GH concentrations (P = 0.015) and stimulated pulsatile GH secretion
(frequency P = 0.037, mass per burst P = 0.038). Compared with placebo, T attenuated exogenous IGF-I’s
inhibition of GH secretory-burst mass (P < 0.038) without restoring pulse number, basal secretion, or pattern
regularity.

Conclusion: The capability of systemic T to mute IGF-I feedback on pulsatile GH secretion suggests a novel
mechanism for augmenting GH production.

Adipose Visceral Fat Negatively correlated with effectiveness of GHRH & GHRP-2

Joint Regulation of Pulsatile GH Secretion by Estradiol, Dihydrotestosterone and Abdominal Visceral-Fat Mass
in Healthy Older Men: A Paradigm of Aromatase and 5-alpha-Reductase Types I and II Blockade, J Veldhuis, K
Mielke, J Miles, C Bowers

Background Dissecting the relative roles estradiol (E2), 5-alpha-dihydrotestosterone (DHT), and abdominal
visceral fat mass (AVF) in the specific mechanistic regulation of GH secretion remains difficult. In part the
impasse reflects interdependency among Te-derived sex steroids due to interconversion by aromatization
and 5-alpha reduction, and in part the separate but interactive nature of hypothalamo-pituitary pathways
driving (GHRH and ghrelin/GHRP-2) or inhibiting (somatostatin-14, SS-14) GH secretion.

Subjects Eleven healthy men ages 61-79 yr.

Methods Subjects were each studied 5 times fasting on separate mornings in random order. Secretagogues
comprised saline, SS-14 withdrawal, bolus GHRH or GHRP-2, and L-arginine infusion followed by bolus
injection of both peptides (to estimate maximal pituitary GH secretion).

AVF (adipose visceral fat) estimates were made by single-slice CT scan.

Outcomes

Regression analyses revealed that unstimulated GH secretion was most strongly determined by AVF
(standardized coefficient, sc = -0.648, P = 0.031).

SS-14 withdrawal-induced GH release tended to correlate with E2 (sc = +0.589, P = 0.071).

The response to GHRH bolus was strongly determined by AVF (sc = -0.712, P = 0.014) and weakly by DHT(sc =
+0.596, P = 0.053).

In contrast, GH peaks induced by GHRP-2 and triple-secretagogue infusions were associated with only AVF(sc
= -0.689, P = 0.019).

Summary E2 and DHT are positively predictive of GH responses to specific, rather than all, secretagogues,
whereas AVF is negatively correlated with GH responses to all secretagogues except SS-14 withdrawal.
Conclusion Sex steroids specifically and visceral adiposity generally determine peptide-selective drive of GH
secretion in healthy older men. The precise pathways that mediate the interdigitating mechanisms are not
known.

Here is another way to compare GHRPs & GH dosing vs effect

This study * caught my attention because it examined the pharmacokinetics of GHRP-2 and in so doing
compared it to synthetic GH administration.

Basically they found 1mcg/kg of GHRP-2 half as effective as 43mcg/kg of synthetic GH...they found a linear
relationship and therefore they conjectured that 2mcg/kg of GHRP-2 would be as effective as 43mcg/kg of
synthetic GH.

However the studies participants were prepubescent children of short stature so we should use their
weights. Googling revealed that 40lbs would be a decent approximation of such a young undersized male
child. That converts to about 18 kilograms.

For synthetic GH that would mean the children received 43mcg * 18kg = 774mcg of GH.

Nutropin reveals that 1 iu of their GH is equal to 333 mcg so that equates to aproximately 2.3iu of GH.

For GHRP-2 that would mean the children received 1mcg * 18kg = 18mcg of GHRP-2.

Using the studies statement that 2mcg/kg of GHRP-2 equalled the synthetic GH dose we arrive at 2mcg *
18kg = 36mcg of GHRP-2 equally 2.3iu of synthetic GH...or further extrapolation 100mcg of GHRP-2
approximately = 6iu of synthetic GH.

I think the above extrapolation is too liberal for adults & thus flawed. So lets be real conservative in our
approach and recognize that the studies used saturation doses (1mcg/kg). For adults I would like to stick with
the definition of saturation dose of 1mcg/kg... and use that for adults so for a 100kg man that equals 100mcg
of GHRP-2. That would mean a single 100mcg dose of GHRP-2 would equal 1.15iu of synthtic GH.

All this approach assumes is that the saturation dose for children produced the equivalent of 1.15iu of
synthetic GH therefore the saturation dose for adults will do the same.

So 3 100mcg doses of GHRP-2 per day will conservatively equate to (1.15 x 3) about 3.5iu of synthetic GH.
Note that if the average weight of the study children were really 50 pounds then this 3.5iu estimate becomes
4.2ius of synthetic GH.

So it is probably not unrealistic to figure that 100mcg of GHRP-6 dosed three times a day will yield the
approximate equivalent of 3.5 to 4 ius of synthetic GH per day in a young adult male.
• Pharmacokinetics and Pharmacodynamics of Growth Hormone-Releasing Peptide-2: A Phase I Study in
Children Catherine Pihoker, Gregory L. Kearns, Daniel French and Cyril Y. Bowers, The Journal of Clinical
Endocrinology & Metabolism 1998 Vol. 83, No. 4 1168-1172

Abstract

Administration of GH-releasing peptide-2 (GHRP-2) represents a potential mode of therapy for children of
short stature with inadequate secretion of GH. Requisite information to determine the dosing route and
frequency for GHRP-2 consists of the pharmacokinetics (PK) and pharmacodynamics (PD) for this compound,
neither of which have been previously evaluated in children. The purpose of this study was to characterize
the PK and PD of GHRP-2 in children with short stature. Ten prepubertal children (nine boys and one girl; 7.7
± 2.4 yr old) received a single 1 µg/kg iv dose of GHRP-2 over 1 min, followed by repeated (n = 9) blood
sampling over 2 h. GHRP-2 and GH were quantitated by specific RIA methods. PK parameters were calculated
from curve fitting of GHRP-2 and GH vs. time data. Posttreatment plasma GH concentrations (normalized for
pretreatment values) were used as the effect measurement....

Discussion

The pharmacokinetics of GHRP-2 found in our cohort of pediatric patients are similar to those previously
reported in healthy adult volunteers after iv administration of the peptide (3). A comparison of the maximum
GH response observed after GHRP-2 administration between these two studies revealed similarities in both
the magnitude (i.e. mean values = 44 µg/L in children vs. 55 µg/L in adults) and time of maximal response (i.e.
average values = 45–60 min for both). The GH responses observed after iv or sc GHRP-2 are also similar to
those previously reported after the parenteral administration of GHRP-6, GHRP-1, or GHRH (3, 4, 23, 24).

To our knowledge, our data represent not only the first report of GHRP-2 pharmacokinetics in pediatric
patients, but also the first pharmacodynamic assessment of this peptide. Comparison of the serum
concentration vs. time profiles for both GHRP-2 and GH in our subjects reveals an equilibration delay in the
attainment of peak GH response, a period that we believe corresponds to the time course of GHRP-2 action.
This assertion is supported in part by the consistent observation of an equilibration delay between the serum
concentrations of GHRP-2 vs. effect (i.e. change GHt) curves, reflected by the production of a
counterclockwise hysteresis and our success in using the sigmoid Emax model to effectively determine the
pharmacodynamic parameters for GHRP-2. As previously reported by Holdford and Sheiner (22), the
successful application of this pharmacodynamic model suggests both linearity and predictability in the drug
concentration vs. effect relationship. Given the fact that GH is a proximate biological marker of GHRP (and
presumably, GHRP-2) activity (23, 24), our assumptions entailed in the pharmacodynamic analysis of our data
appear valid and reflective of the expected pharmacological response of GHRP-2.

Despite the apparent differences in serum GH pharmacokinetics reported after exogenous administration of
the hormone (25) as opposed to the administration of GH secretagogues (26, 27, 28, 29, 30), both the
pharmacokinetic and pharmacodynamic data from our study can be used to address the potential
therapeutic efficacy of GHRP-2 in pediatric patients with GH insufficiency. First, the mean AUC for GH after
the iv administration of a single 1 µg/kg dose of GHRP-2 (i.e. 50.7 ng/mL•h) was approximately 50% of the
AUC at steady state (i.e. 114.2 ± 32.7 ng/mL•h) previously reported in a study of pediatric patients who
received daily sc doses of 43 µg/kg methionyl GH (25). If one assumes linearity in the dose-response
relationship for iv GHRP-2, administration of a single 2 µg/kg iv dose would be expected to produce an AUC
for GH that would be virtually identical to that observed under steady state conditions after sc administration
of the currently recommended daily doses of recombinant human GH (25), doses that have been shown to
produce acceptable rates of linear growth in children who are GH deficient (30). Second, both the Cmax
(mean, 50.7 ng/mL) and Emax values for GHRP-2 in our patient cohort (mean GH, 67.5 ng/mL) actually
exceeded the average Cmax values for GH (37.6 ± 11.6 ng/mL; range, 17.6–49.5 ng/mL) after a single sc dose
of 0.1 mg/kg methionyl GH to GH-deficient children (25). Finally, the EC50 for GHRP-2 in our study cohort (1.1
± 0.6 ng/mL) was substantially less than the Cmax value (7.4 ± 3.8 ng/mL). This particular finding not only
supports the adequacy of the 1 µg/kg iv dose of GHRP-2 in producing a desirable biological effect, but also
suggests that extravascular administration of this peptide by a route that could be associated with up to a
50% reduction in bioavailability may still produce an acceptable increase in the serum GH concentration
sufficient to initiate and sustain a desired growth response. This hypothesis is being tested by our group in
dose-ranging studies of oral and intranasal GHRP-2 that are currently underway.

In conclusion, both the pharmacokinetics and pharmacodynamics of iv administered GHRP-2 in short children
are predictable and reflective of the potential for therapeutic application of this peptide. The data produced
in this investigation will enable the selection of GHRP-2 doses for future evaluation of their bioavailability,
safety, tolerance, and efficacy in children.

Dat Knows MGF (you might as well learn something as well)

To quickly summarize the difference in function, MGF stimulates muscle stem cells (satellite cells) to reenter
the cell cycle and proliferate, whereas IGF-1 is necessary for the differentiation of newly generated muscle
precursor cells into myoblasts and myofibers.

Growth Hormone bound to its receptor in the liver activates the STAT5b signaling pathway which promotes
movement of that activated signaling protein to the nucleus where it induces transcription of the IGF-1 gene.
From studies in mice and humans, it is evident that GH induces expression of both the endocrine form of IGF-
1, the muscle form of IGF-1 and MGF. 1 Mice deficient in GH (lit/lit mice) respond to administration of GH
with an acute increase in MGF, but not IGF-1, in skeletal muscle, although IGF-1 in liver is increased. 2
However the precise mechanism by which GH has distinct effects on IGF-1 and MGF expression in muscle is
not completely known.

What is known is that in response to stretch overload and the presence of growth hormone combined gene
transcription in muscle and its subsequent "blueprint" assembly" are induced to create mechano growth
factor (MGF also known as IGF-1Ec in humans or IGF-1EB in mice) instead of muscle IGF-1. 3
How does the behavior of IGF-1 and MGF differ?

"MGF is a non-secreted form of IGF-1 that can be found in the nucleus of cells in culture or in a perinuclear
location in hippocampal cells after ischemia (restriction in blood supply)".

In other words MGF never leaves the cell it was created in. For emphasis I quote from another source:

"...MGF... is not normally secreted."

Geoffrey Goldspink has written "that MGF increases myoblast proliferation via a different signalling pathway"
then IGF-1.

To reiterate & expand upon this concept I quote from another source:

"IGF-1 isoforms differ in the signaling pathways they activate. By over-expressing IGF-1Ea and MGF in muscle,
it has been shown that both isoforms can activate IGF-1R and AKT phosphorylation. In addition, MGF was
shown to induce phosphorylation of ERK, a property not shared with IGF-1Ea."

So IGF-1 and MGF work through different pathways not receptors. There is only one receptor, IGF-1-receptor
(also insulin, IGF-II & hybrid receptors which are not relevant to this discussion). There is no MGF receptor.
The reason why it would be nonsensical to have an MGF receptor is that MGF does not leave the cell.

This contrasts with IGF-1 which is released from the liver into circulation and which is created in muscle and
translocates to the cell surface. Both events result in IGF-1 binding to the IGF-1 receptor.

Primobolan (Methenolone)
Methenolone aka Primo, Primobolan — DHB/DHT derivative. Rated 88:57. Mild. No sides, dry, lean gains,
collagen synthesis, immune system benefits, “The perfect steroid.” Pricy (±3× test). Experience thread.

Chemical Name: 17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one

Chemical Formula: C20H30O2
Molecular Weight of Base: 302.4558
Molecular Weight of Acetate Ester (oral): 60.0524
Molecular Weight of Enanthate Ester (injectable): 130.1864
Active Life of Oral: 4-6hrs
Active Life of Injectable: 10-14 days
Anabolic/Androgenic Ratio (Range): 88/44-57

Primobolan is one of the unique compounds that can be administered either orally or by injection. The only
difference in the compounds is the ester attached, the oral version using acetate and the injectable version
using enanthate. However regardless of the method of administration or ester used methenolone is
considered by most to be a relatively mild compound. For the most part users should not expect to make
major gains in muscle mass from this drug but rather lean gains in muscular body weight.
In some animal studies1,2 it has been demonstrated that methenolone has the potential to increase muscular
size and strength. However the anecdotal evidence from users suggest that any mass gains using the
compound will not be overly significant. However it has been noted as quite an effective "cutting" drug
because of it's ability to bind to the androgen receptors in the body3. Of course the ability to bind to androgen
receptors has been shown to promote fat burning in individuals. This effect would obviously be highly
desirable during "cutting" phases or to simply limit the amount of body fat one puts on during a bulking
phase.

Promonolan does not convert to estrogen and therefore estrogenic side effects should not be a concern with
this compound. As well, unlike other oral anabolic steroids it is not 17 alpha alkylated. This means that it is far
less stressful to the liver than other oral steroids. However the process that oral methenolone does go
through to make it orally active, 1 alkylation and 17-beta esterification, does not protect it during the first
pass through the liver very well at all. This requires that the oral version of methenolone must be run at
higher doses than would be expected with the injectable version. For this reason it is often said that the
injectable version of the drug is far more efficient at producing gains.

In terms of therapeutic/medical use of methenolone, it has been argued by some researchers that it has
shown some ability to promote immune system function in AIDS patients. This is different than the anti-
muscle wasting properties that some anabolic steroids are used for. In several studies it's been demonstrated
that methenolone does not exhibit this capability. However in terms of enhancing immune function this
could be attributed to the increased nitrogen retention that methenolone promotes4 . While this effect alone
won't prevent muscle wasting in those suffering from AIDS, it can help to maintain muscle mass in less severe
circumstances, such as calorie restricted diets. But despite these advantages methenolone is not approved
for any type of medical use in North America.

Use/Dosing

The difference in the dosing that is required for the oral and injectable versions of methenolone, as described
earlier, is due to the action of the liver and the fact that the majority of the oral compound will not make it to
circulation in the body. Also, due to the differing esters/structures of the compounds the frequency with
which a user must administer them is also different. The oral form of methenolone should be administered at
least once per day to maintain consistent blood levels of the drug, while the active life of the injectable
version of the drug is such that administering it once per week is possible because of the enanthate ester,
although splitting the doses to twice per week would provide much more consistent blood levels of the drug.

For the oral version of the compound to be effective most male users of methenolone will need to administer
roughly 80 to 150 milligrams per day. This demonstrates truly how much of the drug does not make it past
the liver intact. Compare it to the 200 to 400 milligrams per week many users anecdotally report they
administer of the injectable version and have good results with. Of course many users will increase dosages
beyond these with amounts ranging from 600 to 800 milligrams per week or higher of the injectable
compound not being uncommon.

For women that are inexperienced with methenolone doses of the oral version of the drug have anecdotally
reported ranging from about 40 to 75 milligrams per day. For the injectable, 50 to 150 milligrams per week
should produce very noticeable gains in muscle mass and quality. At these dosages very little in the way of
virilizing effects should be experienced by the majority of female users. However as dosages are increased, so
is the likelihood that these effects will become evident.

As for the length of time that methenolone can be run, due to the lack of toxicity issues associated with the
compound and the relatively mild nature of it in terms of side effects there is little to worry about even if
using it for weeks at a time. Liver, kidney or other organ damage should not be a concern for healthy
individuals. Suppression of natural testosterone production in males does of course occur, but only the usual
protocol of post-cycle therapy is needed to regain this.

Female users have reported that methenolone is quite effective if run alone, however some will stack it with
other compounds for an extra anabolic effect. Male users will rarely run methenolone by itself, instead
choosing to add it with any number of other potential compounds. This is primarily due to the mild nature of
the drug. Used in conjunction with other drugs it can offer several benefits, but alone it will likely leave the
user unsatisfied. However anecdotally users report that if used in combination with other compounds it can
be effective in "cutting" or "bulking" phases. This is despite the fact that methenolone itself will not result in
major gains in muscle mass. It does however help and is quite effective at preserving muscle mass while
dieting as well as enhancing the appearance of a user's muscles.

Risks/Side Effects

For the most part, side effects are almost non-existent with methenolone. However due to it being a DHT
derived steroid prostate problems and the exacerbation hair loss if a user is prone to male pattern baldness
can occur for users of the compound. Many will use ketoconazole and/or finasteride to help with these
effects.

Due to the fact that methenolone does not aromatize, estrogenic side effects are of no concern with this
compound. This is another reason why it is often utilized by bodybuilders during their pre-contest
preparations. Water retention, gynecomastia, and a rise in blood pressure should not occur from use of
methenolone. Due to this, there is no need for anti-estrogen or anti-aromatase compounds while cycling this
drug. In fact, there is some evidence that methenolone can act as an anti-estrogen itself, much in the same
way that drostanolone does. However this effect is weak and should not be relied up for these purposes.

In terms of organ toxicity, methenolone shows no signs that it is capable of causing organ damage in healthy
individuals, even at relatively heavy doses. If dosages are kept within reason, there should be little in the way
of concern about possible organ damage while using methenolone.
 The same can be said for virilizing effects in women. While such things are deepening of the voice, menstrual
irregularity, and body/facial hair growth, among others, are definitely possible, they should be minimized if
female users do not use the drug to excess. These effects are of course permanent if they do manifest
themselves.

References

1. Fritzsche D, Krakor R, Asmussen G, Widera R, Caffier P, Berkei J, Cesla M.Anabolic steroids (metenolone)
improve muscle performance and hemodynamic characteristics in cardiomyoplasty. Ann Thorac Surg. 1995
pr;59(4):961-9
2. Fritzsche D, Krakor R, Asmussen G, Lange S, Kaufmann A, Zapf P, Mehlhorn G, Berkei J, Widera R. Effect of an
anabolic steroid (Metenolon) on contractile performance of the chronically stimulated latissimus dorsi in
sheep. Eur J Cardiothorac Surg. 1994;8(4):214-9
3. Saartok T, Dahlberg E, Gustafsson JA. Relative binding affinity of anabolic-androgenic steroids: comparison of
the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding
globulin. Endocrinology. 1984 Jun;114(6):2100-6
4. van Wayjen RG. Metabolic effects of anabolic steroids. Wien Med Wochenschr. 1993;143(14-15):368-75

Proviron (Mesterolone)

Chemical structure: 1 alpha-methyl-17 beta-hydroxy-5 alpha-androstan-3-one

Molecular weight of base: 304.4716
Active Life: 8-12 hours (effects last about 24 hours)
Anabolic/Androgenic Ratio (Range): 100-150/30-40
Mesterolone is an oral androgen primarily prescribed to treat sexual dysfunction, lagging libido and/or
impotency in men. To a lesser extent it has also been used in an attempt to increase sperm count in some
individuals with varying degrees of success1 . It can be run for long periods of time due to the fact that it is
not a 17 alpha alkylated compound. This enables it to not be quite as toxic since its not alkylated in the same
fashion, but at the 1 position, which reduces hepatic breakdown. However, the anabolic effect of
mesterolone is not strong enough for it to be used for muscle building purposes1 .

Since mesterolone is not used for anabolic purposes for the most part, there must be other reasons why
steroid users administer this compound. First, there is some evidence that by using this compound when
cycling testosterone, it may actually increase it's potency. It appears that the mesterolone will attach to the
sex hormone-binding globulin (SHBG) and albumin. This leaves a larger percentage of free testosterone to
conduct anabolic actions.

Mesterolone can also be used for it's action as an anti-aromatase. It is because of this function that many
users will use it when stacking other compounds that may partially convert to estrogen. Mesterolone will
bind to the aromatase enzyme. This in turn does not allow other steroids to interact with the enzyme and
form estrogen.

Some competitive bodybuilders will also add mesterolone to their pre-contest preparation as many believe
that it will improve muscle density and hardness. This could be attributed to the ability of the compound to
decrease water retention and reduce the amount of circulating estrogen in the body, similar to many other
androgenic compounds. However, as discussed earlier, there are several other drugs that could be
substituted for mesterolone that are much more effective for this purpose.

Many steroid users who have had adverse reactions to testosterone, or otherwise do not wish to use
testosterone in their cycle, will often add mesterolone to their cycles for it's ability to increase the libido of a
user. Often times when a user does not include testosterone, or simply not enough testosterone in relation
to the other compounds that he is using, libido will be reduced and including mesterolone may help alleviate
this. Obviously, the dihydrotestosterone effect of the compound plays a key role in this process 2 .

Use/Dosing

The majority of male users will find that dosing in the range of 25 to 100 milligrams per day of mesterolone
will be enough to achieve their desired results. Females most often remain at about 25 milligrams per day,
but many have experimented with levels far higher. Due to the active life of the compound, splitting the
dosage of the drug so that it can be taken twice per day is beneficial, but the effects of the compound should
remain for a full twenty four hours so it is not completely necessary3 .

Due to the fact that many other compounds are available that are much more potent and effective than
mesterolone for the same purposes, it is seemingly unnecessary to increase a user's dosage far higher than
100mgs per day. Instead one would most likely be better served to switch compounds are try a much more
potent drug if the desired results are not achieved.

Side Effects/Risks

Mesterolone is an oral alkylated steroid. If used throughout a longer cycle it may elevate liver values slightly.
However, this would be far less than would be expected with a 17-alpha-alkylated steroid. Its not quite as
toxic since its not alkylated in the same fashion, but at the 1 position, which reduces hepatic breakdown. This
change in the alkylated position would be due to the fact that the 17-alpha position reduces the affinity for
sex hormone binding proteins thereby decreasing the ability of the compound to free testosterone3 ,
obviously something that would make the drug far less effective for it's intended purposes. It is because of all
of this that liver toxicity should be of little concern to the user running mesterolone even if it is for long
periods of time, keeping in mind that other compounds still pose a threat.
The main concern with the compound is the possibility of androgenic side effects. Usually in male users these
side effects will only appear if a user is administering rather large doses of the drug. An individual may
encounter the typical side effects of oily skin, acne, exacerbation of male pattern baldness if the condition
 already exists, and body/facial hair growth. As should be expected with a compound in which
dihydrotestosterone plays such a major role, prostate problems are also not uncommon with users. Women
should also be aware that virilization symptoms are also a possibility with use of the compound. Deepening
of the voice, menstrual irregulation, and other symptoms could all occur1,3 .

References

1. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 140-1

2. Schulte-Beerbuhl M., Nieschlag E., Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and
follicle-stimulating hormone in serum after injection of testosterone enthanate or testosterone cypionate.
Fertility and Sterility 33 (1980) 201-3.
3. Rea, Author L., 2002, Chemical Muscle Enhancement: Bodybuilder’s Desk Reference

Superdrol/Methyldrostanolone/Methasterone

Androgenic Rating = 20
Anabolic Rating = 400
Estrogenic Activity = none
Progestational Activity = no data available
Chemical Name(s): 2a,17a-dimethyl-5a-androst-3-one-17b-ol 2a,17a-dimethyl-etiocholan-3-one-17b-ol
Chemical Formula: C21H34O2
Molecular Weight: 318
Oral Bioavailability: Estimated at 50%
AR Binding Affinity: NA
SHBG Binding Affinity: High
Half Life: ~8 hours
Legal Status (US): Schedule III (FDA 2012)
Average Dose: 10-30 mg/day standalone, 5-10 mg/day when stacked
Compound Experience Thread

Methyldrostanolone, also known as methasteron, is a potent oral anabolic steroid that was never sold as a
prescription drug. In structure, this steroid is a close derivative of drostanolone (Masteron). The only
difference in this case is the addition of a c-17 alpha methyl group, a modification that gives this steroid high
oral bioavailability. The two agents remain very comparable, however.

Both methyldrostanolone and drostanolone are non-aromatizable, so there is no difference in the

estrogenicity of these two steroids , and both steroids retain favorable anabolic to androgenic ratios. Lab
assays do put Superdrol ahead here, however, showing it to possess 4 times the anabolic potency of oral
methyltestosterone while displaying only 20% of the androgenicity (a 20:1 ratio, compared to 3:1). The exact
real-world relevance of these figures remains to be seen, however. Methyldrostanolone is favored by
athletes for its moderate anabolic properties, which are usually accompanied by fat loss and minimal
androgenic side effects.

History

Methyldrostanolone was first described in 1959. This steroid was developed by the international
pharmaceuticals giant Syntex, alongside such other well known anabolic agents as drostanolone propionate
and Oxymetholone. Unlike drostanolone and oxymetholone, however, this steroid (at least in its basic form)
was never released as a medicinal product. It was only sold for a brief period of time as a modified hormone
called dimethazine. Dimethazine is made from two molecules of Methyldrostanolone that are bonded
together, which are later metabolically separated to yield free Methyldrostanolone. So while technically
Methyldrostanolone itself was never sold as a prescription agent, we can say that the drug was one utilized
medicinally.

Otherwise, the methyldrostanolone molecule Methyldrostanolone remained an obscure research steroid

only, and was never itself approved for use in humans. Methyldrostanolone was released in early 2005 as an
over the counter "grey market" anabolic steroid in the United States. The drug was being sold without
restrictions as a nutritional supplement product, barring some minimum age disclaimers by the
manufacturer. No State or Federal laws identify this drug as an anabolic steroid, which remove the legalities
associated with being a Class III controlled substance like other steroids. This is simply due to the fact that
methyldrostanolone was not in commerce at the time such laws were written, and was unknown to
lawmakers. It was never legal to sell as a dietary supplement, however, and in late 2005 the FDA angrily
acknowledged methyldrostanolone was being sold on the sports supplement market. In early 2006, the FDA
sent letters to the manufacturer and a distributor demanding it be pulled from commerce. Superdrol has
since been discontinued.

Characteristics

Methyldrostanolone is a C-17 alpha alkylated steroid, originally developed by the American pharmaceutical
company Syntex. This steroid is already active and does not require conversion. Methyldrostanolone is the
17aa version of the injectable steroid drostanolone (Masteron). This extra methylation makes this steroid
about 3-4x more anabolic than Masteron, and slightly more anabolic than oxandrolone (Anavar ). Due to the
dimethylation, the toxicity of methyldrostanolone is greater than most other oral steroids .

There have been many reported cases of heptatoxicity with this compound. (1-3) Despite the fact that
methyldrostanolone is a DHT derivative and cannot convert to estrogen, some users have still reported gyno
like symptoms during or after a cycle. This effect is likely related to the strong SHBG binding effect and
increase in freely circulating estrogen (and testosterone) from SHBG. Gyno symptoms may also be related to
the fact that methldrostanolone lacks a strong DHT metabolite to antagonize the effects of estrogen (while
also having a relatively low intrinsic androgenic value).

Having a fairly low androgenic value will mean that methyldrostanolone will be light on the hairline for most
men. However those susceptible to male pattern baldness may still noticed accelerated hair loss during a
cycle.

Because of the di-methylation, methlydrostanolone is considerably more resistant to breakdown, thus more
potent per mg than most other steroids. However this makes it more liver toxic than other single methylated
17aa orals. Negative effects on the liver generally manifest as a condition known as reversible cholestasis.
This is essentially a slowing or complete blockage of bile acids from the liver. Immediate signs of
compromised liver function included reduced appetite and general sickness, which will soon be accompanied
by yellowing of the eyes (jaundice), excessive itchiness and very dark urine. If these effects are noticed,
methyldrostanolone should be discontinued immediately.

Because the effects on the liver, it is very important to use a liver protecting supplement during any
methyldrostanolone cycle. If not using a supplement to protect your liver, methyldrostanolone should never
be used any longer than 2 weeks, with a maximum cycle length of 4 weeks with liver protection. Other
reversible side effects from methyldrostanolone may include increased blood pressure, reduced HDL
cholesterol and lower back pumps.

Results-wise, users should expect extreme strength increases and weight gain in a relatively short 2-4 week
period. Weight gain upwards of 20lbs in 4 weeks is not unheard of with this incredibly potent compound.
Although subcutaneous water gain would be minimal, intramuscular water retention should be expected.
This is due to inhibition of 11b-hydroxylase and build-up of mineralcorticoids which encourage salt and water
retention within the muscles.

The most obvious physical effects will be improved vascularity, aggressive muscular pumps, and oily skin.
While methyldrostanolone can stack well with most other steroids, it should never be stacked with another
methylated (17aa) steroid.

Side Effects

Methyldrostanolone is not aromatized by the body, and is not measurably estrogenic. An anti-estrogen is not
necessary when using this steroid, as gynecomastia should not be a concern even among sensitive
individuals. Since estrogen is the usual culprit with water retention, methyldrostanolone instead produces a
lean, quality look to the physique with no fear of excess subcutaneous fluid retention. This makes it a
favorable steroid to use during bulking or cutting cycles, when water and fat retention are major concerns.

Despite the fact that methyldrostanolone is a DHT derivative and cannot convert to estrogen, some users
have still reported gyno like symptoms during or after a cycle. This effect is likely related to the strong SHBG
binding effect and increase in freely circulating estrogen (and testosterone) from SHBG. Gyno symptoms may
also be related to the fact that methldrostanolone lacks a strong DHT metabolite to antagonize the effects of
estrogen (while also having a relatively low intrinsic androgenic value).

Having a fairly low androgenic value will mean that methyldrostanolone will be light on the hairline for most
men. However those susceptible to male pattern baldness may still noticed accelerated hair loss during a
cycle.

Because of the di-methylation, methlydrostanolone is considerably more resistant to breakdown, thus more
potent per mg than most other steroids. However this makes it more liver toxic than other single methylated
17aa orals. It is believed that this is the cause for why some users report lethargy.

Negative effects on the liver generally manifest as a condition known as reversible cholestasis. This is
essentially a slowing or complete blockage of bile acids from the liver. Immediate signs of compromised liver
function included reduced appetite and general sickness, which will soon be accompanied by yellowing of the
eyes (jaundice), excessive itchiness and very dark urine. If these effects are noticed, methyldrostanolone
should be discontinued immediately.

Other reversible side effects from methyldrostanolone may include increased blood pressure, reduced HDL
cholesterol and lower back pumps.

Administration

Methydrostanolone was never approved for use in humans. Prescribing guidelines are unavailable. An
effective dosage of methyldrostanolone for physique or performance-enhancing purposes seems to begin in
the range of 10-20 mg per day, taken for no longer than 6 weeks.

At this level it seems to impart a measurable muscle-building effect, which is usually accompanied by fat loss
and increased definition. Don't expect to gain 30 pounds on this agent (its name, which is short for "Super
Anadrol " is more marketing than reality), but many do walk away with more than 10 pounds of solid muscle
gain when using this agent alone.

In determining an optimal daily dosage, some do find the drug to be measurably more effective when
venturing up to the 30 mg range. Potential hepatotoxicity should definitely be taken into account with such
use, however.

A USER POST ON SUPERDROLFROM ANOTHER FORUM: THE SUPERDROL WRITEUP (THANKS TO /U/GUMPO1)
Chemistry

Superdrol (methasteron) is definitely not a prohormone: it is a very active form of a designer supplement.
Superdrol gets its name from the fact that it is a super-saturated, or 2-reduced, form of Anadrol. Anadrol has
a =C-OH at the 2nd position, and if this is totally saturated (reduced) with hydrogen, it gives -CH3. Another
way to describe it is that it is a 2a-17a-dimethyl of drostanolone (Masteron). Masteron has a single methyl
group at the 2nd position. Superdrol is a modification of this structure by adding another methyl group at the
17th position, like M1T or M-Dien.

However you may wish to look at it, it is by this simple-looking transformation that Superdrol comes to
occupy the sweet spot between the chemical natures of Anadrol and Masteron. Since it is already reduced at
the 5th position, it cannot make estrogen. Progesterone is not an issue: perhaps 0.1% can aromatize, in
theory. In fact, this compound should not have any major metabolites at all. Maybe a few hydroxylated
adrenal metabolites, but only traces. It is basically excreted unchanged as the conjugated glucuronate.

The extra electron density at the 2 makes Superdrol 2-3x as anabolic (mg for mg) than Anadrol. To borrow
from the language of genetics, Superdrol is a fine example of hybrid vigor: it has only the best attributes of
each, and none of the worst. This is a supplement designed to have it all.

Anadrol (oxymetholone) = 17ß-hydroxy-2-hydroxymethylene-17a-methyl-5a-androstan-3-one

Superdrol (methasteron) = 2a,17a-Dimethyl-17ß-hydroxy-5a-androstan-3-one
Masteron (drostanolone) = 2a-methyl-17ß -hydroxy-5a-androstan-3-one
Proviron (mesterolone) = 1a-methyl-17ß -hydroxy-5a-androstan-3-one
Effects
Anabolic effects & dosing requirements

As fascinating as all this chemistry might be, you are probably much more interested in how well Superdrol is
going to work. What you are going to gain, and how much it will take you to make these gains? The gains
from Superdrol are very dry and lean, so numbers do not tell the whole story, but let us look at them
nonetheless.

According to the book values, Superdrol should be 20% as androgenic as the reference standard methyl-test,
and 400-800% as anabolic, while M1T is 910-1600%, and Anadrol closer to 300%, while being twice as
androgenic as Superdrol, mg for mg. So in theory, Superdrol should be half as anabolic as the same dosage of
M1T, and 10-20% as androgenic. This would mean that it should take twice the dosage of Superdrol to match
the anabolic effects of M1T, at which dosage its androgenic side-effects would be 20-40% of those from M1T.

Fortunately in the case of Superdrol it exceeds in practice its theoretical promise. All testers – who were
selected in part because of their experience with M1T – found that the muscle gains produced from
Superdrol were no less than 2/3 of what a comparable dose of M1T would have given them. Moreover, they
found very few side-effects to complain about.

What this means for you is that you will need somewhere between 10 and 40 mg of Superdrol per day.
Period. There was, certainly, a desire to get this product to market before the ban, but because we were able
to keep its chemistry secret, competition did not force it to be rushed, as was the case with M-Dien.
Accordingly, proper testing was carried out, allowing us to determine real world dosing recommendations,
not ballpark theoretical numbers.

The following recommendations are honest and accurate: 10-15 mg will be sufficient for beginners under 200
lbs; 20-25 mg for those advanced lifters under 200 lbs, or for those above 200 lbs but untrained; 30-35 mg for
men who have seriously trained themselves but are under 240 lbs. For men who think they need to run a
dose which falls between the use of whole capsules, one extra 10 mg capsule can be taken before workouts,
such that the weekly average is appropriate as a rule of thumb,

Superdrol will require 50% more of a dose than M1T to give you comparable gains in muscle. Any women
who are entertaining the possibility of using Superdrol should reduce the weight to accord with their sex and
their height, and then divide these dosages by a factor of no less than ten. Capsules will then have to be
diluted in liquid to be measured accurately.

For men, 40 mg is a dose only for the very large or the true non-responders, by which I mean people who do
not see results on less than 30 mg of M1T. Very few people will need 40 mg of Superdrol, and no one will
need above 50 mg. If used in a stack reduce the daily dose by 5-10 mg, which would be very prudent given
how well Superdrol will stack, and if not its expense, then your very limited supply.

The testers whose dosing fit the above guidelines gained, on average, five pounds of muscle in under three
weeks, while losing water and gaining no fat on hyper caloric bulking diets. The quality of the gains from
Superdrol comes from its likeness to Masteron while the quantity comes from its similarity to Anadrol.
Masteron, expensive and very rare, is almost a perfect cutting steroid, being highly androgenic and anti-
estrogenic.

If you must have a rough comparison to something already out there, one tester described the quality of
gains as being akin to those from fina or a test/halo combo, but such comparisons are bound to be inexact.
Gains are very dry, and it makes muscles noticeably more hard and dense. The explosive gains from Anadrol
are accompanied by a great deal of water retention and fat. M1T, as you surely well know, produces
explosive gains not unlike those of Anadrol, but this comes at a cost. More on this later.

As to how difficult it is to retain the gains from Superdrol, you are invited to follow the testers’ post-cycle
results. To date, the results are promising, with no loss of mass or vascularity. The gains from Superdrol will
be impressive, and they will not take long to start, but they will be more gradual to be recognized than those
which come from aromatizing steroids. Your numbers in the gym and on the tape measure will go up, not
explosively, but they will go up surely and steadily.

The diuretic effect of Superdrol will at first mask the gains as you lose water and gain muscle. When mass
begins to increase, it should do so disproportionately compared to tape-measurements. So if you are only
checking the scale, or if you are not lean enough to notice the loss of water, persist and be rewarded.
Strength

Anadrol is famous for explosive gains in strength. M1T is not. Superdrol shares with Anadrol a capacity for
impressive, but consistent, gains in strength. Testers experienced dramatic and immediate strength gains,
when consuming sufficient calories. To their surprise and our delight, every single one became stronger every
single workout, and many personal bests were recorded, while volume increased.

Being a DHT derivative, it is a fair question to ask whether the strength gains from Superdrol can be
maintained, or whether they will not dissipate shortly after one terminates use of the drug. In response to
this, consider that 1) the strength gains from pure androgens are not generally accompanied by proportional
gains in mass, and 2) the gains in both strength and mass which result from dianabol/M1,4ADD are—besides
being accompanied by bloating—diminished soon after one goes off, they don’t just disappear, but they are
hard to keep.

If the mass gains from Superdrol are solid rather than fleeting, then the strength which came with this
increase in muscle mass should be much easier to maintain than those which can result from the use of
Anadrol, Dianabol/M1,4ADD, or many of the pure androgens, which achieve a significant amount of their
effect on strength through their psychotropic effects on focus and aggression.

Athletic Performance

Along with marked increases in strength, all testers observed undeniable increases in their endurance,
whether in cardio or adding to the sets they could perform. Breathing and heart rates were not as high as
expected. Given Superdrol’s chemical relation to Anadrol and Masteron, it was speculated that this could be
due to an increase in red blood cell (RBC) count, which would allow the use of more oxygen. Masteron has
also been used as an Anadrol alternative for aplastic anemia, so it should be a strong immune stimulator and
RBC booster, as many 5-reduced compounds are.

In Anadrol, the extra stamina which should accompany the known increase in RBC is largely counteracted by
the estrogen related effects. Because these are absent with Superdrol, increased RBC count may seemed a
probable explanation for the increase in endurance. But because the increased endurance occurred quickly, I
am hesitant to assert that an increased RBC count is the reason. Shortly after this appears in print, there
should be blood work available to confirm or deny this. No matter the explanation, Superdrol does increase
endurance significantly.

Fluid Retention

Masteron and Anadrol are on the opposite ends of the spectrum in regards to fluid retention. In this regard,
Superdrol lies close to Masteron, which – being unable either to convert to estrogen or mimic the effects of
estrogen – has typically been used for reducing water retention while increasing muscle hardness and
density. The rapid gains in mass caused by Anadrol involve not a little water retention: bloating is
unavoidable, as with Dianabol/M1,4ADD.
With Superdrol, there is no extra water retention. There is not even facial bloating. It forms no estrogen, so
the renin-angiotensin-aldosterone (RAAS) system cannot be activated to cause any water retention. M1T has
the unfortunate effect of causing water retention in the kidneys, which can be painful, and is definitely
unhealthy.

The pumps for which Anadrol is known are caused by an increase in the volume of blood, some of it RBC but
much of it water. Blood pressure rises accordingly, and can lead to headaches, other forms of discomfort, or
worse. The pumps from Superdrol could well be the result of the volumization of blood without the water
gain, as noted above. It is in fact a mild diuretic. This helps contribute to the unmatched vascularity noticed in
lean individuals.

Because it dries you out, unless you are cutting for a reason, like a contest, you should increase your water
intake accordingly. You can expect to drop at least several pounds of water in your first few days of use. From
testers who monitored their blood pressure, there was no indication that it rose significantly, nor were there
in others symptoms of high BP, for example, face turning beet red, or feeling nauseous after a few light sets.

The pumps and increased vascularity from Superdrol are pleasant - “my biceps feel flexed when at rest” in
the words of one tester. That is, until the dose is becomes too high, at which point Superdrol shares with
Anadrol back pumps, cramps, or aches. These can inhibit workouts. At proper doses, these are fleeting, not
unlike those from M1T, but not as severe. However, the tester who challenged the highest dose experienced
such discomfort that he literally had to lay on the gym floor in between sets. It seems that Superdrol has a
built in mechanism, harmless enough, to prevent its abuse.

Fat

Masteron is very effective in cutting cycles to reduce bodyfat; Anadrol does not mind putting on a few
pounds ‘for the winter.’ Superdrol testers were all eating well, no one was cutting, and mass was going up
faster than tape-measurements. It was wondered whether Superdrol exhibited fat-burning properties like
tren. This can be discounted, and explained instead as a diuretic effect: testers size did not change
dramatically because they lost water, while their muscles grew and became more dense.

So in regard to fat, Superdrol falls right between Masteron and Anadrol: one could say that it neutral in terms
of partitioning. When using Superdrol, fat will not magically melt away, but nor will it especially inhibit fat
loss on a cut. It will not especially prime you for fat gains on a bulk, but if you do not watch your diet you can
get fat.

Psychological Effects

The psychological effects of Anadrol and Masteron are noticeable, if not as pronounced as with some other
DHT derivatives. It was not clear what, if any, psychological effects should have been expected from
Superdrol, given how little its androgenic effects looked to be on paper. What the testers found, to begin
with was that Superdrol felt “somatically clean,” meaning that there was zero sense of physical malaise or
indisposition which is common to Anadrol and especially M1T. On the contrary, testers had a sense of
physical well-being, a clean feeling of being ‘on'—as distinct from the sure knowledge that one is growing,
even if one doesn’t feel well, that one gets from M1T or Anadrol.

This feeling was not as pronounced as with Dianabol. Psychologically, the following were attributed to the
use of Superdrol: confidence, assertiveness, focus, increased libido, the need to do something,
aggressiveness in the gym, a command mindset, and some irritability—especially upon ramping up to the
next dosing level.

One tester described the CNS stimulation he got from doing 30 mg at once as being stronger than 50 mg of
M5, 32 mg of M4OHN, or EC. Endurance and strength should be mentioned here as well, because while
above I have offered physical explanations for them, some of this effect could well be psychological, in which
case it would dissipate upon cessation of the use of Superdrol. There was some increase in appetite for some
of the testers, a decrease for others; in either case this was not overwhelming.

Recovery

Recovery time on Superdrol was improved, slightly but noticeably - not on a par, however, with a similar dose
of M1T, let alone Anadrol. In this light you should be reminded that the increases in strength which you will
experience on Superdrol do not come with a proportional increase in the strength of connective tissue. So
when using Superdrol, you should observe strict form in the gym or else you invites injury, which obviously
defeats the purpose of any kind of performance enhancing agent.

Adverse effects

Across the board, testers were astounded by the virtual absence of unwelcome side-effects from Superdrol
use. One tester, already balding, mentioned an occasional itchy scalp. The only exception to the clean bill
given to Superdrol was noted earlier, lower back pain at excessive doses. This lack of side effects can be
attributed to Superdrol’s very low androgenic capacity and its anti-estrogenic effects.

References

Cholestatic Jaundice and IgA Nephropathy Induced by OTC Muscle Building Agent Superdrol. Beata
Jasiurkowski MD, et al. The American Journal of Gastroenterology (2006) 101, 2659-2662.

Severe Cholestasis and Renal Failure Associated with the Use of the Designer Steroid Superdrol
(Methasteron): A Case Report and Literature Review. John Nasr and Jawad Ahmad. Digestive Diseases and
Sciences.

Methasteron-Associated Cholestatic Liver Injury: Clinicopathologic Findings in 5 Cases” Neeral L. et al. Clinical
Gastroenterology and Hepatology, Volume 6, Issue 2, February 2008, Pages 255-258.
Identification of drostanolone and 17-methyldrostanolone metabolites produced by cryopreserved human
hepatocytes.” Julie Gauthier, Danielle Goudreault, Donald Poirier and Christiane Ayotte. Steroids; Volume 74,
Issue 3, March 2009, Pages 306-314.

Sustanon 250

Pharmaceutical Name: Testosterone (with propionate, phenylpropionate, isocaproate and decanoate ester)
Molecular Weight of Base: 288.429
Molecular Weight of Esters:
Propionate: 362.5082
Phenylpropionate: 438.6058
Isocaproate: 404.5886
Decanoate: 460.6958 Formula of Base: C19 H28 O2
Melting Point of Base: 155 Celsius
Active life: approximately 21 days
Anabolic/Androgenic ratio: 100/100
Originally developed as use primarily for hormone replacement therapy, Sustanon 250 is a blend of
testosterone esters thought to provide a long lasting testosterone release1. It was thought that by using short,
medium and long acting esters that a stable flow of the compound could be maintained and that extremely
infrequent injections would be needed. However, this theory was proven wrong as blood levels of the
compound peak rather quickly and slowly taper down as time passes. To maintain stable blood levels the
drug must be injected just as frequently as other short estered compounds.

Sustanon 250 is blended with estered testosterone of the following amounts: 30mg propionate, 60mg
phenylpropionate, 60mg isocaproate, 100mg decanoate. It should also be noted that there is a Sustanon 100.
It is as follows: 20mg propionate, 40mg phenylpropionate, 40mg isocaproate. Due to Sustanon 100 not
having the decanoate ester the active life of the compound is shorter than that of Sustanon 250. Other than
that difference, the compounds are fairly similar. However, in this profile Sustanon 250 will only be dealt
with.

Sustanon 250, outside of the blend of esters, offers no unique advantages to other testosterone compounds.
The effects for the most part should be the same as any testosterone compound. In terms of the effects of
esters, Sustanon 250 seemingly has the worst of both. Many users complain that they suffer from water
retention while using the compound due to the long acting esters, but because of the short acting esters, the
compound should be injected frequently. This has led many users to simply choose another testosterone
ester better designed for their goals.

Testosterone is able to promote strength increases and muscular growth via numerous mechanisms. Of
course first off testosterone promotes nitrogen retention in muscle therefore allowing the muscles to hold
more protein and enabling repair and growth of those muscles. Secondly testosterone binds to the androgen
receptor to promote receptor dependant mechanisms for muscular growth and fat loss2 . Testosterone also
helps to increase the concentrations of androgen receptors in cells that are important for muscle growth and
repair in muscle.
As mentioned, testosterone can play a role in promoting fat loss. Testosterone has the ability to bind to the
androgen receptors in fat cells. This can enable the breakdown of body fat while and also deters new fat
formation3 . Of course due to the fact that testosterone will encourage muscular growth, indirectly it will
promote fat reduction because any excess calories are likely to be used in the muscle building process rather
than being added as body fat.

Like most anabolic steroids, testosterone also increases red blood cell production. An increased number of
red blood cells in the blood can improve endurance via better oxygenated blood as well as improving a user's
ability to recuperate after strenuous physical activity. However it should be noted that there are other
steroids and compounds out there that are far more adept at this function.

Among the other mechanisms that testosterone can help promote anabolism are via the increased
production of insulin growth factor 1 it encourages, as well as suppressing the action of catabolic hormones
in the body. In terms of performance enhancement, testosterone also offers numerous advantages. Namely
it has the ability to increase the number of motor neurons in muscles and thereby improving muscular
contraction. Like many other anabolic steroids testosterone also promotes glycogen synthesis (4). This will of
course help to improve a user's endurance and strength by providing more fuel for intense workouts thus
increasing endurance and strength, as glycogen is stored carbohydrates used as a fuel during exercise.

Use/Dosing

As with the other testosterone compounds, the doses of the drug that are taken by users varies to a great
degree depending on the experience and goals of the user. Doses as low as 200-250mgs per week have been
reported by users who say they have made good gains, with experienced users administering several grams
of testosterone per week. The range of use is very wide. This also includes women administering
testosterone. It is because of the long active life of some of the esters in Sustanon 250, it is not
recommended that women who choose to administer testosterone use it or other long-estered formulas.
This is due to the fact that slow acting esters can not be quickly altered if negative side effects become overly
burdensome. By having to deal with the slow release of the testosterone and not being able to lower doses
or cease administration of the compound immediately, it makes it much more likely that any side effects that
are experienced will be more pronounced and/or exaggerated. For this reason, females who use testosterone
may want to begin with testosterone propionate or suspension when choosing which ester to use and not
Sustanon 250.

In terms of an actual injection schedule, to maintain stable blood levels of the compound individuals should
inject at least every other day, with every day injections of course being preferred. This is due to the short
acting esters that Sustanon 250 contains. If one chooses to inject less frequently they are likely to experience
fluctuating levels and this can lead to harsher side effects in some users. However due to the long acting
esters users must wait approximately 21 days after the last injection to have the compound clear their
system so that they can begin post-cycle therapy. One may want to begin using a short acting estered
testosterone during this time due to the declining testosterone levels. This would surely lead to a smoother
transition to coming off of the compound.

Risks/Side Effects

Most of the side effects that result from using testosterone in males is related to testosterone's high
tendency to convert into estrogen via the aromatase enzyme. These side effects can include water retention
and gynecomastia. Users often complain that water retention is much more severe with longer acting esters
than with shorter acting esters such as propionate. To combat these side effects users can use aromatase
inhibitors and/or selective estrogen receptor modulators. Of course the likelihood of estrogen related side
effects increase as the dosages are raised. However these should be controllable if the proper precautions
taken.

Of course being testosterone, user's should also expect to deal with androgenic side effects as a possibility.
These side effects can include facial/body hair growth, exacerbation of male pattern baldness, and oily
skin/acne, among others. Some users may wish to use products such as Proscar/Propecia to reduce the
amount of testosterone that converts to dihydrotestosterone. Finasteride is also an option that users' can
pursue.

Due to the suppression of natural testosterone levels, testicular atrophy is also likely to occur in some
individuals. Use of human chorionic gonadotropin can help to prevent this, among it's other effects. Of
course a proper post-cycle therapy should be run once administration of the compound is completed to help
recover fully functioning natural testosterone production.

Far more than the other testosterone esters, for the possible exception of propionate, users of Sustanon will
often complain of injection site irratation and swelling. Some individuals find that the reaction that they
experience with the compound is so bad in fact that they will have to cease administration of it. As well, due
to the frequent injections of the compound and the possibility of injection site irritation, it is advisible that
users rotate injection sites as frequently as possible so that no complications arise.

Women may find that other shorter acting esters are more manageable than longer acting such as some of
those found in Sustanon 250. This is due to the fact that the fast acting esters can be controlled easier and
that the dosing and administration of the compound can be quickly altered if negative side effects become
overly burdensome. With longer acting esters these adjustments are much more difficult to make rapidly and
side effects could become more pronounced and/or exaggerated. For this reason, females who use
testosterone may want to at least begin with shorter acting esters if they experiment with testosterone.
 Of course with women using testosterone there is a possiblity that virilizing symptoms could occur.
Deepening of the voice, body/facial hair growth, and enlargement of the clitoris are all possible side effects of
testosterone use. These are for the most part irreversible5 .

References

1. Cantrill JA, Dewis P, Large DM et al. Which testosterone replacement therapy? Clin Endocrinol (oxf) 21 (1984)
97-107
2. Toth M., Zakar, T. Relative binding affinities of testosterone, 19-nortestosterone and their 5-alpha reduced
derivatives to the androgen receptor and to other androgen-binding proteins: A suggested role of 5alpha-
reductive steroid metabolism in the dissociation of "myotropic" and "androgenic" activities of 19-
nortestosterone. J Steroid Biochem 17 (1982) 653-60
3. Sjogren J, Li M, Bjorntorp P. Androgen hormone binding to adipose tissue in rats. Biochim Biophys Acta. 1995
May 11;1244(1):117-20
4. Ramamani A, Aruldhas MM, Govindarajulu P. Differential response of rat skeletal muscle glycogen
metabolism to testosterone and estradiol. Can J Physiol Pharmacol. 1999 Apr;77(4):300-4
5. Bolour S, Braunstein G. Testosterone therapy in women: a review. Int J Impot Res. 2005 May 1

Testosterone Cypionate

Chemical structure: 17b-hydroxy-4-androsten-3-one

Chemical Formula: C27 H40 O3
Molecular Weight (base): 288.429
Molecular Weight (ester): 132.1184
Active life: 8 days
Detection Time: 3 months
Anabolic/Androgenic ratio: 100/100

Testosterone Cypionate is a synthetic version of the naturally produced testosterone hormone. This hormone
is responsible for many different physical and mental characteristics in males. It promotes sex drive, fat loss,
helps with gaining and maintaining lean muscle mass, increases bone density, and may even protect against
heart disease. Whether it is naturally produced or through the use of Testosterone Cypionate, these traits do
not change. All other steroids are actually the testosterone molecule that has been altered to change the
properties of the hormone. Testosterone Cypionate carries a rating of 100 when measuring its
anabolic/androgenic structure and this rating is used to measure all other steroids. This would make
testosterone the "father" of all anabolic steroids used by athletes today. It should be noted; all testosterone
compounds, including Testosterone Cypionate carry this anabolic/androgenic score of 100, as they are all
merely testosterone.
Testosterone Cypionate is a highly anabolic and androgenic hormone making it a great steroid to use if one is
in pursuit of more size and strength. Testosterone Cypionate promotes nitrogen retention in the muscle and
the more nitrogen the muscles hold the more protein the muscles store. Testosterone Cypionate can also
increase the levels of another anabolic hormone, IGF-1 in muscle tissue providing even more anabolic
activity. Testosterone Cypionate also has the amazing ability to increase the activity of satellite cells. These
cells play an active role in repairing damaged muscle. Testosterone also binds to the androgen receptor to
promote androgen receptor dependent mechanisms for muscle gain and fat loss.

Testosterone Cypionate induces changes in shape, size and can also change the appearance and the number
of muscle fibers. Androgens like testosterone can protect your hard earned muscle from the catabolic
(muscle wasting) glucocorticoid hormones, in-turn inhibiting the related adverse reactions. In addition,
Testosterone Cypionate has the ability to increase red blood cell production and a higher red blood cell count
will improve endurance through increased oxygenation in the blood. More red blood cells can also improve
recovery from strenuous physical activity. Even so, Testosterones anabolic/androgenic effects are dose
dependent; the higher the dose the higher the muscle building effect.

Many athletes display massive strength gains while using Testosterone Cypionate as the hormone improves
muscle contraction by increasing the number of motor neutrons in muscle and improves neuromuscular
transmission. It also promotes glycogen synthesis providing more fuel for intense workouts thereby
increasing endurance and strength.

Testosterone Cypionate also has the ability to promote fat loss through an enhancement of metabolic
activity. Testosterone binds to the androgen receptor fairly well resulting in fat breakdown, and further
prevents new fat cell formation. Another indirect action of fat loss that testosterone produces is the nutrient
portioning effect it has on muscle and fat. Since the body is building muscle at an accelerated rate more of
the food you eat is shuttled to muscle tissue instead of being stored as fat; nutrient efficiency is enhanced.

Testosterone Cypionate will also play a crucial role revolving around creatine. Creatine is essential to
adenosine triphosphate (ATP), the source of energy for our muscles and when the muscles are stimulated
ATP is broken down into adenosine diphosphate (ADP) and this is what releases energy. Unfortunately, the
process is often too slow during strenuous activity but through the use of Testosterone Cypionate, this
demand is met as ATP is replenished at a much faster rate.

Effects of Testosterone Cypionate

With a well-planned Testosterone Cypionate cycle, nearly every anabolic steroid benefit can be obtained. For
the off-season athlete, more lean muscle mass can be built with less body fat gain. In-order to grow, you
must consume enough calories and fat gain will occur, but Testosterone Cypionate will ensure the brunt of
your weight gain is the weight you want.
While off-season bulking use is the most common, the effects of Testosterone Cypionate can be
tremendously beneficial during the cutting phase too. During this period of use, we are able to preserve far
more lean muscle tissue that would otherwise be lost. In-order to lose body fat, we must burn more calories
than we consume and this can and often does lead to muscle and strength loss. Further, the longer and
harder you diet the more muscle and strength will be at risk, but due to the traits of Testosterone Cypionate
muscle tissue and strength are protected.

Regardless of the purpose of use, Testosterone Cypionate defines performance enhancement by its ability to
promote recovery and endurance. With a performance level dose of Testosterone Cypionate your body can
recover faster and you wont tire out as quickly. This will allow you to workout longer and harder, and more
progress can be made. This is performance enhancement at its best!

Testosterone Cypionate Administration

Testosterone Cypionate is only available in an injectable form and is regularly used to treat conditions such as
low testosterone. More than twenty million men in the U.S. alone suffer from some form of low
testosterone, and such a condition can severely diminish ones quality of life. Symptoms such as loss of
muscle mass and strength, a decrease in libido and sexual performance, an increase in body fat, and low
energy levels are all common characteristics of low testosterone. Further, when ignored low testosterone can
be a gateway to Alzheimers, diabetes, osteoporosis and many other serious conditions. Most men will find
one injection every seven to ten days at 100mg to 200mg per injection to completely eradicate such a
problem.

For performance enhancement, one injection per week is often enough; however, in many cases two smaller
yet equal sized injections will prove to be far more efficient. The reason for multiple injections is to keep
blood levels peaked; further, it is often needed to control side effects that may occur with performance level
dosing. Like most anabolic steroids, the more you take the greater the reward, but the more you take the
greater the risk. By splitting the injections up into smaller more frequent injections, you are introducing
smaller amounts of the hormone for your body to deal with all at once. As for the actual performance doses,
this can range anywhere from 200mg per week all the way to 1,000mg per week depending on needs and
desires.

The typical dose for those who are using Cypionate to counteract the lowering of testosterone due to the use
of other steroids is normally 200mg. If it is being used for direct performance purposes, most will find 400mg
to 600mg per week will be effective, but it is important to note that higher doses will greatly increase the
risk.

Regardless of the total dose, most steroid users will find this to be an extremely well-tolerated anabolic
steroid and one that can be used for long periods of time. 12 weeks of total use is quite commonplace, as is
16 weeks. There's nothing magical about these numbers, but they are solid guidelines in-order for the
individual to plan out his desired goals.

Regardless of the total dosing or the cycles length, you will need to design a post cycle therapy (PCT) plan
once your Testosterone Cypionate use comes to an end. For most men, if you are discontinuing the use of
anabolic steroids for more than ten weeks, you will need PCT but if your off period is less then it can be
skipped. For full post cycle information and planning, please see the Post Cycle Therapy page on Steroid.com.

It should be noted; when it comes to performance enhancement, Testosterone Cypionate for women is not
recommended. This is a steroid that carries far too much androgenic activity; after all, it is the primary male
androgen. Women can suffer from low testosterone and there can be therapeutic benefits from the use of
Testosterone Cypionate; however such treatment plans will be tremendously low dosed and should be
watched closely for virilization symptoms.

The Side Effects of Testosterone Cypionate

As an extremely well-tolerated hormone for most men, the side effects of Testosterone Cypionate are in
many ways easy to control. When it comes to such adverse reactions, keep in mind they largely fall into the
realm of possible and are by no means guaranteed. Even so, total dosing, genetic predispositions and your
overall state of health will play a role.

As for the side effects themselves, Testosterone Cypionate like all testosterone compounds carries a high
level of aromatase activity; aromatization referring to the conversion of testosterone into estrogen. As
estrogen levels rise, this can lead to gynecomastia (male breast enlargement) and excess water retention.
This excess water retention can even negatively affect blood pressure. In-order to combat such effects,
especially gynecomastia, many turn to Selective Estrogen Receptor Modulators (SERMs) such as Tamoxifen
Citrate (Nolvadex) and for more serious protection Aromatase Inhibitors (AIs) such as Anastrozole (Arimidex).
Without question, AIs are the most effective; however, they can also prove to be problematic when it comes
to cholesterol and caution is advised.

Beyond these effects, Testosterone Cypionate can promote dihydrotestosterone (DHT) related side effects
such as acne, hair loss and prostate enlargement; however, it should go without saying DHT steroids will be
the prime culprits. In-order to provide protection, a 5-alpha reductase inhibitor such as Finasteride can be
useful as it is an androgen suppressor and the androgen DHT is causing the problem. It must be noted; hair
loss is only possible in men predisposed to male pattern baldness.

Testosterone Enanthate

Pharmaceutical Name: Testosterone (with enanthate ester)

Molecular Weight: 412.6112
Molecular Weight of Base: 288.429
Molecular Weight of Ester: 130.1864
Formula of Base: C19 H28 O2
Formula of Ester: C7 H12 O
Active life: 15-16 days
Anabolic/Androgenic ratio:100/100

Testosterone is responsible for the development and maintenance of male secondary sex characteristics. This
includes it being a highly anabolic and androgenic hormone, therefore being capable of increasing users'
muscle mass and strength/power when administered at larger than normal doses in the body. The
testosterone enanthate compound itself is an injectable oil which contains testosterone with the enanthate
ester attached to the testosterone molecule. When the enanthate ester is adding to testosterone base, it
creates a long-acting form of testosterone. This requires a user to only inject the compound once or twice per
week to maintain fairly stable levels of the compound, something that is obviously an advantage. Blood levels
of testosterone enanthate will fall rather dramatically five days after it is administered, however the level of
the compound should still be well above baseline after a week. This is quite similar to the cypionate ester. In
fact, testosterone cypionate and enanthate are basically interchangeable in terms of active life and half life,
including almost identical release patterns. Enanthate was primarily manufactured in other areas of the
world outside of North America. Cypionate was the ester of choice for North American companies in the
early stages of anabolic steroid development. However now both of these esters are used throughout the
world having both maintained their popularity with users. They are both widely available.

Testosterone is able to promote strength increases and muscular growth via numerous mechanisms. Of
course first off testosterone promotes nitrogen retention in muscle therefore allowing the muscles to hold
more protein and enabling repair and growth of those muscles. Secondly testosterone binds to the androgen
receptor to promote receptor dependant mechanisms for muscular growth and fat loss. Testosterone also
helps to increase the concentrations of androgen receptors in cells that are important for muscle growth and
repair in muscle1 .
As mentioned, testosterone can play a role in promoting fat loss. Testosterone has the ability to bind to the
androgen receptors in fat cells. This can enable the breakdown of body fat while and also deters new fat
formation2 . Of course due to the fact that testosterone will encourage muscular growth, indirectly it will
promote fat reduction because any excess calories are likely to be used in the muscle building process rather
than being added as body fat.

Like most anabolic steroids, testosterone also increases red blood cell production. An increased number of
red blood cells in the blood can improve endurance via better oxygenated blood as well as improving a user's
ability to recuperate after strenuous physical activity. However it should be noted that there are other
steroids and compounds out there that are far more adept at this function.
Among the other mechanisms that testosterone can help promote anabolism are via the increased
production of insulin growth factor 1 it encourages, as well as suppressing the action of catabolic hormones
in the body. In terms of performance enhancement, testosterone also offers numerous advantages. Namely
it has the ability to increase the number of motor neurons in muscles and thereby improving muscular
contraction. Like many other anabolic steroids testosterone also promotes glycogen synthesis. This will of
course help to improve a user's endurance and strength by providing more fuel for intense workouts thus
increasing endurance and strength, as glycogen is stored carbohydrates used as a fuel during exercise3 .

Some users believe that testosterone enanthate should be reserved for "bulking" cycles and is not
appropriate for those cycles in which a user is hoping to reduce body fat. However this is a misnomer as the
ester of the compound can not alter it's physiological effects. Depending on the diet and training routine of
the user, testosterone enanthate can be used quite effectively for either mass building or cutting cycles. This
belief that enanthate should only be used for bulking cycles may originate from the fact that a majority of
users anecdotally report that they experience more water retention/bloat while using testosterone
enanthate in comparison to other shorter acting testosterone esters. This water retention and bloat would
seemingly make the user appear "puffy" and therefore may lead the individual to believe that they are
indeed increasing their body fat, while the lack of water retention that they experience with the shorter
acting esters may make them think that they are reducing their body fat when that may not be the case.

However, a minority of users also report that they hold less water while using testosterone enanthate than
testosterone propionate. This again demonstrates that individuals react quite differently to various
compounds. Experimentation with the various compounds is the only sure way to see how you react.

Use/Dosing

The ester enanthate is seven carbons in length. Due to this length the majority of the compound is stored in
the adipose tissue when injected intramuscularly. In doing so it is steadily released over a period of time. A
peak in the blood level of the compound is reached after 24-48 hours after the injection followed by a slow
decline. This requires that a user wait about fourteen days after the last injection to begin their post-cycle
therapy to ensure that the compound has completely cleared the system of the user.

In terms of an actual injection schedule most users will inject testosterone enanthate twice per week.
However, some users will administer the compound only once per week or may choose to inject several
times per week. The more frequently a user injects the more stable the blood levels of the compound will be,
assuming of course that the doses are equally distributed and of the same amount.

As with the other testosterone esters, the doses of the drug that are taken by users varies to a great degree
depending on the experience and goals of the user. Doses as low as 200-250mgs per week have been
reported by users who say they have made good gains, with experienced users administering several grams
of testosterone per week. The range of use is very wide. This also includes women administering
testosterone. It is because of the long active life of the enanthate ester, it is not recommended that women
who choose to administer testosterone use it or other long-estered formulas. This is due to the fact that slow
acting esters can not be quickly altered if negative side effects become overly burdensome. By having to deal
with the slow release of the testosterone and not being able to lower doses or cease administration of the
compound immediately, it makes it much more likely that any side effects that are experienced will be more
pronounced and/or exaggerated. For this reason, females who use testosterone may want to begin with
testosterone propionate or suspension when choosing which ester to use and not enanthate.

Risks/Side Effects

Most of the side effects that result from using testosterone in males is related to testosterone's high
tendency to convert into estrogen via the aromatase enzyme. These side effects can include water retention
and gynecomastia. Users often complain that water retention is much more severe with longer acting esters
than with shorter acting esters such as propionate. To combat these side effects users can use aromatase
inhibitors and/or selective estrogen receptor modulators. Of course the likelihood of estrogen related side
effects increase as the dosages are raised. However these should be controllable if the proper precautions
taken.

Of course being testosterone, user's should also expect to deal with androgenic side effects as a possibility.
These side effects can include facial/body hair growth, exacerbation of male pattern baldness, and oily
skin/acne, among others. Some users may wish to use products such as Proscar/Propecia to reduce the
amount of testosterone that converts to dihydrotestosterone. Finasteride is also an option that users' can
pursue.

Due to the suppression of natural testosterone levels, testicular atrophy is also likely to occur in some
individuals. Use of human chorionic gonadotropin can help to prevent this, among it's other effects. Of
course a proper post-cycle therapy should be run once administration of the compound is completed to help
recover fully functioning natural testosterone production.

Women may find that other shorter acting esters are more manageable than longer acting such as
testosterone enanthate. This is due to the fact that the fast acting esters can be controlled easier and that
the dosing and administration of the compound can be quickly altered if negative side effects become overly
burdensome. With longer acting esters these adjustments are much more difficult to make rapidly and side
effects could become more pronounced and/or exaggerated. For this reason, females who use testosterone
may want to at least begin with shorter acting esters if they experiment with testosterone.

Of course with women using testosterone there is a possiblity that virilizing symptoms could occur.
Deepening of the voice, body/facial hair growth, and enlargement of the clitoris are all possible side effects of
testosterone use. These are for the most part irreversible4 .
 References

1. Schulte-Beerbuhl M, Nieschlag E. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and

follicle-stimulating hormone in serum after injection of testosterone enanthate or testosterone cypionate.
Fertility and Sterility 33 (1980) 201-3.
2. Corcoran C, Grinspoon S. The use of testosterone in the AIDS wasting syndrome. AIDS Clin Care. 1999
Apr;11(4):25-6, 33-4
3. Crawford BA, Liu PY, Kean MT, Bleasel JF, Handelsman DJ. Randomized placebo-controlled trial of androgen
effects on muscle and bone in men requiring long-term systemic glucocorticoid treatment. J Clin Endocrinol
Metab. 2003 Jul;88(7):3167-76
4. Bolour S, Braunstein G. Testosterone therapy in women: a review. Int J Impot Res. 2005 May 12

Testosterone Propionate

Pharmaceutical Name: Testosterone (with propionate ester)

Molecular weight of base: 288.429
Molecular weight of ester: 74.0792 (propionic acid, 3 carbons)
Chemical structure: 4-androstene-3-one,17beta-ol
Active Life: 2-3 days
Anabolic/Androgenic Ratio: 100/100
Often considered the mildest of the testosterone esters1,2 , testosterone propionate offers some unique
advantages to the other testosterones with longer acting esters. However like the other testosterone
compounds, testosterone propionate offers the same benefits in a medical sense. It is only the dosing
schedule of the drug that changes, although the propionate ester may cause certain unique reactions in some
individuals that will be detailed later in this profile.

The main advantage of testosterone propionate over other testosterone esters is that it's effects will be
realized much quicker than with other compounds. Due to the quick release of the hormone users often
report anecdotally that they will begin to notice the effects of the compound within the first 5-7 days of first
administering the drug in some cases. However with this advantage comes the requirement that a user inject
the compound every day or every other day to maintain stable blood levels of the drug. This frequent
injection schedule often deters many inexperienced users from using the propionate ester in their first few
cycles.

Some users believe that testosterone propionate should be reserved for "cutting" cycles and is not
appropriate for those cycles in which a user is hoping to build mass. However this is a misnomer as the ester
of the compound can not alter it's physiological effects. Depending on the diet and training routine of the
user, testosterone propionate can be used quite effectively for either mass building or cutting cycles. This
belief that propionate should only be used for cutting cycles may originate from the fact that a majority of
users anecdotally report that they have far less water retention while using testosterone propionate in
comparison to other longer acting testosterone esters. This lack of water retention and bloat would
seemingly make the user appear leaner and therefore may lead the individual to believe that they are indeed
reducing their body fat, while the water retention that they experience with the longer acting esters may
make them think that they are gaining body fat when that is not the case.

However, a minority of users also report that they hold more water while using testosterone propionate than
either testosterone cypionate or enanthate. This again demonstrates that individuals react quite differently
to various compounds.

Use/Dosing

Levels of the compound will peak after 24-36 hours of administering the drug and begin tapering from
there1,3 . Therefore most individuals will inject testosterone propionate every day or every other day. This
dosing schedule allows an individual to maintain a fairly consistent blood level of the compound, with
injections every day obviously providing the more stable of the two options.

As with the other testosterone esters, the doses of the drug that are taken by users varies to a great degree
depending on the experience and goals of the user. This also includes women administering testosterone.
Women may find that testosterone propionate is the most manageable of the testosterone esters, along with
possibly testosterone suspension or non-estered compounds, due to the fact that it is fast acting and that the
dosing and administration of the compound can be quickly altered if negative side effects become overly
burdensome. With longer acting esters these adjustments are much more difficult to make rapidly and side
effects could become more pronounced and/or exaggerated. For this reason, females who use testosterone
may want to begin with testosterone propionate when choosing which ester to use.

Many users will also often "kick start" their cycles that use long acting estered compounds with testosterone
propionate so that they begin experiencing anabolic and androgenic effects much quicker in their cycles,
without having to endure injections every day or every other day throughout their cycle. This "kick start" will
usually last for three to five weeks until the long acting estered compounds have reached their peak blood
concentrations. To do this, the user simply administers the testosterone propionate along with the long
acting estered compounds.

Individuals may also end their cycles with testosterone propionate and/or other short acting esters so that
their start time for their post cycle therapy is much closer to their last injection and blood levels remain more
stable until the end of the steroid cycle.

Side Effects/Risks

Since testosterone propionate is indeed simply another form of injectable testosterone, the side effects
associated with it are for the most part those commonly encountered with any type of testoserone
 compound. For more specific information about these, including those that may effect women, see the
testosterone enanthate profile in this forum. In this section the side effects, and the characteristics of them,
that are unique to testosterone propionate alone will be dealt with.

Far more than the other testosterone esters, for the possible exception of Sustanon, users of testosterone
propionate will often complain of injection site irratation and swelling2 . Some individuals find that the
reaction that they experience with the ester is so bad in fact that they will have to cease administration of
the compound. As well, due to the frequent injections of the compound and the possibility of injection site
irritation, it is advisible that users rotate injection sites as frequently as possible so that no complications
arise.

Some users also anecdotally report that they are much more likely to experience low grade fevers when using
testosterone propionate in comparison to other testosterone compounds. This symptom will usually only
persist for a few days to a week or more, but can sometimes last far longer.

As should be expected with an ester such as propionate, suppression of endogenous testosterone production
will occur quite soon after the intial administration of the drug1,3 . The usual protocal of post-cycle therapy
and possibly the use of human chorionic gonadotropin during the cycle should be followed, but no special
considerations need to be taken into account because of this.

References

1. Fujioka M., Shinohara Y., Baba S., et al. Pharmacokinetic properties of testosterone propionate in normal
men. J Clin Endocrinol Metab 63 (1986), pp. 1361-4
2. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp.160-2
3. Pope, H.G, Kouri, E.M., & Hudson, J.I. Effects of supraphysiologic doses of testosterone on mood and
aggression in normal men: A randomized controlled trial. Archives of General Psychiatry, 2000, 57, pp. 133-
140

Trenbolone Acetate

Chemical Formula: C20 H24 O3

Molecular Weight of Base: 270.3706
Molecular Weight of Ester: 60.0524
Formula of Base: C18 H22 O2
Formula of Ester: C2 H4 O2
Active life: 2-3 days
Anabolic/Androgenic ratio: 500/500

Trenbolone aka finaplix is often considered the ideal muscle-building compound that can be utilized by
strength athletes and bodybuilders. Its appeal is that it is strong androgen but has no estrogenic activity. This
combination, along with the fat-burning properties of the drug that will be detailed later, makes it a potent
compound that offers several advantages. These advantages however are tempered by some serious
consequences if used improperly.

Trenbolone is a 19-nor steroid and is derived from the compound nandrolone. The difference between it and
nandrolone are the c9 and c11 double bonds. The c9-10 double bond is the reason that trenbolone has no
estrogenic activity. This bond is necessary for the aromatization of the A ring to be possible and by occupying
this bond, no aromatization can occur (1,2).

Trenbolone can affect muscle growth in several different ways, making it one of the best compounds for both
maintaining and adding quality muscle mass. First, trenbolone can greatly increases the level of IGF-1 within
muscle tissue. It also causes muscle satellite cells, those responsible for repairing damaged muscle fibers, to
be more sensitive to IGF-1 and other growth factors. The amount of DNA per muscle cell may also be
significantly increased by using trenbolone1 .
Trenbolone has an extremely strong binding affinity for the androgen receptor as well, even surpassing that
of testosterone. This of course supports the assertion that trenbolone is extremely anabolic as by binding to
the androgen receptor a compound is able to activate the anabolic mechanisms that are dependent upon the
androgen receptor, one of the many ways that anabolic steroids aid muscle growth. Like most other anabolic
steroids, trenbolone also increases nitrogen retention in muscle tissue. However a rather unique
characteristic of the drug is its anti-catabolic abilities. Trenbolone binds with the receptors that interact with
glucocorticoid hormones, these being catabolic hormones3 . By being able to inhibit cortisol and some other
catabolic hormones in the body trenbolone is ideal for those users that are attempting to reduce body fat as
the compound will help to minimize muscle wasting when running a calorie deficit.

Due to the fact that trenbolone is manufactured for the sole purpose of use in animals, there are a few
studies that address its potential effects in humans. Therefore it should be noted that the effects and safety
of trenbolone for human use are being extrapolated from animal studies. This is not to say that nothing can
be learned from animal-based research, but the findings of these studies are simply not one hundred percent
transferable to use in humans.

Despite this caution, trenbolone does have tremendous results with commercially raised livestock and these
results have led countless strength athletes and bodybuilders to experiment with the compound. Most often
it is the concept of "feed efficiency" that is cited when people expound the virtues of trenbolone. Basically
the concept refers to the ratio of feed that results in meat from the animal that can be sold commercially.
Trenbolone has been shown in countless studies and real world use to add muscle to livestock without any
changes in diet. This improved feed efficiency is a result of trenbolone ability to have the body more
efficiently process and use the feed given an animal, as well as utilizing the vitamins and minerals ingested at
a greater rate. This is exactly what a user would hope for in a compound and anecdotally users of trenbolone
have reported that the compound does indeed deliver on its potential, providing the user with dramatic
gains.
Use/Dosing

Like other steroids that are extremely androgenic, trenbolone offers several advantages for a user. First, due
to the androgenic nature of the drug a user can expect a large increase in their strength. This makes the
compound extremely popular with strength athletes. However bodybuilders looking to reduce their body fat
also find that trenbolone can help them achieve their goals as well. This ability to help in the reduction of
body fat stems from the drug's affinity for binding to the androgen receptors. These androgen receptors are
located in, among other places, fat cells. When these androgens bind to the androgen receptors they can
affect these cells and increase fat-burning. When this is combined with the fact that trenbolone has a cortisol
reducing effect along with the ability to bind to the glucocorticoid receptor, it can be understood why this
compound is so highly touted for dieting and the reduction of body fat4 .

As for the ester of trenbolone acetate, acetate is a relatively short-chain ester. It has an active life of two to
three days. Ideally a user would use daily injections to keep blood levels of the compound fairly stable,
however injections every other day will suffice. The acetate ester provides a rapid and high concentration of
the hormone which is beneficial to those seeking quick gains, and coupled with a rapid clearing time the
acetate ester can be discontinued on the onset of adverse side effects without having to wait days or even
weeks for it's effects to diminish.

In terms of cycle length, due to the liver toxicity associated with trenbolone most inexperienced users will
limit their use of the compound to about eight to ten weeks. However, like most compounds, more
experienced users have stretched these limits to accommodate their goals. However if a user chooses to
extend their use of the compound for lengthy periods of time it is imperative that kidney and liver values are
monitored to ensure that no damage to the organs is being done.

Dosages for users are highly dependent on how they react individually to the compound. Many users
anecdotally report that side effects are minimal if doses are kept at certain levels but can turn rather harsh if
doses are increased even slightly. For this reason it is important that inexperienced users start with low doses
of the compound to judge their reaction to it. 50mgs per day is often cited as the standard starting point for
most. However doses even lower than this, such as 75mgs every other day, are used by some with good
results.

Risks/Side Effects

Trenbolone does not exhibit any estrogenic activity and therefore estrogenic side effects are not a concern
with this compound. It is also resistant to the 5 alpha reductase enzyme, but this is of little comfort to a user
as trenbolone is already of the most androgenic drugs in common use by steroid users. For this reason
androgenic side effects should be expected by most users that undertake a cycle of this drug. Prostate
enlargement and oily skin/acne are commonly reported by users. As well anecdotally many users have
reported that trenbolone is one of, if not the, harshest compound for losing one's hair. If a user is genetically
predisposed to male pattern baldness he may want to avoid trenbolone.
Having listed the harsh androgenic nature and side effects associated with trenbolone, it should come as no
surprise that women are not recommended to use this compound. The usual virilizing effects such as
deepening of the voice, body/facial hair growth, and enlargement of the clitoris, among others are likely to
cause problems for female users. These effects can appear at even relatively low doses. Trenbolone is not a
compound that women should attempt to administer.

Now due to the lack of estrogenic side effects associated with trenbolone it would seem that users would
have little to worry about in terms of side effects like gynecomastia, water retention, etc. However
trenbolone is a progestin, meaning that it has the ability to bind to receptors of the female sex hormone
progesterone2 . Also, like other 19-nor compounds trenbolone increases prolactin levels. Side effects related
to these reactions can include breast growth and lactation. To prevent these side effects as they relate to
increased prolactin levels a user can use several compounds including bromocriptine, vitamin b6, and/or
cabergoline. Letrozole can also be used to lower progesterone levels. It should also be noted that trenbolone
lowers thyroid levels temporarily which in turn raises prolactin levels5 . It is therefore advisable that users
may want to use the compound T3 to combat this effect in part.

Being a progestin, trenbolone also has a dramatic effect on users’ natural testosterone production. Much in
the same way that nandrolone does, trenbolone can suppress the natural production of testosterone for
weeks after a user has ceased administering it. For this reason it is advisable that users use testosterone in
conjunction with trenbolone if they wish to avoid sexual dysfunction, libido problems, or mental side effects
associated with a lack of testosterone. Anecdotally many users have also reported that testicular atrophy is
nearly always a problem when using trenbolone and that it is much more dramatic than with other
compounds. Users may wish to administer human chorionic gonadotropin to help counteract this.

The psychological effects of trenbolone use are also quite distinct in some users. Of course the obvious effect
would be a reaction to the androgenic nature of the compound. An increase in aggressiveness is often
reported by users, as androgens help to affect brain chemistry and may cause feelings of well-being, angst,
aggression, or anxiety. As well, anecdotally some users have also reported that they experience vivid dreams
while using the compound.

Kidney and liver function is negatively affected by trenbolone use as well. It is recommended that users
closely monitor these throughout a cycle making sure that no problems arise. As well, users will also report
that darker than normal urine is a common side effect of use of trenbolone. This should not be a cause of
alarm among users; however they should ensure that there is no blood in the urine as this is obviously a sign
of trouble.

Overdoing Tren can cause cholestasis which is indicated by high bilirubin levels, so it is a good idea to include
total bilirubin along with your ALT, AST, GGT markers for liver health6 .
Notes

Tren, Estradiol and Labcorp, Roche ECLIA blood work, Bilirubin bloodwork
The Roche ECLIA assay starts by introducing antibodies that are designed to bind specifically to the what’s
being tested for (in this case estradiol). The antigen also has a ruthenium molecule attached to it that can
emit light with electrical current (through electron excitation). The amount of light that is emitted later
reveals the concentration of the compound being tested for such that the more light detected, the lower the
concentration. But here’s where tren causes problems…

While the antibodies are very specific to estradiol in this particular test, there is cross-reactivity and roughly
0.1% will bind to trenbolone. Doesn’t sound like much, but trenbolone’s structure reduces the excitability of
the ruthenium complex from before, meaning it takes more electricity (and thus electrons flowing through)
to generate any light. Remember, the less light emitted, the higher the concentration of E2 is thought to exist
with this method.

Next, these tiny magnetic beads that are coated with a streptavidin protein are added to the blood. These
beads bind to the estradiol and some of the tren that already attached to the first antibody added (with the
ruthenium that emits light under electrical current).

Now before the electricity flows to detect light, another compound is introduced in a known quantity. in this
case, it is more estradiol that has already been “biotinylated” (estradiol with a vitamin b7 attached to it).
Biotin and streptavidin are extremely attracted to each other, so this new estradiol (that will not emit light)
competes with the existing estradiol to bind to the magnetic beads. The idea is that the more estradiol that
was already in the blood, the more of this new labeled estradiol gets competed off and because this alters
the total light emission, you can extrapolate how much estradiol was in the sample originally.

Unfortunately, the tren doesn’t ever lose its fight to keep its little microbead against the biotinylated
estradiol because tren is king. And as reactions continue, more and more tren ends up swooping in and
dominating like the alpha that it is.

Finally, a magnetic plate pulls all of the compounds that matter out of the solution, and the rest of the blood
is washed away, including your true estradiol levels.

How ECLIA works.

If you need to know your true estradiol levels while running trenbolone, you should request the estradiol
sensitive assay.

References

1.Thompson SH, Boxhorn LK, Kong WY, Allen RE, Trenbolone alters the responsiveness of skeletal muscle
satellite cells to fibroblast growth factor and insulin-like growth factor I, Endocrinology 1989 May, 124 (5) :
2110-7
2. Ojasoo T, Raynaud JP. Unique steroid congeners for receptor studies. Cancer Research 38 (1978) 4186-98
3. Bauer, Meyer et al. Characterisation of the affinity of different anabolics and synthetic hormones to the
human androgen receptor, human sex hormone binding globulin and to the bovine progestin receptor. Acta
Pathol Microbiol Imunol Scand Suppl 108 (2000) 838-46
4. St John LC, Ekeren PA, Crouse JD, Schanbacher BD, Smith SB, lipogenesis in adipose tissue from
ovariectomized and intact heifers immunized against estradiol and/or implanted with trenbolone acetate, J
Anim Sci 1987 May, 64 (5):1428-33
5. Donaldson IA, Hart IC, Heitzman RJ. Growth hormone, insulin, prolactin and total thyroxine in the plasma of
sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol. Res Vet Sci. 1981
Jan;30(1):7-13.
6. ASAIO J. 2006 Jan-Feb;52(1):117-8. Cholestasis induced by parabolan successfully treated with the
molecular adsorbent recirculating system. Anand JS1, Chodorowski Z, Hajduk A, Waldman W.

Trestolone

aka Trestolone Acetate, 7α-methyl-19-nortestosterone (MENT)

Anabolic/Androgenic Ratio: 2300:650
CAS#: 3764-87-2
Chemical Structure: 7α-Methylestr-4-en-17β-ol-3-one
Molecular Weight: 288.431 g/mol g·mol(sup)-1

Description

Trestolone (MENT) is an experimental androgen/anabolic steroid (AAS) and progestogen medication under
development by the USG and university partners for potential use as a form of hormonal birth control for
men and in androgen replacement therapy for low testosterone levels in men, but has never been marketed
for medical use. The compound is an extremely potent 19-nor derivative oft-described as a cross between
tren and deca—but without any of the negative sides of either. Perhaps more so than any other compound,
MENT is highly capable of eliciting serious gains in mass and strength over a relatively short period of time.
Trestolone delivers 10x more myotropic effect of testosterone. The myotropic effect is the effect of building
muscle, making trestolone more effective in building muscle than any other commercial steroid in existence.
In fact, trestolone outperforms trenbolone by a whopping 250% in this area. It's oft-described as “test on
steroids” or “supercharged test.”

Metabolic Equivalence to Testosterone

Trestolone is the only steroid in production today that is capable of sustaining normal male physiology in the
complete absence of testosterone, including sexual functioning.
Trestolone has an anabolic/androgenic rating of 2300:650. In rats, it was found to be roughly ten times as
myotropic as methyltestosterone.

The psychological effects MENT conveys include a positive sense of confidence, euthymia and well-being that
are noted to be more heightened even than those conveyed by testosterone or DHT derivatives Proviron and
Masteron.

Clinical Studies

In a 1992 study in rats investigating the pharmacology of MENT, researchers found the anabolic potency of
MENT to be 10X greater than that of testosterone, while also being 12X more suppressive on HTPA. This
means that if your average male produces 4-7mg of testosterone daily to keep muscle mass and sexual
function, only 400-700mcg of MENT is needed to produce the same results.

In this same study, MENT acetate was used to determine the rate of hydrolysis of the acetate ester and how
quickly elevated MENT plasma levels were reached. The half-life is also VERY short, calculated to be only 40
min for the unesterified compound (not the acetate, which should extend the half-life slightly).

A comprehensive human study conducted on male subjects compared the effects of MENT to testosterone,
both accompanied with the progestin etonogestrel, on spermatogenesis, as well as sex drive and safety
biomarkers associated with androgen use. This was a robust study, containing 29 subjects tested for 48
weeks.8
Participants either received two implant pellets each containing 135mg of MENT acetate calculated to
release 400mcg daily, or three 600mg testosterone pellets, with one given every 12 weeks. Both groups
received 68mg of etonogestrel. Both groups experienced significant reduction in sperm production, with 80%
of both groups going from an average of 55 x 106 mL to just 1 x 106 mL after 12 weeks of supplementation.8
Recovery from MENT was much more rapid than from testosterone. The recovery period was 16 weeks for
the MENT group, in which semen concentration increased to over 20 x 106 mL—whereas the testosterone
group still had azoospermia until after 28 weeks.8

Dosage Guidelines

Weekly dosage is low. In clinical studies, the injectable pellets used released between 400-700 micrograms
per day as replacement for natural testosterone production values between 4-7 milligrams per day—ten
times the strength of testosterone.

A common dose for AAS users is 10 mg per day, or 70 mg per week. Megablast dosages are anywhere from
25-50 mg per day, or 175-350 mg per week, even on up to 100 mg/day. Cycle duration is oft-limited to 6-8
weeks due to extremely rapid physique changes.
 References

1. Wikipedia: Trestolone
2. Reddit Compound Experience Thread: Trestolone
3. Anderson, Richard A., et al. “Evidence for tissue selectivity of the synthetic androgen 7α-methyl-19-
nortestosterone in hypogonadal men.” The Journal of Clinical Endocrinology & Metabolism 88.6 (2003): 2784-
2793.
4. Sundaram, Kalyan, Narender Kumar, and C. Wayne Bardin. “7α-methyl-19-nortestosterone (MENT): the
optimal androgen for male contraception.” Annals of Medicine 25.2 (1993): 199-205.
5. Liu, Aijun, Kathryn E. Carlson, and John A. Katzenellenbogen. “Synthesis of high-affinity fluorine-substituted
ligands for the androgen receptor. Potential agents for imaging prostatic cancer by positron emission
tomography.” Journal of Medicinal Chemistry 35.11 (1992): 2113-2129.
6. Kumar, Narender, et al. “Pharmacokinetics of 7α-methyl-19-nortestosterone in Men and Cynomolgus
Monkeys.” Journal of Andrology 18.4 (1997): 352-358.
7. Walton, Melanie J., et al. "7α-methyl-19-nortestosterone (MENT) vs Testosterone in Combination With
Etonogestrel Implants for Spermatogenic Suppression in Healthy Men." Journal of Andrology 28.5 (2007):
679-688.

Winstrol (Stanozolol)

Chemical structure: 17 alpha-methyl-5alpha- androstano [3,2-c]pyrazol-17 beta-ol

Molecular Formula: C22H36N2O
Molecular weight of base: 344.5392
Active Life: 8 hours for most orals, 48 hours for injectable
Anabolic/Androgenic Ratio: 320/30

One of the most popular and widely recognized anabolic steroids, stanozolol enjoys a high popularity among
steroid users. However, it may actually be one of the more over-used compounds as it's abilities and effects
will only be fully realized by a minority of users who are administering it for a specific purpose.

Stanozolol is a derivative of dihydrotestosterone. Despite this most users of the drug will find that its activity is
quite mild compared to other compounds with similar chemical origins. Individuals that are looking for mass
gains will likely be disappointed if using stanozolol for this purpose. It is widely considered a cutting
compound. Due to the lack of water retention most users find that they can acheive a dry look to their physique
as long as their body fat is relatively low. For the most part, the anabolic effects that are acheived via the use of
this drug are a result of it's ability to increase protein synthesizing and nitrogen retention2,4 . However as stated
previously these effects are mild at best.

Anecdotally a majority of users will report that their joints and ligaments have a dry feeling when using
stanozolol, complaining often of ligament pain when lifting heavy. This would seemingly make the drug a
poor choice for athletes other than bodybuilders who are trying to acheive a specific "look", but there is some
scientific evidence that suggests that stanozolol could in fact strengthen tendons and ligaments. However, with
the vast majority of users reporting ligament and joint pain while on the compound it is difficult to recommend
any attempt to administer the drug if peak performance is desired for athletic competition.

Like most anabolic steroids oral administration of stanozolol has a rather dramatic effect on levels of sex
hormone-binding globulin in the body. In the case of stanozolol however, it can be quite potent relatively
speaking. It is because plasma binding proteins, like sex hormone-binding globulin, act to temporarily prevent
steroid hormones from exerting their intended activities. By limiting this, it results in a greater percentage of
free steroid hormone circulating in the body. This may actually result in a mechanism whereby stanozolol
could help to increase the potency of a concurrently used steroid5 . Whether this benefit would be worth
actually running stanozolol in a cycle that would otherwise not include it would be something that the user
would have to experiment with him or herself as there is simply not enough evidence to make a definitive
conclusion one way or the other.

Use/Dosing

Stanozolol is available as both an oral steroid as well as an injectable. While there are no differences in the
compound itself, there are several advantages and disadvantages to using each compound. First, in an animal
study, it was demonstrated that the injectable version of the compound was far superior to the oral
administration of the drug for nitrogen retention2 . This of course means that it is better able to help preserve or
build lean-body mass, something obviously one who is using the compound would be seeking.

Another advantage of injecting stanozolol is that it will negate the first pass of the compound through the liver
and therefore is less toxic to the organ. Despite these advantages however, there are a few disadvantages of
choosing to inject, namely the comfort of the user. Stanozolol is notorious for causing pain at the injection site
upon administration and for possibly several days afterwards, as anecdotally reported by users. This will often
cause users to begin administering the compound orally, especially when due to the compound's unique
structure, the injectable version can be taken orally as well.

With the active life of stanozolol being only eight hours, multiple doses of the oral compound throughout the
day is recommended. As for injections, once a day is optimal to maintain stable blood levels of the compound,
but every other day should be adequate due to it's active life.

Male users will often find that doses in the range of 25-100mgs per day to be adequate for seeing results with
this compound. It is often anecdotally reported that most first time users will usually administer 50mgs per day
and are generally happy with the effects.

Stanozolol is a drug that is fairly popular with women as well. This is primarily due to the compound's
anabolic nature, with the likelihood of androgenic side effects being rather small. First time female users
anecdotally report that doses ranging from 5-15mgs per day will result in quite dramatic gains. However like
 most compounds, users have experimented with doses far higher with the risks of the associated side effects
becoming more pronounced as the dosages increase.

Due to the toxicity issues related to stanozolol it is most often recommended that users limit their cycles of the
compound to six weeks or less. However many users have exceed this limit while running high doses and have
reported little to no complications. If an individual does decide to run stanozolol for an extended period of time
he or she should monitor their liver values via blood tests to ensure that no permanent damage occurs.

Side Effects/Risks

The oral form of stanozolol is a 17-alpha-alkylated substrate and due to this liver toxicity should be a concern
to those who take this compound. Elevated liver values will undoubtedly occur while running this drug. Even
with the injectable version, liver damage can occur so precautions need to be taken.

Stanozolol is also very harsh on the user’s cholesterol levels often lowering HDL and raising LDL at the same
time, even at extremely small doses. Users with histories of health problems related to cholesterol should be
wary of using this compound.

Androgen related side effects such as acne, prostate enlargement and an aggravation of male pattern baldness
are often reported by users. Anecdotally many users have reported that stanozolol is one of the harshest drugs
in terms of hair loss. Many will simply not risk running the compound because of this.

As mentioned previously estrogenic side effects are not a factor with this compound as it does not aromatize.
Virilizing side effects in women are much less likely to occur than with most other anabolic compounds, but
there is still a risk that these may develop, especially with larger doses. As always these include deepening of
the voice, body/facial hair growth, and enlargement of the clitoris, among others.

References

1. Ellis AJ, Cawston TE, Mackie EJ., The differential effects of stanozolol on human skin
and synovial fibroblasts in vitro: DNA synthesis and receptor binding., Agents Actions
1994 Mar;41(1-2):37-43
2. Olson ME, Morck DW, Quinn KB. The effect of stanozolol on 15nitrogen retention in the
dog. Can J Vet Res. 2000 Oct;64(4):246-8
3. Minuto F, Barreca A, Melioli G. Indirect evidence of hormone abuse. Proof of doping? J
Endocrinol Invest. 2003 Sep;26(9):919-23.
4. Brestel EP, Thrush LB., The treatment of glucocorticosteroid-dependent chronic
urticaria with stanozolol., J Allergy Clin Immunol 1988 Aug;82(2):265-9
5. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 173-5
 15 HEPATOTOXICITY
It is a well-known fact that most oral anabolic steroids, as well as a select few injectable anabolic steroids
induce a measure of liver toxicity (properly referred to as hepatotoxicity) in the body. The range of
hepatotoxicity that these compounds can cause varies a great deal, ranging from very minor to serious life-
threatening damage. The word "liver toxicity" and "hepatotoxicity" is thrown around a lot in bodybuilding
circles and throughout the anabolic steroid using community, but how many people actually understand
what these terms mean? How many people actually know what specifically it is that is "toxic" about the
anabolic steroid in the liver? What is it that actually happens to the liver cells (hepatocytes)? The majority of
people who throw around the words "liver toxic" will not be able to answer those questions at all. This is
where that should change. After reading through this post, you will understand why certain anabolic steroids
cause hepatotoxicity, what hepatotoxicity actually is, and how it affects the body, and most importantly:
what you can do about it and what liver protectants to take.

Drug Metabolism

When it comes to drug metabolism, the liver’s primary function is to metabolize the drug into a form that is
suitable for elimination by the kidneys. The main goals of this metabolism is to reduce fat solubility, make the
drug water soluble, and to decrease its biological activity so that it stops working. This occurs for not only
foreign substances (known as xenobiotics, which drugs are considered), but also endogenous chemicals. Drug
metabolism in the liver exists in two main phases, phase I and phase II.

• Phase I: Phase I metabolism happens primarily in the smooth endoplasmic reticulum of hepatocytes. The
main purpose of this phase is to make lipid soluble compounds water soluble. This typically renders the
metabolites of the drug to be inactive, but not always. This is the phase that we want to focus on with oral
steroids, and is where the C17aa comes into play in protecting the steroid from being degraded by the liver.
• Phase II: Phase II metabolism takes place in the cytosol of hepatocytes. In this phase, the products from
phase I will undergo conjugation to increase their water solubility.

The efficacy of the enzymes used in drug metabolism are age-dependent. In newborns and the geriatric, the
ability to metabolize drugs is greatly decreased. Smoking can increase the efficacy of drug metabolism
through the inhalation of polycyclic aromatic hydrocarbons. This is most noticeably manifested in the
increased metabolic activity of caffeine.

Anabolic Androgenic Steroids

C17-Alpha Alkylation & What It Does

It's common knowledge that oral steroids are known as being liver toxic, while injectable anabolic steroids
are not (at least not to as great of an extent as orals are). There is a reason for this, and that is: C17-alpha
alkylation (C17aa). Without the C17aa modification, very little of the anabolic steroid when ingested will
survive hepatic metabolism (liver metabolism), and not enough of it will reach the bloodstream to produce
any noticeable effects. It was then discovered at one point, that by modifying the chemical structure by
adding a methyl group (also known as an alkyl group) to the 17th carbon on the steroid structure (also known
as carbon 17-alpha), it would allow the anabolic steroid to become more resistant to the hepatic metabolism
that would previously render the majority of the ingested steroid into inactive metabolites. This chemical
bonding of a methyl group onto the 17th carbon is what is known as C17-alpha alkylation. It is because of
C17-alpha alkylation, that the anabolic steroid becomes orally active and bioavailable – without it, the
anabolic steroid would not survive liver metabolism. However, the negative downside in this case is that of
increased hepatotoxicity (increased liver toxicity). C17-alpha alkylation allows an anabolic steroid to become
more resistant to hepatic breakdown, and any compound that is further resistant to hepatic breakdown will
always have greater hepatotoxicity associated with it for various reasons. But how does this happen?

C17aa effectively alters the chemical structure enough to block the enzyme 17beta-hydroxysteroid
dehydrogenase (17beta-HSD) from interacting with the hormone in the liver, which would normally
metabolize the steroid into an inactive metabolite. However, the liver is now forced to metabolize the
anabolic steroid through other means. At this point in time, it is unknown as to how exactly the C17aa
modification causes hepatotoxicity, but it is strongly hypothesized that because the liver contains a high
concentration of androgen receptors[1] , the now unaltered and unmetabolized anabolic steroid (which is now
instantly highly active) that is making the first pass through the liver will exhibit heavy amounts of androgenic
activity in the liver because its metabolism has been blocked. Because it is being ingested orally, and
therefore makes the first pass through the liver, the liver then becomes exposed to massive concentrations
of these active anabolic steroids immediately, rather than through the injection route of administration
where the anabolic steroid does not have to make a first pass through the liver (and therefore the liver is not
exposed to massive amounts of active androgens all at once). The fact that studies have demonstrated that
the greater the androgenic strength an oral anabolic steroid exhibits, the worse the hepatotoxicity is, lends
credence to the theory that androgenic activity is correlated with hepatotoxicity in oral AAS.[2][3]

Trenbolone
Trenbolone does not possess C17-alpha alkylation, however, it is known to possess ever so small amounts of
hepatotoxicity. This is believed to be because of the nature of Trenbolone’s chemical structure, which causes
Trenbolone to exhibit a higher resistance to hepatic metabolism and breakdown even though it is not C17-
alpha alkylated. The small amount of hepatotoxicity is not a large cause for concern at all, as Trenbolone’s
minute amount of liver toxicity does not even reach the amounts of toxicity exhibited by oral C17-alpha
alkylated anabolic steroids. The slight hepatotoxicity can be a concern for individuals with pre-existing liver
problems (known or unknown) and this should be kept in mind. Every potential Trenbolone user should
always have blood work (see Liver Function Tests below) done in order to monitor liver enzyme readings
regardless, and a proven liver support supplement (see Liver Protection below) can be utilized during a
Trenbolone cycle for the extra assurance of proper liver function.
 Drug Induced Hepatotoxicity

Drug induced hepatotoxicity can have many causes. Some medications cause direct damage to hepatocytes
while others block certain metabolic processes. As an example, acetaminophen itself is not the source of
hepatotoxicity, but rather one of its metabolites. When taken in extreme quantities, this metabolite
accumulates because the enzymes required are unable to keep up in phase II metabolism and cell damage
occurs. Likewise, mitochondrial damage can increase oxidative stress which can damage hepatocytes.

These causes are categorized in seven general categories based on the mechanism of hepatotoxicity. The
main categories where AAS and ancillaries are implicated are:

• Steatosis: Steatosis is the accumulation of triglycerides in the liver. Liver function tests (LFTs) are unreliable
when it comes to the diagnosis of hepatic steatosis. Often will have an AST/ALT ratio < 1. Imaging and
possible biopsy is required to make an accurate diagnosis. AST and ALT both upwards of 4 times ULN.
Tamoxifen and Raloxifene have been shown to induce hepatic steatosis.
• Zonal Necrosis: Zonal necrosis is essentially the death of cells in a specific zone of the liver. This is the most
common manifestation of hepatotoxicity. This will cause an increase in ALT with normal ALP levels. This can
be caused by C-17-alpha-alkylated (C17aa) steroids.
• Cholestasis: Cholestasis is the impediment of biliary flow from the liver through the biliary tract. This is the
cause of jaundice. The increase in bilirubin causes a yellowing of the skin and that is occurs with itching.
C17aa steroids may cause hepatotoxic cholestasis. This can be seen on labs as normal levels of ALT and > 2
times ULN ALP. The mechanism of this is not well known. Testosterone and 19-nortestosterone compounds
have been implicated in cases of hyperbilirubinemia, but rarely to the point of jaundice. (More on this
below).
• Hyperplasia and Neoplasia: C17aa compounds have been implicated in cases of hepatic hyperplasia and
neoplasia, essentially cancer. However, non-C17aa steroids have also been noted as a cause of liver cancer in
medical case reports.
• Vascular Lesions: These vascular lesions are known as Peliosis Hepatis. These lesions are present on
endothelial cells of hepatic vasculature and is typically asymptomatic. This can eventually lead to
hepatomegaly (enlarged liver) and frequently death if untreated.

Effects of liver damage include jaundice, ankle edema, gynecomastia, increased bleeding due to decrease in
clotting factor synthesis. Most of these effects come from deficiencies in synthesis of their respective plasma
proteins. For example, damage to hepatocytes that are responsible for synthesis of SHBG will result in a
decrease in SHBG. This will alter the free estrogen/free androgen ratio, potentially inducing gynecomasta.
Likewise, a decrease in plasma proteins will change the blood colloid osmotic pressure, causing a change in
capillary net filtration pressure leading to edema in the lower extremities.
 Cholestasis
Cholestasis is the most common form of liver damage that is characteristic of the use/abuse of oral anabolic
steroids.[4] As already stated, it is the condition whereby bile is unable to properly flow throughout the liver
and into the duodenum (the first section of the small intestine that connects to the stomach). This can occur
as the result of a physical (also known as a mechanical) blockage, such as gallstones or a tumor formation
causing blockage. The other form of blockage is in the form of a chemical blockage (also known as metabolic
cholestasis), which is cholestasis that is resultant of a disruption of the hepatic cells' ability to properly
manufacture and flow bile. C17aa anabolic steroids cause metabolic (chemical) cholestasis. Metabolic
cholestasis can also be the result of a hereditary genetic dysfunction, and there are plenty of other
substances, drugs, and medications that can cause cholestasis as well. In order to understand cholestasis, it is
important to know what bile is and what it does for us.

Bile is a dark green/yellow to brown fluid that is manufactured by the cells of the liver, and consists of 85%
water, 10% bile salts, 3% muscuous and pigments, 1% fats, and 0.7% inorganic salts. The primary function of
bile is to digest fats that are consumed in food, making it a very important component in the digestion and
processing of food. Because it is involved in the digestion and breakdown of fats, it is very important for the
proper breakdown and absorption of fat-based and fat soluble compounds (such as many types of vitamins).
In addition to this, bile serves to act as an excretion vehicle for the transport of metabolites out of the liver,
such as bilirubin which is a metabolic byproduct as a result of the liver cells recycling red blood cells. Finally,
an additional function that bile serves (and this is very important) is the neutralizing of acidity of the contents
of the stomach (as a result of stomach acid) before it enters the intestines. A simultaneous role bile plays in
that process is also a disinfectant, killing bacteria that could be in the ingested food.

When the C17aa anabolic steroids inhibit the flow of bile in the liver, bile will build up in the small bile ducts
of the liver forming plugs (known as canalicular bile plugs). The cells of the liver (hepatocytes) will continue to
attempt to excrete bile as they normally would, but as bile accumulates due to the plugs, enough pressure
will build until the lining cells of the bile ducts rupture. As a result, bile spills out onto other cells and tissue,
resulting in cell death. Cells will begin to build up with bile as well (more common in intrahepatic
chemical/metabolic cholestasis), and without proper flow of bile, the cells will die. This build-up of bile is
known as a bile pool, and while not all of the bile acids contained in the bile pool are hepatotoxic, most of
them are, and this is why the bile pool accumulation results in liver cell death. C17aa anabolic steroids cause
intracellular bile retention within the hepatocytes (bile accumulation inside the liver cells).

Symptoms of Cholestasis:

• Nausea

• Malaise

• Anorexia, loss of appetite

• Vomiting

• Abdominal pain/burning (almost like heartburn/burning sensations due to the lack of bile being excreted to
neutralize the acidity of stomach content entering the duodenum).

VERY IMPORTANT: what is commonly mistaken for heartburn by many people while using oral C17aa
anabolic steroids is actually varying stages of cholestasis.

• Pruritus (itching)

• Clay colored dark stool

• Pale stool (strong indication of physical/mechanical cholestasis rather than metabolic/chemical cholestasis)

• Dark amber colored urine

• Jaundice (strong indication of physical/mechanical cholestasis, but can occur with metabolic/chemical
intrahepatic cholestasis if it reaches worsened stages)

Although cholestasis can normally be recovered from if C17aa steroids are halted early enough, the body
might require months before liver function is properly restored, and this is why it is very important to
maintain proper liver function during the use of C17aa compounds with the supplementation of a proper
liver support compound.

Liver Function Tests

Liver Function Tests can be done to assess hepatic function. These are not exactly conclusive and require
some sort of follow up to assess the degree of severity. Often this will be some sort of imaging or biopsy.
Most of these biomarkers are assessed in a multiplication of the upper limit of normal (ULN), which is the top
end of the normal range.

Aminotransferases: Aminotransferases are enzymes that are used in the synthesis of amino acids. There are
two aminotransferases that are checked as part of an LFT.
• Aspartate Transaminase (AST): Reference range: 8 - 40 IU/L. While AST is found in the liver, this enzyme is
also found in great quantities in cardiac and skeletal muscle. Because of these other sources, AST alone is not
a good indicator of liver damage. Essentially, AST does not require the entire cell to be damaged for it to
enter the plasma, where ALT does. This is due to its location within the cell. If AST is elevated then there is a
good possibility that the source of the AST is from muscle damage. This can be caused by myocardial
infarction (heart attack), rhadomyolysis, and even resistance training. This is why slightly elevated AST levels
should not be of concern if you lift frequently.
• Alanine Transaminase (ALT): Reference range: ≤ 52 IU/L. Much like AST, ALT is an enzyme used to catalyze
the synthesis of amino acids. Unlike AST, ALT is found predominantly in the liver and requires significant
damage to hepatocytes for it to be released in to the plasma.
AST to Platelet Ratio Index (APRI): This typically won’t be included in lab tests, but it is easy to figure out. An
online calculator can be found here. APRI has been shown to be a predictor of liver cirrhosis.
Alkaline Phosphatase (ALP): Reference rage: 30 - 120 IU/L. ALP is an enzyme that is located within hepatic
biliary ducts. Elevations in plasma concentrations of this enzyme are indicative of either cholestasis or biliary
obstruction. In these pathologies, ALT and AST may remain unaffected.
Total Bilirubin: Reference range: 0.1-1.0 mg/dL. Bilirubin is a byproduct of hemoglobin catabolism. The heme
group of hemoglobin is broken down into biliverdin, then bilirubin, which is transported to the liver for the
production of bile salts along with urobilin (the pigment that makes urine yellow) and stercobilin (the
pigment that makes feces brown). High hepatic sources of bilirubin are indicative of cirrhosis or hepatitis.
5'-nucleotidase (5'NTD): Another biomarker used int he diagnosis of cholestasis.

Liver Protection

TUDCA / UDCA

For Additional Information & Studies, Be Sure To Visit The Examine Page

Tauroursodeoxycholic acid (TUDCA) and Ursodeoxycholic acid (UDCA) are bile acids themselves that are non-
toxic to the liver and in fact have been proven to exhibit the exact opposite - they assist in bile flow through
various different pathways which will be covered shortly. TUDCA is simply the taurine conjugate of UDCA
(UDCA with a taurine amino acid bound to it), which has been claimed to exhibit greater oral bioavailability,
but both variants have been proven to work very effectively. TUDCA and UDCA used to be extracted from the
liver of bears, but synthetic methods have since been developed in order to manufacture these compounds,
as well as the ability to derive them from other sources.

By far the most effective liver support compound available, TUDCA and UDCA are compounds that serve to
speed up the metabolic transition of toxic bile acids to less toxic bile acids, and they also serve to increase the
manufacture of non-toxic bile acids from cholesterol.[5] The result is a decrease in the toxicity of the bile pool.
Remember when I mentioned above that liver toxicity from oral anabolic steroids (in the really bad stages)
results in bile building up in the hepatocytes (liver cells) until they rupture and bile spills out onto other cells
killing them? Well, the bile being spilled out consists of mostly toxic bile salts. TUDCA and UDCA are beneficial
non-toxic bile salts that will essentially balance out the toxicity of the bile pool and serve to neutralize the
toxicity making it less toxic to the surrounding resident liver cells. TUDCA and UDCA have also shown to
increase amounts of the bile salt export pump (a transporter protein) in the liver cells, thus increasing the
flow of bile as a result.[6] What this means is that they will facilitate the flow of bile in the liver so that the bile
pool will not remain stagnant damage the surrounding liver cells. A good analogy to explain this is using the
'hot potato' analogy where a group of people in a circle are throwing a hot potato around from person to
person fairly quickly. As long as the hot potato is passed around at a constant pace, no single person's hand
will get burned, but if the hot potato is to remain in one person's hand for too long, they will end up doing
damage to their hands by being burned (which is much like a stagnant bile pool in the liver damaging the
 surrounding cells). These compounds have also demonstrated to serve as antiapoptotics in liver cells, which
means they effectively block the transcription factor known as AP-1, which is activated during cholestasis due
to various toxic bile salts that will activate death receptors on liver cells.[7]
TUDCA and UDCA are by far the best quintessential treatments for both the prevention of cholestasis, as well
as the recovery from it. They are, quite literally, the compounds specific to the treatment and mitigation of
oral C17-alpha alkylated anabolic steroid liver toxicity - this cannot be said of any other liver support
supplement/compound. In addition to treating cholestasis very effectively, it has demonstrated in studies to
also reduce the risk of hepatitis B, where they had significantly decreased the risk of having abnormal serum
alanine aminotransferase activity at the end of treatment compared to the beginning.[8] Other studies have
also shown that UDCA and TUDCA are beneficial in the treatment necroinflammatory liver disease, such as
(and especially for) hepatitis C-related chronic hepatitis in which bile duct damage and some degree of
cholestasis are frequently seen at histology, and the study had observed that TUDCA had significantly
improved the biochemical expression of chronic hepatitis.[9] In general, TUDCA seems to prevent hepatic cell
death.[10]
Dosing of TUDCA and UDCA: 500-1000mg daily for the maintenance of healthy liver function during the use
of a C17aa oral during a cycle. 1,000mg or higher daily for the purpose of repairing the liver following heavy
hepatotoxicity and hepatocyte damage from cholestasis (and/or for individuals with serious liver disorders).
IMPORTANT: Do not exceed 8 weeks of TUDCA/UDCA use, as it can increase negative cholesterol values and
decrease HDL. It is recommended to use these bile salts only during a cycle of oral C17aa anabolic steroids, or
for the purpose of liver repair following periods of significant hepatotoxicity from the use of these
compounds. Other compounds should be sought after for general year-round liver support.
According to this study (taken from Examine), TUDCA has been shown to decrease HDL levels when taken for
extended periods of time. In normal people, this really isn't a big deal. In people who are constantly using
steroids, like blasting and cruising (B&C), it can become counter-intuitive to run TUDCA for no reason due to
decreased HDL levels. For example, on a cruise one wants to let their body recover, and ideally see good
bloodwork before blasting again. One key reading on the bloodwork is the HDL, as HDL is one marker that
almost always drops significantly while taking exogenous steroids in large dosages.

Also, according to the FDA as listed in UDCA's medication safety profile (two sources below), UDCA should
not be taken without direct indication to do so, i.e. gallstones or primary biliary cirrhosis. The pros of taking
TUDCA and UDCA while not on oral steroids or having one of the aforementioned indications do not
outweigh the cons. TUDCA should not be used for year round general liver support, as there are other
options (discussed below) which do not have these negative drawbacks, thus making the choice clear.

• Product Information: URSO 250(R) oral tablets, ursodiol oral tablets. Aptalis Pharma US, Inc. (per FDA),
Bridgewater, NJ, 2013.
• Product Information: URSO Forte(R) oral tablets, ursodiol oral tablets. Aptalis Pharma US, Inc. (per FDA),
Bridgewater, NJ, 2013.
NAC (N-acetylcysteine)

For Additional Information & Studies, Be Sure To Visit The Examine Page
NAC (N-acetylcysteine) is an excellent liver protectant/support compound that has demonstrated
effectiveness in mitigating hepatotoxicity[11] as well as successfully treating acetaminophen (Tylenol) induced
hepatotoxicity,[12] which is an added benefit for NAC that TUDCA does not do. NAC has also demonstrated
some pretty good effectiveness at mitigating and preventing cholestasis as evidenced by studies. One
particular study administered 300mg/kg of NAC orally to rats for 28 days, and not only did NAC
administration reduce elevations of liver enzyme values that would otherwise be high without NAC
administration, it also seemed to improve renal (kidney) function as well![13] That same study indicated,
though, that NAC's activity in ameliorating cholestasis is not through the same pathway as TUDCA. NAC's
ability to prevent or cure cholestasis stems from its antioxidant and immunomodulatory properties.
Acetylcysteine serves to increase the glutathione reserves in the body and, together with glutathione, they
both directly bind to toxic metabolites. This serves to protect hepatocytes (liver cells) from succumbing to
toxicity from Tylenol or cholestasis. TUDCA instead operates through the direct action of essentially
'balancing' the content of bile salts (TUDCA is itself a bile salt), and while it does assist in mitigating
cholestasis, it does not do anything for Tylenol-related toxicity. Another study also investigated NAC's ability
to help alleviate cholestasis, which focused a little more on the observation of the renal (kidney) related
effects, and found that in addition to improved liver enzyme values, NAC had the ability to vastly improve
markers of kidney function and was actually able to even double the rate of sodium excretion.[14] This would
also strongly indicate that NAC might prove very useful for the elimination of sodium and its related water
retention in the body, which is something that might be of particular interest for anabolic steroid using
individuals who might be having problems with water retention during a cycle.
The problem, however, with NAC is that it has demonstrated very poor oral bioavailability,[15] and this is the
reason as to why high oral doses of NAC were utilized in studies for the treatment of Tylenol poisoning
compared to when the subjects were administered NAC through the IV (intravenous) route of administration.
Aside from NAC's ability as a nephroprotective (kidney protecting) and hepatoprotective (liver protecting)
agent, it is well documented to serve a myriad of other benefits to the body. Although these benefits of NAC
do not pertain to the main topic at hand (liver support during anabolic steroid use), it is very informative and
helpful to know and understand that NAC has potential applications that are extremely far reaching beyond
simply liver and kidney function.
Dosing of NAC: As previously mentioned, there are issues in regards to poor oral bioavailability with NAC. IV
and inhalation formats of NAC do exist, but are generally prescription-only, depending on which country.
However, the oral format of NAC is generally widely available for purchase almost anywhere. Be sure to look
for a NAC product that has chelated it to an element or compound to provide greater bioavailability. With
that being said, a proper dose for the purpose of maintenance of liver health during a cycle of C17-alpha
alkylated anabolic steroids would be in the range of 1,000mg - 2,000mg of NAC per day. NAC can be used
year-round as a general liver support, and should be run at 1,000mg per day or less when not utilizing C17-
alpha alkylated oral anabolic steroids.
IMPORTANT: Studies have demonstrated that high doses of NAC can cause lung and heart damage in
mice[16] due to the fact that NAC is metabolized in the body to S-nitroso-N-acetylcysteine (SNOAC). In large
enough amounts, SNOAC leads to significantly increased blood pressure in the lungs and the right ventricle of
the heart. This is why it is advised to not exceed the standard dose of 1,000mg - 2,000mg per day while on
C17aa oral anabolic steroids. Other than this warning, it should be mentioned that the implications of long-
term NAC use (at any dose range) are currently unknown and have not been investigated. This is not to say
that long term use is a bad thing, but that we simply do not know if the outcome is indeed good or bad.

What About Other Liver Protectants?

TUDCA and UDCA should be considered first above all else when using hepatotoxic anabolic steroids, as they
treat the mechanisms specific to cholestasis. NAC is very beneficial as well. The other options, are just
secondary aids as they are not nearly as beneficial for C17aa.

Choline & Inositol

For Additional Information & Studies On Choline, Be Sure To Visit The Examine Page

Choline can be used as a daily supplement for general health and/or a liver protector while on oral steroid
course. Choline cannot replace TUDCA and should be used in addition to TUDCA while taking oral steroids.
Choline should be used in conjunction with Inositol and many products that you will find will contain both
anyway.

Deficiency in dietary choline can lead to triglyceride accumulation (hepatic fatty acids) and impair TG release
from the liver due to less phosphatidylcholine being made.

For general liver health take 250-500 mg of choline once per day

For liver protection while on oral steroids take 1-2 g in two even doses per day (ie 1000mg or 1 g is 500 mg
twice a day, 12 hours apart or so)

For Additional Information & Studies On Inositol, Be Sure To Visit The Examine Page

Inositol may also be used as both a daily supplement for general health and/or as adjunct liver protection to
TUDCA while on oral steroids. Again, taking inositol and choline together is important.

Inositol the word itself refers to a group of 9 molecules that all have similar structures, termed
stereoisomers. The key isomer that we are focusing on is MYO-INOSITOL and this is the isomer that we want
to supplement and take. Pretty much all OTC supplements with inositol will be this isomer, but always double
check to be sure you are getting the right one.
 Inositol shows promising effects in restoring insulin sensitivity and decreasing LDL and acne, and has many
other slight positive beneficial effects which can be found under the "Human Effect Matrix" category on the
examine.com page linked just above.

For general liver health and oral steroid protection, inositol doses will typically be in the 2g-4g range, and it is
advised to take these doses in two split even doses per day, roughly 12 hours apart.

Milk Thistle
For Additional Information & Studies, Be Sure To Visit The Examine Page

Milk thistle, which contains silymarin and silybin are known as being powerful antioxidants in the liver in
particular. Many studies have been conducted on the efficiency and have demonstrated them to exhibit a
plethora of beneficial properties in liver tissue. However, milk thistle is not very effective for treating
cholestasis in particular. As a general liver health support, it is not too bad. However, almost all of the studies
performed on milk thistle’s effectiveness had administered the test subjects the compound via injection,
which would provide near 100% bioavailability. Milk thistle consumed orally is a different story. Milk thistle
can serve as a beneficial addition to TUDCA and UDCA, but should not be substituted as a first-line treatment
for cholestasis. TUDCA should be reserved for the first-line treatment of cholestasis and should be the
primary liver protectant while on a cycle of C17-alpha alkylated oral anabolic steroids.

Liv.52 (LiverCare)
Liv.52 is an herbal medicine used widely in Europe and Asia to support metabolic and liver health. While in
some countries this product is regarded as a drug, it contains all natural ingredients including capparis
spinosa, terminalia arjuna, cichorium intybus, achillea millefolium, solanum nigrum, tamarix gallica, and
cassia occidentalis. There have been medical studies have been conducted on Liv.52 in recent years, many of
which involve its ability to protect the liver from damage by alcohol or other toxins. Note that while these
studies lend support for the use of a natural remedy like Liv.52 during hepatotoxic steroid administration,
they do not provide complete assurance that this remedy can prevent liver damage. Also some of the studies
may have some bias, so be sure to use caution when reviewing them.

A Final Word

• TUDCA or UDCA should be every anabolic steroid user's first choice for on-cycle liver protection during the
use of oral C17-alpha alkylated anabolic steroids.

• Following this, NAC is an excellent choice to go along TUDCA / UDCA, and also is a great choice for year-round
general liver protectant.

• Another great choice for year-round general liver protectant is Choline & Inositol, but it shouldn't be your
choice for liver protection during use of oral C17-alpha alkylated anabolic steroids.
• Milk Thistle & Liv.52 (LiverCare) can provide some benefits, but they in NO WAY should be your only liver
protection during use of oral C17-alpha alkylated anabolic steroids.

References

The majority of this wiki page was taken and expanded from this thread by /u/canal_of_schlemm, as well as a
thread by DanC
1. Cellular distribution of androgen receptors in the liver. Hinchliffe SA, Woods S, Gray S, Burt AD. J Clin Pathol.
1996 May;49(5):418-20.
2. Liver toxicity of a new anabolic agent: methyltrienolone (17-alpha-methyl-4,9,11-estratriene-17 beta-ol-3-
one). Kruskemper, Noell. steroids. 1966 Jul;8(1):13-24.
3. T. Feyel-Cabanes, Compt. Rend. Soc. Biol. 157, 1428 (1963).
4. anabolic-androgenic steroids and liver injury. M Sanchez-Osorio et al. Liver International ISSN 1478-3223 p.
278-82.
5. Ursodeoxycholic acid and bile-acid mimetics as therapeutic agents for cholestatic liver diseases: an overview
of their mechanisms of action. Poupon R. Clin Res Hepatol Gastroenterol. 2012 Sep;36 Suppl 1:S3-12. doi:
10.1016/S2210-7401(12)70015-3.
6. Tauroursodeoxycholic acid inserts the bile salt export pump into canalicular membranes of cholestatic rat
liver. Dombrowski F, Stieger B, Beuers U. Lab Invest. 2006 Feb;86(2):166-74.
7. Tauroursodeoxycholic acid reduces bile acid-induced apoptosis by modulation of AP-1. Pusl T, Vennegeerts T,
Wimmer R, Denk GU, Beuers U, Rust C. Biochem Biophys Res Commun. 2008 Feb 29;367(1):208-12. doi:
10.1016/j.bbrc.2007.12.122. Epub 2007 Dec 27.
8. Bile acids for viral hepatitis. Chen W, Liu J, Gluud C. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003181.
9. Tauroursodeoxycholic acid for the treatment of HCV-related chronic hepatitis: a multicenter placebo-
controlled study. Crosignani A, Budillon G, Cimino L, Del Vecchio Blanco C, Loguercio C, Ideo G, Raimondo G,
Stabilini R, Podda M. Hepatogastroenterology. 1998 Sep-Oct;45(23):1624-9.
10. Effect of tauroursodeoxycholic acid on bile acid-induced apoptosis in primary human hepatocytes. Benz,
Angermüller, Otto, Sauer, Stremmel, Stiehl. European Journal of Clinical Investigation Volume 30, Issue 3,
pages 203–209, March 2000.
11. The protective effects of n-acetylcysteine against acute hepatotoxicity. Sahin S, Alatas O. Indian J
Gastroenterol. 2013 Mar 10.
12. The biochemistry of acetaminophen hepatotoxicity and rescue: a mathematical model. Ben-Shachar R, Chen
Y, Luo S, Hartman C, Reed M, Nijhout HF. Theor Biol Med Model. 2012 Dec 19;9:55. doi: 10.1186/1742-4682-
9-55.
13. Antifibrotic and antioxidant effects of N-acetylcysteine in an experimental cholestatic model. Galicia-Moreno
M, Favari L, Muriel P. Eur J Gastroenterol Hepatol. 2012 Feb;24(2):179-85. doi:
10.1097/MEG.0b013e32834f3123.
14. Acute cholestasis-induced renal failure: effects of antioxidants and ligands for the thromboxane A2 receptor.
Holt S, Marley R, Fernando B, Harry D, Anand R, Goodier D, Moore K. Kidney Int. 1999 Jan;55(1):271-7.
15. Pharmacokinetics of N-acetylcysteine in man. Borgström, L.; Kågedal, B.; Paulsen, O. (1986). European Journal
of Clinical Pharmacology 31 (2): 217–222. doi:10.1007/BF00606662. PMID 3803419.
16. S-Nitrosothiols signal hypoxia-mimetic vascular pathology. Palmer, Lisa A.; Doctor, Allan; Chhabra, Preeti;
Sheram, Mary Lynn; Laubach, Victor E.; Karlinsey, Molly Z.; Forbes, Michael S.; MacDonald, Timothy; Gaston,
Benjamin (2007). Journal of Clinical Investigation 117 (9): 2592–601. doi:10.1172/JCI29444. PMC 1952618.
PMID 17786245.
17. Drug Induced Cholestasis

16 ANCILLARIES / RELATED
Compounds in this section are sometimes used to support AAS use in general. They cover a wide range of
uses, and, as with most AAAS use, these are typically used for purposes which are off label. Therefore,
information and actual studies are hard to obtain. Aromatase Inhibitor (AI), Reversible, Non-steroidal --
These drugs inhibit aromatization by reversible competition for the aromatase enzyme. By using up the
aromatase molecules in the system, it is unavailable to participate in the aromatization of Testosterone
which greatly slows down the process.

Aromatase Inhibitor (AI), Irreversable, Steroidal -- These drugs form a permanent and deactivating bond
with the aromatase enzyme. This prohibits the aromatase molecule from participating in the aromatization of
testosterone.
Dinitrophenols -- A group of non-naturally occurring chemical compounds which are nitro derivatives of
phenol.
Dopamine Receptor Agonists -- A chemical that binds to the dopamine receptor and triggers a response.
Used to stop the production of prolactin.
GnRH Agonist (Gonadotropin-releasing Hormone Agonists) -- A synthetic peptide modeled after the
hypothalamic neurohormone GnRH that interacts with the gonadotropin-releasing hormone receptor to elicit
its biologic response, the release of the pituitary hormones FSH and LH.
Leukotriene Receptor Antagonist (Leukast) -- Block the actions of cysteinyl leukotrienes at the CysLT1
receptor on target cells such as bronchial smooth muscle.
SARMs (Selective Androgen Receptor Modulators) -- SARMs are intended to have the same kind of effects as
androgenic drugs like anabolic steroids but be much more selective in their action, allowing them to be used
for many more clinical indications than the relatively limited legitimate uses that anabolic steroids are
currently approved for.
SERMs (Selective Estrogen Receptor Modulators) -- This class of drugs are estrogen antagonists and do not
lower the amount of estrogen that is in the system; they act by binding to the estrogen receptor without
generating a biological response. Different SERMs can block the estrogen receptors in different areas of the
body. The ones listed block them in breast tissue.
Sympathomimetic Amine -- Sympathomimetic drugs mimic the effects of transmitter substances of the
sympathetic nervous system. Amines are organic compounds and functional groups that contain a basic
nitrogen atom with a lone pair. Amines are derivatives of ammonia, wherein one or more hydrogen atoms
have been replaced by a substituent such as an alkyl or aryl group.

FAQ

Q: Can Nolvadex (Tamoxifene) and Arimidex (Anastrozole) be used together?

There is a lot of confusing information on wether or not these two compounds can be ran together. Looking
at drug interaction charts, Medscape has the following:
tamoxifen + anastrozole
tamoxifen decreases levels of anastrozole by unspecified interaction mechanism. High likelihood serious or
life-threatening interaction. Contraindicated unless benefits outweigh risks and no alternatives available.
Never use combination. Anastrozole and tamoxifen should not be administered together.

This information has been contradited by a few studies.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362190/
In conclusion, the results of this study confirm that anastrozole does not affect the pharmacokinetics of
tamoxifen when the two drugs are given in combination to post-menopausal women with early breast
cancer. In addition, the oestradiol suppressant effects of anastrozole appear unaffected by tamoxifen.
http://publications.icr.ac.uk/629/
As a result of (a) the lack of effect of anastrozole on tamoxifen and DMT levels and (b) the observed fall in
blood anastrozole levels having no significant effect on oestradiol suppression by anastrozole, we conclude
that the observed reduction in anastrozole levels by tamoxifen is unlikely to be of clinical significance when
anastrozole and tamoxifen are administered together.
The actual ATAC trial that this information comes from. Pharmacokinetic details can be found here
http://www.nature.com/bjc/journal/v85/n3/pdf/6691925a.pdf
"...the observed fall in blood anastrozole levels having no significant effect on oestradiol suppression by
anastrozole, we conclude that the observed reduction in anastrozole levels by tamoxifen is unlikely to be of
clinical significance when anastrozole and tamoxifen are administered together."*
A: Taking arimidex with tamoxifen decreases the serum concentration of anastrozole by 27%, but has no
effect on the pharmacodynamics of either

Q: Does Aromasin need to be taken with fat?

A: It works better when taken with a high fatty meal, yes.
http://www.rxlist.com/aromasin-drug.htm
Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in
water
http://www.rxlist.com/aromasin-drug/indications-dosage.htm
the recommended dose of AROMASIN is 50 mg once daily after a meal.
http://www.drugs.com/monograph/aromasin.html
High-fat meal increases plasma exemestane concentrations by approximately 40%.
http://labeling.pfizer.com/showlabeling.aspx?id=523
Absorption: Following oral administration of radiolabeled exemestane, at least 42% of radioactivity was
absorbed from the gastrointestinal tract. Exemestane plasma levels increased by approximately 40% after a
high-fat breakfast.
http://www.drugs.com/monograph/aromasin.html
Dosages >25 mg daily not shown to provide substantially greater suppression of plasma estrogens but may
increase adverse effects

Accutane

Acne prevention. Do not give blood if using.

https://en.wikipedia.org/wiki/Isotretinoin

Arimidex (Anastrozole)

Drug Class: Aromatase Inhibitor

Active Life: 48 hours
Anastrozole is an aromatase inhibitor. Aromatase inhibitors prevent the conversion of androgens into
estrogen in fat, muscle, breast, and brain1 . The medical use of Anastrozole is primarily to inhibit the
progression and growth of breast cancer in women by blocking the aromatase enzyme. It has also been used
by some doctors to try and treat low testosterone production in men, as well as being used in conjunction
with testosterone replacement therapy.
For bodybuilders and strength athletes, Anastrozole is used to minimize the aromatization of anabolic
steroids, and to a lesser extent for it's ability to raise testosterone levels in users. By reducing the amount of
estrogen in a steroid user's body he will be able to avoid estrogen related side effects such as water
retention, gynocomastia, etc2 . Obviously this is something that users should be hoping to limit as much as
possible.
Interestingly, in addition to decreasing estrogen it has been demonstrated that anastrozole can also increase
testosterone levels by up to 58%, along with also raising levels of lutenizing hormone3 . This is quite
significant especially when one considers that anastrozole can be used in conjunction with other compounds
during a user's post cycle therapy to raise natural testosterone levels once administration of anabolics
steroids is completed via the hypothalamic testicular pituitary axis.
 Use/Dosing

In the majority of users, .5mgs per day should be enough to prevent any estrogen related side effects related
to anabolic steroid use. Even when doses were increased to 1 mg per day there was no change in the amount
of estrogen that was able to be reduced as compared to doses of .5mgs per day3 . This would seem to
indicate that raising your dosage will show no further results if estrogenic side effects continue to be a
problem at a dosage of .5mgs. If symptoms persist the user may have to try a more potent compound such as
Femara4 .

Having said all of this however, dosing is user dependent and you should get blood work to dial in your dose,
but MOST users will find .5 mg of Arimidex E3D or E3.5D to be a good starting dose for 500-600 mg
Testosterone (just for a reference). Some may need more frequent (EOD) dosing or some may even need less
than E3.5D; this is really something that varies person-to-person too much and without blood work there is
no way to know for sure what dosage you need. Another obvious factor that will cause variance is how much
aromatizing compounds you are taking (i.e.Test, Deca, etc. etc.).

For users using anastrozole during their post cycle therapy the same dosages should apply. There is no need
to increase or decrease dosages. It can be run throughout the post cycle period with no ill effects.

Blood levels of the compound should stabilize and reach their peak at about 7-10 days after first
administering the drug5 . Therefore it is unlikely that a user would need to frontload with anastrozole or
begin taking it before they start administering the anabolics that they plan on taking.

Side Effects/Risks

Anastrozole is seemingly very mild on blood lipids (cholesterol) and has not been shown to affect them
adversely6,7 . However it should be noted that in theory if one was to consistently suppress your natural
estrogen levels for a long period of time, this would negatively impact your health (including your
cholesterol). Despite this there is no scientific evidence that anastrozole can be dangerous for healthy
individuals to use, even for extended periods of time.

It would seem then that anastrozole has little in the way of negative side effects associated with it's use. It is
by far one of the safest compounds that an athlete can use.

References

1. Preclinical pharmacology of "Arimidex" (anastrozole: ZD1033)--a potent, selective aromatase inhibitor. J

Steroid Biochem Mol Biol 1996 Jul;58(4):439-45
2. The ATAC Trialists Group. The ATAC (Arimidex, Tamoxifen, Alone or in Combination) adjuvant breast cancer
trial in post-menopausal women with early breast cancer. Lancet 2002; 359: 2131-39
3. Mauras N, O'Brien KO, Klein KO, Hayes V. "Estrogen suppression in males: metabolic effects." J Clin Endocrinol
Metab. 2000 Jul;85(7):2370-7.
4. Leder BZ, et al. "Effects of aromatase inhibition in elderly men with low or borderline-low serum Testosterone
levels." J Clin Endocrinol Metab. 2004 Mar;89(3):1174-80.
5. Taxel P, et al. "The effect of aromatase inhibition on sex steroids, gonadotropins, and markers of bone
turnover in older men. J Clin Endocrinol Metab 2000 86:2869—2874*
6. Dougherty RH, et al. "Effect of aromatase inhibition on lipids and inflammatory markers of cardiovascular
disease in elderly men with low Testosterone levels." Clin Endocrinol (Oxf). 2005 Feb;62(2):228-35.
7. Hayes FJ, et al. "Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback." J
Clin Endocrinol Metab. 2000 Sep;85(9):3027-35.

Aromasin (Exemestane)

Drug Class: Aromatase Inhibitor

Active Life: 24-30 hours

Exemestane is a steroidal suicide aromatase inhibitor/irreversible aromatase inactivator, lowering production

of estrogen in the body by blocking the aromatase enzyme. Similar in structure to formestane, exemestane’s
medical use like most aromatase inhibitors is for treatment of estrogen-dependent breast cancer. It is usually
only prescribed in those cases where therapies using less aggressive compounds have not produced the results
hoped for, such as selective estrogen receptor modulators.

For use by strength athletes and bodybuilders, exemestane has several properties that would be beneficial.
First, exemestane reportedly can lower estrogen 85% on average1 . In doing so of course this will aid in the
prevention of estrogen related side effects caused by aromatizing steroids. The drug also raises testosterone
levels in users which can be advantageous if used during post-cycle therapy2 . Add to this the fact that there is
some evidence that exemestane may elevate levels of insulin growth factor [IGF]3 .
Like other aromatase inhibitors, there is also conflicting information and studies regarding the effect that
exemestane has on users blood lipids/cholesterol, with some studies indicating that the compound has little to
no effect while others say that it is quite harsh4,5 .

Use/Dosing

Exemestane reaches peak plasma concentrations within 2 hours following the oral administration of a 25 mg
dose1 . The active life of the drug is between 24 and 30 hours. This is significant since it is quite shorter than
for the non-steroidal inhibitors1 . A single oral dose of 25 milligrams of exemestane causes a relatively long-
lasting reduction in plasma and urinary estrogen levels, with maximal suppression occurring approximately 2
to 3 days after dosing and persists for about 4 to 5 days1,4 .
It has been shown that 25 milligrams of exemestane is basically just as effective as 50 milligrams at
suppressing estrogen, raising testosterone levels, and levels of IGF2 . It is therefore unnecessary to go higher in
doses than 25 milligrams per day. Due to the active life of the compound exemestane should be administered
roughly once every twenty-four hours.

It appears that the only negative aspect of the compound in terms of the dosing schedule is that it takes
approximately seven days for it to reach steady blood plasma levels. However, this is not a major hindrance to
its use. It just simply requires that a user begin using exemestane a week prior to when they want the effect of
the compound to be full realized.

Risks/Side Effects

Exemestane has no significant drug toxicity at doses up to 600 milligrams per day. It is well tolerated by most
users with the maximum tolerated dose toxicity not yet being identified1 . Negative side effects related to the
use of this compound are usually quite mild and can include things such as transient gastrointestinal effects,
hot flashes, nausea, and/or fatigue1, 2 . As previously mentioned, the effect of exemestane on the blood
lipids/cholesterol are unknown due to the conflicting research and therefore should be monitored when using
the compound. Sexual dysfunction is also a possibility due to the lowering of estrogen levels as well. However
reports of this are relatively rare.

Due to the mild negative side effects associated with the compound, as well as the potency of the drug in
alleviating estrogen-related side effects when administering aromatizing anabolic steroids, exemestane is
seemingly a relatively safe choice when looking for an aromatase inhibitor.

FAQ

Q: Does Aromasin work better with a fatty meal?

A: It works better when taken with a high fatty meal, yes.
http://www.rxlist.com/aromasin-drug.htm
Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in
water
http://www.rxlist.com/aromasin-drug/indications-dosage.htm
the recommended dose of AROMASIN is 50 mg once daily after a meal.
http://www.drugs.com/monograph/aromasin.html
High-fat meal increases plasma exemestane concentrations by approximately 40%.
http://labeling.pfizer.com/showlabeling.aspx?id=523
Absorption: Following oral administration of radiolabeled exemestane, at least 42% of radioactivity was
absorbed from the gastrointestinal tract. Exemestane plasma levels increased by approximately 40% after a
high-fat breakfast.
http://www.drugs.com/monograph/aromasin.html
Dosages >25 mg daily not shown to provide substantially greater suppression of plasma estrogens but may
increase adverse effects
 Related Posts

Switching from Arimidex to Aromasin.

References

1. Brueggemeier RW. Overview of the pharmacology of the aromatase inactivator

exemestane. Breast Cancer Res Treat 2002;74:177-185.
2. Mauras N, Lima J, Patel D, Rini A, di Salle E, Kwok A, Lippe B. Pharmacokinetics and
dose finding of a potent aromatase inhibitor, aromasin (exemestane), in young males. J
Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
3. Martinetti A, Zilembo N, Ferrari L, Massimini G, Polli A, La Torre I, Giovanazzi R,
Pozzi P, Bidoli P, De Candis D, Seregni E, Bombardieri E, Bajetta E. Bone turnover
markers and insulin-like growth factor components in metastatic breast cancer: results
from a randomised trial of exemestane vs megestrol acetate. Anticancer Res. 2003 Jul-
Aug;23(4):3485-91.
4. Buzdar AU. An overview of the pharmacology and pharmacokinetics of the newer
generation aromatase inhibitors anastrozole, letrozole, and exemestane. Cancer. 2002
Nov 1;95(9):2006-16.
5. Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C, Cufer T,
Lobelle JP, Mattiaci MR, Piccart M, Paridaens R. The effect of exemestane on serum
lipid profile in postmenopausal women with metastatic breast cancer: a companion study
to EORTC Trial 10951, 'Randomized phase II study in first line hormonal treatment for
metastatic breast cancer with exemestane or tamoxifen in postmenopausal patients'. Ann
Oncol. 2004 Feb;15(2):211-7.

Bazedoxifene
https://en.wikipedia.org/wiki/Bazedoxifene

Cabergoline (Dostinex)

Drug Classification: Dopamine-Receptor Agonist

Active Life: approximately 7 days
Cabergoline is a drug most often medically prescribed for its ability to inhibit prolactin secretion via its action
as a dopamine agonist. Used in the treatment of such diseases as Parkinson's disease1 , acromegaly2 , restless
leg syndrome3 , Cushing’s syndrome4 , hyperprolactinemia5 , among others, the drug has been adopted by
bodybuilders and strength athletes as a means to combat prolactin related side effects caused by certain
anabolic steroids. For this purpose cabergoline is extremely effective while presenting little risk in terms of
serious side effects to the health of the user when used for this purpose.
Steroid users should be concerned about excessive prolactin levels because of the side effects associated
with them. Prolactin is a naturally occurring hormone primarily produced by the lactotrophs located in the
pituitary gland, with a minority amount of the hormone being produced by other tissues/cells of the body.
Prolactin plays a major role in lactation in most mammals including humans. It both stimulates milk
production as well as inducing lobuloalveolar growth of the mammary gland. Obviously both of these side
effects would be of great concern to bodybuilders and strength athletes from both a health and cosmetic
standpoint. Decreased sex drive, sperm production and sexual function may also be related to elevated levels
of this hormone6,7 . In fact even in men with regular healthy levels of prolactin cabergoline can help to
temporarily reduce the amount of the hormone that is secreted which leads to such advantages as an
increase sex drive, improvement in sexual function (quality of erection) as well as reducing the refractory
period for users (the amount of time between erections)8 .

Cabergoline works to inhibit secretion of prolactin because it is a dopamine receptor agonist. This means that
it acts upon dopamine receptors in the same way as dopamine does in the body. Dopamine acts as a
prolactin inhibitor by binding to receptors in the lactotrophs in the pituitary gland and signals for these to
cease the synthesis and secretion of prolactin.

While dopamine exhibits an ability to inhibit the secretion of prolactin it of course has numerous other
functions in the body, with cabergoline being able to mimic the action of dopamine and also performing
many of these. These functions include creating a sense of wellbeing or contentment via a chemical reaction
in the body, most often released during pleasurable or satisfying physical actions. It has even been shown
that dopamine-receptor agonists such as cabergoline can help increase the likelihood that individuals that are
quitting smoking be successful9 . Dopamine can also help improve brain function. For this reason cabergoline
is sometimes prescribed to sufferers of Parkinson’s disease. For the average user however it may help in
improving memory or even motor functions, although if normal dopamine levels are already being produced
by the user this effect will likely be minimal at best. However the primary reason for use of cabergoline by
steroid users remains for the treatment of prolactin related side effects.

The anabolic steroids that can lead to excessive levels of prolactin are primarily nandrolone and nandrolone-
derived compounds. Steroids such as deca durabolan, trenbolone, and durabolan all can have this effect. For
this reason users of these drugs may want to have a compound such as cabergoline in their possession to
treat negative side effects related to prolactin if they should develop at any point during a steroid cycle.

A secondary factor in controlling the levels of prolactin in users of anabolic steroids is the amount of
circulating estrogen in their systems. Estrogen has an apparent positive effect on the amount of prolactin
produced, with the more estrogen that is produced being related to the amount of prolactin that is produced
accordingly. Essentially estrogen stimulates the secretion of prolactin via the disruption of the inhibitory
effect of dopamine10 . For this reason often times prolactin can be controlled by way of the reduction of
estrogen levels. Use of aromatase inhibitors can be used for this purpose. However when prolactin levels
reach a point where a reduction of estrogen levels does not inhibit excessive prolactin secretion enough,
administration of cabergoline should be sufficient to inhibit any further overproduction.

Use/Dosing

Due to the extremely long active life of the drug, approximately seven days, users only have to administer
their doses once or twice per week to see good results. In terms of the dosing that healthy individuals would
need to use to suppress prolactin levels raised by their use of anabolic steroids, anecdotally many users
report seeing their best results with dosing in the range of one half of a milligram to one and a half milligrams
of cabergoline per week. This dose range should be sufficient for the majority of users but larger doses can be
used as there appears to be little worry for users in terms of toxicity except at extremely high doses that
would be impractical to administer unintentionally11,12 .
Cabergoline reaches its peak plasma concentration within two to three hours if administered orally. The drug
is metabolised by the liver with a relatively large amount of the drug experiencing a first pass effect13 . Users
are able to take the drug with or without food; there is no impact on the absorption rate or action of the
compound in either case. In healthy subjects it has been determined that the elimination half-life of
cabergoline is between sixty-three and one hundred and nine hours13 . There is no reliable data on the
detection time of the compound.

In terms of the duration of time that users can administer cabergoline, there is very little research that has
been completed on the subject. As will be discussed in the Risks/Side Effects portion of this profile below
there are some indications that there may be risk factors involved in the long term use of the drug but no
definitive conclusions can be made. However, at least in terms of the short term finding, it appears that
cabergoline is a relatively safe drug for use by healthy adults for long periods of time.

Risks/Side Effects

When compared to the other most popular dopamine-receptor agonist bromocriptine mesylate, cabergoline
is seemingly better tolerated and at least as efficient, if not more so, at reducing prolactin levels in users7,14 .
Although bromocriptine mesylate is relatively free of any significant negative side effects users often
complain of serious stomach discomfort and other additional gastrointestinal problems while taking the drug.
Cabergoline has shown a far smaller propensity to produce this effect. However there are still those that find
the drug causes reactions such as stomach upset, vomiting and nausea among some users but less frequently
then with bromocriptine mesylate.
Due to the fact that cabergoline is a relatively new drug there is little long term research that is available that
gages the long term safety of the compound. For this reason there are several sporadic reports of fairly
serious ailments that could be attributed to the drug. For example there have been reports of conditions
including such things as hair loss15 , inhibition of the secretion of adrenal gland hormones16 , and even heart
disease17 . However none of these side effects have been reported in anyway close to being statistically
significant and therefore they are not considered to be a valid concern for users.
 Although for the most part cabergoline will not be used or be beneficial for women in a
bodybuilding/strength athletics sense, the drug itself has been found not to be harmful to women. In fact, it
has been shown that cabergoline will not negatively impact fertility in women long term or short term. There
is even some evidence that use of the drug during pregnancy should not have any negative impacts18 ,
although this should most definitely be considered a risky undertaking for normally healthy women and
should always be used in consultation with a medical doctor.

References

1. Nakatsuka A, Nagai M, Yabe H, Nishikawa N, Nomura T, Moritoyo H, Moritoyo T, Nomoto M. Effect of

clarithromycin on the pharmacokinetics of cabergoline in healthy controls and in patients with Parkinson's
disease. J Pharmacol Sci. 2006 Jan;100(1):59-64.
2. Selvarajah D, Webster J, Ross R, Newell-Price J. Effectiveness of adding dopamine agonist therapy to long-
acting somatostatin analogues in the management of acromegaly. Eur J Endocrinol. 2005 Apr;152(4):569-74.
3. Benes H, Heinrich CR, Ueberall MA, Kohnen R. Long-term safety and efficacy of cabergoline for the treatment
of idiopathic restless legs syndrome: results from an open-label 6-month clinical trial. Sleep. 2004 Jun
15;27(4):674-82.
4. Pivonello R, Ferone D, Lamberts SW, Colao A. Cabergoline plus lanreotide for ectopic Cushing's syndrome. N
Engl J Med. 2005 Jun 9;352(23):2457-8.
5. Jackson J, Safranek S, Daugird A. Clinical inquiries. What is the recommended evaluation and treatment for
elevated serum prolactin? J Fam Pract. 2005 Oct;54(10):897-8, 901.
6. Nickel M, Moleda D, Loew T, Rother W, Gil FP. Cabergoline treatment in men with psychogenic erectile
dysfunction: a randomized, double-blind, placebo-controlled study. Int J Impot Res. 2006 May 18; [Epub ahead
of print]
7. De Rosa M, Colao A, Di Sarno A, Ferone D, Landi ML, Zarrilli S, Paesano L, Merola B, Lombardi G. Cabergoline
treatment rapidly improves gonadal function in hyperprolactinemic males: a comparison with bromocriptine.
Eur J Endocrinol 1998 Mar;138(3):286-93.
8. Kruger TH, Haake P, Haverkamp J, Kramer M, Exton MS, Saller B, Leygraf N, Hartmann U, Schedlowski M.
Effects of acute prolactin manipulation on sexual drive and function in males. J Endocrinol. 2003
Dec;179(3):357-65.
9. Frishman WH, Mitta W, Kupersmith A, Ky T. Nicotine and non-nicotine smoking cessation pharmacotherapies.
Cardiol Rev. 2006 Mar-Apr;14(2):57-73.
10. Gillam MP, Middler S, Freed DJ, Molitch ME. The novel use of very high doses of cabergoline and a
combination of testosterone and an aromatase inhibitor in the treatment of a giant prolactinoma. J Clin
Endocrinol Metab. 2002 Oct;87(10):4447-51.
11. Gillam MP, Fideleff H, Boquete HR, Molitch ME. Prolactin excess: treatment and toxicity. Pediatr Endocrinol
Rev. 2004 Nov;2 Suppl 1:108-14.
12. Johansen SS, Karkov J. A fatal overdose of the ergot derivative cabergoline. Forensic Sci Int. 2004 Nov
10;146(1):47-51.
13. Del Dotto P, Bonuccelli U. Clinical pharmacokinetics of cabergoline. Clin Pharmacokinet. 2003;42(7):633-45.
14. Bolko P, Jaskula M, Wasko R, Wolun M, Sowinski J. The assessment of cabergoline efficacy and tolerability in
patients with pituitary prolactinoma type. Pol Arch Med Wewn. 2003 May;109(5):489-95.
15. Miwa H, Kondo T. Hair loss induced by dopamine agonist: case report and review of the literature.
Parkinsonism Relat Disord. 2003 Oct;10(1):51-2.
16. ;lf[p2fgt54ePivonello R, Ferone D, de Herder WW, de Krijger RR, Waaijers M, Mooij DM, van Koetsveld PM,
Barreca A, De Caro ML, Lombardi G, Colao A, Lamberts SW, Hofland LJ. Dopamine receptor expression and
function in human normal adrenal gland and adrenal tumors. J Clin Endocrinol Metab. 2004 Sep;89(9):4493-
502.
17. Horvath J, Fross RD, Kleiner-Fisman G, Lerch R, Stalder H, Liaudat S, Raskoff WJ, Flachsbart KD, Rakowski H,
Pache JC, Burkhard PR, Lang AE. Severe multivalvular heart disease: a new complication of the ergot
derivative dopamine agonists. Mov Disord. 2004 Jun;19(6):656-62.
18. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A, Rocchi F, Gangi E, Paracchi S, Gasperi M,
Lavezzari M, Nicolosi AE, Ferrero S, Landi ML, Beck-Peccoz P, Bonati M. Pregnancy outcome after cabergoline
treatment in early weeks of gestation. Reprod Toxicol. 2002 Nov-Dec;16(6):791-3.

Clenbuterol, Spiropent, Ventipulmin, Clenasma

Pharmaceutical Name: Clenbuterol Hydrochloride
Formula: C12 H18 Cl2 N2O
Chemical Structure: (RS)-1-(4-Amino-3,5-dichlorophenyl)-2-(tert-butylamino)ethanol
Molecular Weight Of Base: 277.19
Excretion: urine and feces
Half Life: 36-48 hours
Anabolic/Androgenic Ratio (Range): mildly anabolic, not androgenic

Use/Dosing
Clen is primarily used to assist with metabolism increases during cut cycles to aid in fat loss.

Cycles are common in 2-4 week increments with equal on cycle and equal time off cycle.
First timers start with 20 mcg and increase the dose by 20 mcg after 3-4 days. The increases are stopped at
120 mcg for females and 140 mcg for males or when the sides become too much.

Usage can be tapered off in the same manner, although there is significant debate about the necessity of
tapering either way.

More experienced users will start dose at (or near) their personal maximum and run cycle at that level the
entire time.
 After approximately five weeks, your body will become accustomed to Clen and the metabolic effect will be
not work as well.

Side Effects/Risks
• Shaky hands
• Increased sweating
• Nausea
• High Blood Pressure
• Cramps
Most sides will subside after approximately a week of use.
An overdose of Clen has the potential to be fatal. An overdose can have the following symptoms:
• Rapid breathing
• Irregular heartbeat
• Irregular blood pressure
• Unconsciousness
• Trembling / Shaking
• Panic
• Extreme restlessness
• Severe nausea / vomiting
• Diarrhea

From longer term high doses / abuse:

• Cardiac hypertophy

How does Clen work (excerpt from Anabolics)?

The drug will usually elevate the body temperature shortly after therapy is initiated. The rise in temperature
is commonly .5 to 1 degree, sometimes a little more. This elevation is due to one’s body burning excess
energy (largely from fat), and is usually not uncomfortable.

The number of consecutive days clenbuterol hydrochloride is now used is usually dependent on the response
of the individual.To be clear, the athletic benefits of this drug will only last for a limited time and then
diminish, largely due to beta-receptor down regulation. By most accounts clenbuterol hydrochloride seems
to work well for approximately 4 to 6 weeks. During this period, users generally monitor their body
temperature on a regular basis. We are given some level of assurance that clenbuterol hydrochloride is
working by the temperature elevation. Once the temperature drops back to normal, receptor
downregulation has probably diminished the efficacy of the drug. At this point increasing the dosage is
usually not regarded as effective, and instead clenbuterol hydrochloride is discontinued for a period of no
less than 4-6 weeks.
 Many bodybuilding competitors enhance the fat burning effect of clenbuterol hydrochloride with the use of
additional substances. Many have commented that when the drug is combined with thyroid hormones,
specifically the powerful Cytomel®, the thermogenic effect can become extremely dramatic. Such a mix is
often further used during a steroid cycle, helping the individual elicit a much more toned physique from the
drugs. A clenbuterol/thyroid mix is also common when using growth hormone, which is believed to enhance
the thermogenic and anabolic effect of HGH therapy. Lastly, ketotifen has also been a popular adjunct to
clenbuterol hydrochloride, which is an antihistamine that upregulates beta-2 receptor density. It seems
capable of not only increasing the potency of each dose of clenbuterol hydrochloride (allowing the user to
take less clenbuterol), but also of perhaps even slowing receptor downregulation (see the Ketotifen profile
for a more comprehensive discussion).

Visit the Wiki for more detailed information.

Companion Supplement(s)
Taurine is recommended to be taken with Clen at a dose of 3-5g per day. This is done because Clenbuterol
deplete taurine levels in the liver, inhibiting T4 to T3 conversion. In addition, taurine has been reported to
reduce the cramping that often comes with Clenbuterol usage.
Extra water should be taken while on Clenbuterol. On the order of an extra liter per day.

Note:
Clen will slightly assist in fat loss. As with most things in the steroid community, appropriate training regimen
and diet need be followed to experience the benefits of Clen. The "mild anabolic" effect is unproven in
humans and should not be relied on for any kind of capability to stop muscle loss during a cut cycle.

References
1. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp.518
2. http://www.ncbi.nlm.nih.gov/pubmed/4045696

Cialis
Helps blood flow
https://en.wikipedia.org/wiki/Tadalafil

Clomid (Clomiphene Citrate)

Drug Class: Selective Estrogen Receptor Modulator

Active Life: 5-7 days
Originally developed as a female fertility aid, clomiphene citrate has been popular among steroid users for
quite some time now as a post-cycle therapy compound used to help recover natural testosterone
production. The compound works by partially or completely blocking the effects of estrogen in the body. This
is due to the fact that it is a synthetic estrogen with both agonist and antagonist properties1 . With a similar
structure to that of tamoxifen citrate, clomiphene citrate blocks the ability of estrogen to bind with receptors
in certain tissues2,3 , these being located in the hypothalamus and being suprapituitary4 , although this is a
somewhat contentious claim. Tamoxifen citrate is selective to those receptors in the liver, breast, and bone.
So in terms of use as a fertility drug in women, clomiphene citrate helps to eliminate the negative feedback of
estrogens on the hypothalamic-pituitary-ovarian axis and increases the production of luteinizing hormone
and follicle stimulating hormone. This induces ovulation.
Therefore if these results can be translated to strength athletes and bodybuilders, this ability to raise the
levels of luteinizing hormone and follicle stimulating hormone should be quite impressive. An increase in
these hormones will result in an increase in testosterone production in users5,6 . This of course is something
that is desperately desired when coming off of anabolic steroids. If testosterone levels can be raised quickly
after a cycle a user is much more likely to maintain more of his gains than if he suffered through a crash in
testosterone levels and his natural production came back slowly, all the while having to combat the increased
levels of estrogen and cortisol.

While it is true that clomiphene citrate has many "anti-estrogen" properties, there are a multitude of better
options. It's is relatively weak in comparison to tamoxifen citrate and the anti-aromatase compounds that are
available are much more potent in terms of controlling and/or eliminating estrogenic side effects that are
likely to develop. The primary duty of clomiphene citrate should be left to post-cycle therapy.

Use/Dosing

Of course due to the fact that there is little research to do with the use of clomiphene citrate as it relates to
steroid users, much of what we know about the dosing of it has been from anecdotal reports. For the most
part users will maintain doses of the drug between 25mgs to 150mgs per day on a consistent basis. Often
times users will "frontload" the compound using doses of between 200-300mgs on the first day of their post-
cycle therapy and then reduce the subsequent doses. However the side effects associated with large doses of
the compound may hinder some individuals' abilities to do this.

Some users also advocate tapering the dose of clomiphene citrate during the last few weeks of
administration. However this is more a practice that is based upon theory rather than solid medical evidence
of it's productivity.

In terms of dosing length it seems that at least 3 weeks of clomiphene citrate therapy is recommended by
users. Of course each has their own preferences along with individual recovery schedules. Also the types of
compounds used and the duration of a cycle will of course influence the time it takes for a user to recover
and the need for a lengthy post-cycle therapy. Due to the lack of serious side effects associated with the
drug, as well as the fact that there is no risk of toxicity with the clomiphene citrate, users are able to use the
compound for months on end with seemingly no significant negative consequences.
 Risks/Side Effects

Despite these rather inconvenient side effects, for the most part clomiphene citrate can be run for extended
periods of time with no worries of serious negative consequences7,8 . Potentially things such as hot flashes,
nausea, dizziness, and headaches may occur but anecdotally users report that these symptoms are quite rare.
However emotional side effects along with vision problems are frequently reported with use of this drug.
Visual tracers or blurry vision are often reported by users, even some who use extremely low doses of the
compound. These are often reported to become more pronounced at night. However if this symptom
becomes unbearable, it quickly dissipates after administration of the compound is ceased.

In terms of the emotional side effects associated with clomiphene citrate, some users complain that they
become depressed, irritable or more emotional in general when using the drug. This can primarily be
explained by way of clomiphene citrate being a synthetic estrogen. By introducing a type of estrogen into a
user's system some effects should be expected. Coupled with the fact that the natural testosterone
production of the user is already suppressed this obviously could lead to some difficulties. Of course some
users find these effects much more pronounced than others, with many finding clomiphene intolerable while
others have little to no side effects.

Another possible effect of use of the compound is increased acne. This is a direct result in the shifting
hormonal balance that a user would be experiencing while coming off of anabolic steroids and the
introduction of clomiphene citrate to their system. An increase in production of seminal fluid may also be
experienced by some users and therefore the volume of ejaculate may well noticeably increase as well.

References

1. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 188-9

2. Vermeulen A, Comhaire F. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Fertil Steril. 1978 Mar;29(3):320-7.
3. Guay AT, Jacobson J, Perez JB, Hodge MB, Velasquez E. Clomiphene increases free testosterone levels in men
with both secondary hypogonadism and erectile dysfunction: who does and does not benefit? Int J Impot Res.
2003 Jun;15(3):156-65
4. Winters SJ, Troen P. Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin
secretion in men. J Clin Endocrinol Metab 1985 Nov;61(5):842-5
5. Winters SJ, Troen P. Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin
secretion in men. J Clin Endocrinol Metab 1985 Nov;61(5):842-5
6. Tenover JS, Bremner WJ. The effects of normal aging on the response of the pituitary-gonadal axis to chronic
clomiphene administration in men. J Androl. 1991 Jul-Aug;12(4):258-63
7. Purvin VA.Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol. 1995 Apr;113(4):482-4
8. Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk,
Br. J. Cancer 1988 Oct, 58 (4) 497-9
Cyclofenil

Drug Class: Selective Estrogen Receptor Modulator

Active Life: 3-5 days
Cyclofenil is a selective estrogen receptor modulator. It works via the same mechanisms as clomiphene
citrate and tamoxifen citrate1,2 . In acting as an estrogen receptor anatagonist/agonist, medically it is
prescribed to stimulate ovulation in women and can be used to help raise natural testosterone levels in
men3 . In terms of use for strength athletes, bodybuilders and other steroid users, like clomiphene citrate and
tamoxifen citrate, cyclofenil has two primary uses.

The first such use would be for the prevention of estrogen-related gynecomastia. Cyclofenil has the ability to
bind to the estrogen receptors in breast tissue, therefore preventing the formation of gynecomastia.
However it should be noted that cyclofenil appears to be less potent then tamoxifen citrate in achieving this
effect, and therefore users may not want to rely on it if other options are available.

The second use that cyclofenil may be employed for is post-cycle therapy. In addition to targeting the
estrogen receptors in breast tissue, the compound also has the ability to bind to the estrogen receptors in
the hypothalamus. By doing so, cyclofenil is able to block the negative feedback inhibition that is caused by
estrogen3 . This creates an environment where there is an increase in the production of gonadotropin
releasing hormone. This in turn signals the pituitary to raise the amount of luteinizing hormone circulating in
the body, with luteinizing hormone of course being the primary indicator for the testes to increase the rate of
testosterone production. All of this would obviously be of benefit when a steroid user discontinues his use of
anabolic steroids. By being able to increase the natural testosterone production of a user as quickly as
possible, it is more likely that they will be able to maintain more of the muscle mass gained during a cycle as
well as achieving a more natural hormonal balance in a shorter period of time.
It should be noted that due to the similar mechanisms by which they work2 , users that are administering
tamoxifen citrate and/or clomiphene citrate are unlikely to see any increased benefits to adding cyclofenil for
either the purpose of gynecomastia prevention and/or during post-cycle therapy. As long as the clomiphene
citrate/tamoxifen citrate is being taken in adequate dosages, there is no reason to include cyclofenil.

Use/Dosing

As stated above, similar to tamoxifen citrate and clomiphene citrate, cyclofenil is primarily used during the
post-cycle therapy of a male steroid user's cycle. This is due to the ability of the compound to inhibit the
negative feedback loop activated via estrogen. This in turn helps to increase the production of gonadotropin
releasing hormone, thereby stimulating the pituitary to release a larger volume of luteinizing hormone. All of
this brings about a signal for the testes to increase their production of testosterone.
 For the most part, users have anecdotally reported that dosing in the range of 400 to 600mgs per day should
be sufficient to provide the effect sought after by users. The duration of the use of cyclofenil is similar to
clomiphene citrate, usually lasting for approximately four to five weeks for post-cycle therapy.

As for use as a preventive measure for gynecomastia, it can be run throughout the cycle of a user for this
effect as well. The dosage required varies from user to user, however it should be relatively lower then those
needed for post-cycle therapy. A dose of between 200-400 milligrams per day should be sufficient in most
cases.

Some users also advocate tapering the dose of cyclofenil during the last few weeks of administration.
However this is more a practice that is based upon theory rather than solid medical evidence of its
productivity.

Risks/Side Effects

There are no real direct negative side effects associated with the use of cycolfenil. For the most part, any
negative side effects that a user may experience would almost undoubtedly be related to the shift in
hormonal balance that the user is undergoing. Acne, a strained emotional state, oily skin and a change in sex
drive are all symptoms that users may experience once they cease the administration of anabolics steroids
and begin recovering their natural testosterone production.

Other than these concerns, there is little in the way that short-term or long-term use of cycolfenil could cause
damage to in the human body4 . It is seemingly safe in terms of possible effects to the body’s hormonal
production. For the vast majority of users the compound is relatively side effect free and well tolerated.

References

1. Schmidt-Elmendorff H, Kammerling R. [Comparative clinical studies on clomiphen, cyclofenil and epimestrol

(author's transl)] Geburtshilfe Frauenheilkd. 1977 Jun;37(6):531-41
2. Schopman W, Slager E, Hackeng WH, Mulder H. Stimulation of calcitonin secretory capacity by increased
serum levels of testosterone in men treated with tamoxifen. Int J Androl. 1987 Dec;10(6):747-51
3. Cox LW. Stimulation of ovulation and spermatogenesis by drugs and hormones. Mod Med Asia. 1977
Nov;13(11):23-5
4. Herbai G, Ljunghall S. Lipid-lowering effects of two synthetic oestrogen derivatives with weak genital
oestrogen properties. Ups J Med Sci. 1985;90(1):67-72

Cytadren (Aminoglutethimide)

Drug Class: Cortisol and Aromatase Inhibitor Active Life: approximately 24 hours
Aminoglutethimide is a non-steroidal compound that works to inhibit both cortisol production as well as the
aromatization of androgens. It works to block the production of cortisol by stopping the conversion of
cholesterol to pregnenolone1 . This along with the ability to inhibit aromatization of any androgens that a
steroid user may be administering would obviously be beneficial for those hoping to not only minimize
estrogenic side effects but also lowering the levels of the catabolic hormone cortisol.

The medical use of aminoglutethimide is primarily to treat hyperadrenocorticism, also known as Cushing’s
syndrome, which is the excessive production of cortisol by the body. To a lesser extent the drug has also been
used in the treatment of breast cancer, as is the case with other aromatase inhibiting drugs. However since
there are far superior drugs now available aminoglutethimide is not a popular drug in cancer treatment.

In terms of research conducted in athletes or those looking to use the drug for athletic or cosmetic purposes,
there is of course very little as is the case with many drugs used by bodybuilders and strength athletes. For this
reason we are left to extrapolate the best methods to use aminoglutethimide from anecdotal information as well
as trying to form the available research to fit into our needs.

A significant aspect of aminoglutethimide is that along with its ability to inhibit both cortisol and
aromatization, it also suppresses the production of adrenal androgens2 . Obviously this would be a negative for
someone that was not using exogenous hormones, but since it is unlikely that athletes or other steroid users
would be administering aminoglutethimide without also using anabolic steroids this is likely not to be a
concern for most.
The cortisol inhibiting effect of aminoglutethimide is short lived in the body due to the body’s ability to adapt
to the action of the drug. By lowering the natural production of cortisol the body will begin to produce
adrenocorticotropic hormone. The hormone sparks an increase in cortisol production in the body to help
normalize its levels causing the action of the drug to become basically moot3 . It is believed by some that if one
staggers their use of the drug to a schedule similar to two days on and then two days off that this may be
enough to ward off the body’s response to the lowered cortisol levels while still reaping the benefit of partial
suppression. There is little research to indicate that this is true however.

Use/Dosing

To achieve the two primary actions of aminoglutethimide, namely aromatase inhibition and cortisol reduction;
two very different dosing ranges are used. For aromatase inhibition, maximum estrogen suppression is
achieved at 250 to 500 milligrams per day. In some studies it has been demonstrated that as little as 250
milligrams of aminoglutethimide can suppress aromatase activity by 92% in some users, with larger doses only
providing minimally improved results. In contrast, for cortisol suppression dosages typically run in excess of
one gram of aminoglutethimide per day. While running a larger dose the enzyme that is responsible for
converting cholesterol into prognenolone and thereby creating cortisol, the demolase enzyme, should be
maximally inhibited3 .
 As noted earlier however, when running the drug for cortisol suppression, it will provide diminishing results if
run consistently. For this reason administering the drug for only two or three days consecutively should be the
norm for most users. Any more then that and the body will begin to produce more cortisol to compensate. As
for dosing for aromatase inhibition, doses ranging from approximately 250 to 500 milligrams per day, these
should be moderate enough to not affect cortisol levels and therefore there is no need to skip days of
administering the drug. Every day administration at that dosage should not negatively impact the user.

As for the duration of the cycles that include aminoglutethimide, it again depends on the dosages used. If the
user is using doses in the range of 250 to 500 milligrams per day, a duration of six to eight weeks should be
safe for the majority of users. However if one is using it at doses of approximately one gram per day the user
will want to limit their use of the drug to only a few weeks, possibly prior to a competition. This is due to the
potential for liver toxicity that comes with aminoglutethimide, as will be discussed further in the Risks/Side
Effects portion of this profile below.

As a side note, it should be mentioned that unlike many other aromatase inhibitors or other drugs that are said
to have “anti-estrogenic” qualities, aminoglutethimide does not raise other beneficial hormones for strength
athletes and bodybuilders in the body such as luteinizing hormone, gonadotropin releasing hormone and/or
testosterone, among others. For this reason there is no real reason to run this drug during post-cycle therapy as
there are countless other compounds that offer additional benefits that the user should take advantage of.

Risks/Side Effects

It appears that there is a significant risk of hepatoxicity with aminoglutethimide when used over extended
periods of time even at relatively moderate dosages4 . For this reason lengthy use of the drug would not be
recommended for most users and even short cycles of it are likely to increase liver values.

Other potential negative side effects include apathy, insomnia, gastrointestinal distress, and thyroid
dysfunction. As well, like other aromatase inhibitors, cholesterol levels in both men and women may be
negatively affected with long term usage of the drug. With cortisol suppression it is likely that users will also
experience joint discomfort when training along with a feeling of malaise. This is a common side effect and
often reported when users are administering significantly large enough doses of the drug to achieve cortisol
suppression. However, these cortisol-related side effects will only become noticeable if the doses administered
are high enough to produce such an effect. If run at lower doses exclusively for the aromatase inhibitor effect,
these will be less likely to occur.

References

1. Lonning PE. Oestrogen suppression--lessons from clinical studies. Best Pract Res Clin
Endocrinol Metab. 2004 Mar;18(1):33-45.
2. Schmid P, Possinger K. Interactions of antioestrogens and aromatase inhibitors. Forum
(Genova). 2002;12(1):45-59.
3. Dexter RN, Fishman LM, Ney RC et al. Inhibition of adrenal corticosteroid synthesis by
aminoglutethimide: Studies on the mechanism of action. J Clin Endocrinol 27 (1967)
473-80.
4. Perez AM, Guerrero B, Melian C, Ynaraja E, Pena L. Use of aminoglutethimide in the
treatment of pituitary-dependent hyperadrenocorticism in the dog. J Small Anim Pract.
2002 Mar;43(3):104-8.

Dantrolene
Muscle Relaxant. May be able to help for DNP overdose
https://en.wikipedia.org/wiki/Dantrolene

DNP
Also known as: 51-28-5, Aldifen, Solfo Black B, Tertrosulphur PBR, alpha-Dinitrophenol, Phenol, 2,4-dinitro-,
Solfo Black G, Nitro kleenup
Class: Dinitrophenols
Molecular formula: C6 H4 N2 O5
Molecular Weight: 184.10636
Half Life: 36 Hours

Disclaimer: Reading this entire profile is imperative to ensuring proper DNP administration.
What is DNP?
DNP is the most powerful compound available used to drop body fat. On a cycle of 250mg-600mg/day, the
average user will lose 1lb+ of body fat a day. This is not without a price, as DNP side effects can be
debilitating and DNP overdoses are guaranteed to kill the user. Researching DNP as thoroughly as possible is
vital to ensuring maximum safety of use.

The NIH has a very good article on the history and risks of DNP here: 2,4-Dinitrophenol (DNP): A Weight Loss
Agent with Significant Acute Toxicity and Risk of Death
How does DNP work?
DNP inhibits ATP production in cell mitochondria through uncoupling the metabolic pathway oxidative
phosphorylation. This has two consequences which result in fat loss:

• Instead of being converted into ATP, all consumed and stored macromolecules are converted into significant
amounts of heat, which in turn raises body temperature and increases the bodies basal metabolic rate
between 50%-75% depending on dose.

• When your ATP levels fall below the necessary range for your body to function properly, your body attempts
to convert all stored glycogen and fat into ATP. Since the body cannot achieve this, the body burns from
stored "energy reserves (fat)" for the entirety of time that you run DNP.
 While the raise in body temperature determines the effectiveness of DNP supplementation, it is also what is so
dangerous about its use. An overdose of DNP will lead to fatal hyperthermia. The first cycle of DNP use will
ultimately be the most vital to understanding the compound, how your body reacts to it and how to utilize it
safely.

How to use DNP:

Beginner (First) Cycle examples:

Begin use at ~200mg/day for 3-4 days.

• After 4 days, continue 200mg/day for an additional 10-17 days.

or

• If you can handle the side effects, ramp up to 400mg/day for an additional 10 days.
When DNP was in common use, the dose was usually around 300 mg/day. There's a JAMA paper from 1934
on DNP that has details on dosages and cycle lengths. Use of Dinitrophenol in Nutritional Disorders A Critical
Survey of Clinical Results
Advanced Cycles:

Advanced DNP users can safely dose between 200mg-800mg/day. Generally, we see 200mg/day cycles from
advanced users lasting ~30 days. This can be considered a cruise dose. The blast dose of 600mg+ is usually
run for 14-21 days.

A note on safety: The longer DNP is run, the higher %potential for adverse effects.
Some users have been known to run upwards of 1g/day. This is not only overkill but it is also extremely
dangerous, as 1g/day moving into stable blood levels can put you either just below, at, or above the overdose
limit depending on your weight. Most users who will dose 1g, will do so as either a frontload or once a week
as an added boost. Again, this is not necessary or recommended.
Click here - Graph of blood level accumulation based on dose/time

Guidelines for use:

• Do NOT use DNP in hot environments (Extended periods of time in the sun, use in a sauna, steam room, etc.)
This can cause fatal hyperthermia.

• Do NOT consume alcohol while on DNP (This is far more important than the dangers of consuming alcohol
with oral steroids, as this relates to hyperthermia and not liver damage).

• Do NOT take diuretics while using DNP.

• Drink 2-3 gallons of water or more a day.

• Discontinue use if your oral temperature rises above 103 - Continue use of a lower dose when temperature
returns to normal.
• Supplement with electrolytes

• Optional: Supplement with Antioxidants (prevent free radical damage from fat oxidation) and Glycerol (may
prevent muscle catabolism)

Side effects (Mild):

• Intense feelings of heat [Unavoidable]

• Profuse sweating [Unavoidable]

• Lethargy [Simple sugars (fructose) will mitigate]

• Insomnia [Dose/user dependent - do not mistake for heat/sweating causing sleep disturbance]

• Shortness of breath [Dose/user dependent]

• Headache [Dose/user dependent]

• Dry/Sore throat [Dose/user dependent]

• Yellowing of the eyes [Dose/user dependent - NOT A RESULT OF LIVER DAMAGE]

• Yellowing of semen/urine/sweat [Dose/user dependent - often cured by increase in water intake]

Side effects (Harsh)

These side effects are incredibly rare - and are ALL a result of extremely long cycles, overdose, or gender +
age specific.

• Cataracts [In a trial of 100,000 people, less than ~0.1% developed cataracts. These were predominantly
women aged ~45, who used DNP for ~11 months, and developed cataracts ~7-15 months after use. In the
VERY RARE cases of males ~22-25 recently developing cataracts, they ran DNP at 1g+ daily and for extended
periods of time]

• Peripheral Neuropathy [This may first present as numbness. Symptoms include tingling, pain, itching,
crawling, and pins and needles. Pain can become intense enough to require use of opioid (narcotic)
drugs.] See this post for a user's experience.

• Death [Death is due to overdose resulting in fatal hperthermia - Completely avoidable by following the
conservative dosing protocols discussed above]

Additional notes:
• During the first 3-4 days of use, DNP will deplete your body of glycogen. The full range of DNP's side effects
will NOT be observable until after this time frame. This is why ramping up for a first time use is necessary.
• When your body lacks glycogen your muscles appear flat and small. DNP will also force your body to retain a
LOT of water. These two consequences result in a physique opposite of the desired results from DNP use.
THIS IS TEMPORARY - Your body will lose all water weight and replenish glycogen ~5 days after cycle. Until
then, be aware that your appearance and weight will be deceiving.

• DNP is Yellow. DNP has been used as an incredibly strong yellow dye. This potential is what causes yellowing
of the eyes and semen, among other fluids such as sweat and urine. This is nothing to be concerned about,
and increases in water consumption often prevents this.

• If you take DNP and develop a rash or hives IMMEDIATELY discontinue use. A rash indicates allergy to DNP.
The allergic reaction will subside without medical intervention - and there IS a protocol to overcoming the
allergy, but I will not cover it here.

• It is not advised to exercise with any sort of high intensity while on DNP.

• DNP may cause nausea/vomiting, generally cause by dosing on an empty stomach.

• A good protocol for DNP use is before bed (on a single dose) or before bed and upon wake up (on multiple
doses).

• Split large doses equal hours apart if possible.

• Eating carbs while on DNP will cause your body to suffer a temporary heat wave - it is thought the carbs are
being instantly burned away.

• DNP comes it two forms: Crystal and Powder. It is generally believed that powder is more potent than crystal
by a ratio of ~5:4

• Your body cannot build a tolerance to DNP. This is both a positive and negative attribute. While you can take
DNP at a single dose for as long as you want, this is also precisely the reason that a fatal overdose is cause for
alarm. If overdosed, your body does not possess a single method of saving itself.

• DNP will cause your body to stop creating T3. At 200mg/day, this is usually seen around day 10. At 400mg-
600mg/day, this can be seen as early as day 3. Supplementing with T3 is advisable.

DNP is not fully understood and lacks research to validate many claims of harsh side effects not mentioned
here. While this compound profile attempts to explain everything known about DNP in an effort to ensure
maximum safety of use, as with anything - individual use will vary. Always exercise caution when using DNP.

Sources
DNP Explained - Courtesy of /u/HyperactiveGray
DNP In-depth Side effects/Health Risks - Courtesy of /u/IthinkI_likeu
DNP - Cataracts
 DNP discussed on Pubmed - Complete with additional references
Use of Dinitrophenol in Nutritional Disorders. A Critical Survey of Clinical Results, a 1934 paper
from American Journal of Public Health and the Nation's Health.
Cataracts Following the Use of Dinitrophenol: A Summary of Thirty-Two Cases, a 1936 paper from California
and Western Medicine.
THE USE OF 2:4-DINITROPHENOL AS A METABOLIC STIMULANT Br Med J. Mar 24, 1934; 1(3820): 524–527.
DNP Wiki - Complete with additional references
Additional thanks to:
/u/hypnotoadIRL for peeking my interest in DNP
Everyone from the Crowdsource Thread

Ephedrine

Pharmaceutical Name: Ephedrine Hydrochloride

Formula: C10 H15 NO
Chemical Structure: (R,S)-2-(methylamino)-1-phenylpropan-1-ol
Molecular Weight Of Base: 165.23
Excretion: 22-99% renal
Half Life: 3-6 hours
Anabolic/Androgenic Ratio (Range): mildly anabolic, not androgenic

Use/Dosing

Note: all dosage discussion is for ephedrine, not ephedra. See [Ephedra vs Ephedrine]() for discussion.

The primary application for ephedrine among bodybuilders and athletes (off-label) is that of a cutting (fat-
loss) agent. Here, the individual will generally take this drug a few times per day during a dieting phase of
training, at a dosage of 25 to 50 mg per application.

Maximum dosage is 150 mg per day in divided doses. Do not take 150 mg at one time.

Side Effects/Risks:

• Headaches

• Increase in blood pressure

• Shaky hands

• Tremors

• Sweating
• Rapid heartbeat

• Dizziness

• Feelings of inner unrest

Ephedrine is a CNS stimulant with potential for fatal overdose. Signs of overdose may include:

• Rapid breathing

• Blood pressure irregularities

• Irregular heartbeat

• Unconsciousness

• Trembling

• Shaking

• Panic

• Extreme restlessness

• Severe nausea, vomiting, or diarrhea

How does Ephedrine work (excerpt from Anabolics)?

The action of this compound is notably similar to that of the body's primary adrenergic hormone epinephrine
(adrenaline), which also exhibits action toward both alpha and beta receptors. When administered,
ephedrine will notably increase the activity of the central nervous system, as well as have a stimulatory effect
on other target cells. This may produce some effects that can be beneficial to a bodybuilder or athlete. For
starters, the user's body temperature should rise slightly as more free fatty acids are produced from the
breakdown of triglycerides in adipose tissue (stimulating metabolism). This may aid in body fat reductions
and increased vascularity. It is also believed that the anabolic effectiveness of steroids might be increased
with this substance (mildly), as an increase in metabolic rate may equate to an increase in fat, protein and
carbohydrate conversion by the body. The stimulant effect of this drug will also increase the force of skeletal
muscle contractions.

Companion Supplement(s)

See ECA or EC Stack

Note:

Ephedrine will slightly assist in fat loss. As with most things in the steroid community, appropriate training
regimen and diet need be followed to experience the benefits of Ephedrine.

Ephedra vs Ephedrine

Ephedra is a stem extract from ephedra sinica (ma huang) or ephedra vulgaris (aka distachya),
while ephedrine is a sympathomimetic amine found in ephedra. The same results can be achieved taking
ephedra or ephedrine. To obtain the same doses of ephedrine while taking ephedra, compare the ephedra
dose with how much ephedrine is in the extract (typical extracts are standardized to 8-12% ephedrine).
However, ephedra contains several other active ingredients, including norpseudoephedrine (an ephedrine
precursor), several kynurenate compounds, and others. While these compounds have been correlated with
other negative effects, it is highly unlikely to be observed in typical doses of ephedra (in particular, high levels
kynurenate compounds are associated with psychotic symptoms, but the dose of ephedra necessary for such
a concentration would also contain a very fatal amount of ephedrine).

References:

Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp.521

http://www.ncbi.nlm.nih.gov/pubmed/22618982
http://www.ncbi.nlm.nih.gov/pubmed/11454619

ECA or EC Stack

The ECA stack is a commonly used fat burning stack consisting of Ephedrine, Caffeine, and Aspirin.

The main component, Ephedrine, is the main active ingredient for weight loss and the caffeine augments its
efficacy. The aspirin is added to prevent blood clotting (which may be a side effect of ephedrine) and to aid in
the signal transduction of ephedrine via prostaglandin inhibition.

Some proponents of the ECA stack recommend replacing the Aspirin in the stack with either Fish Oil or White
willow bark, as Aspirin is linked to various organ side effects and the previous two compounds share the
same anti-clotting mechanisms. Overall the difference to the stack is negligible.

Studies have shown that the combination of Ephedrine and Caffeine is superior for fat loss than taking each
individually.[1][2][3] As ephedrine can increase heart rate and caffeine may increase blood pressure (in a naive
user), the combination tends to have an additive rather than synergistic toxicological profile.[4]
 Use/Dosing

To get started, compile the necessary ingredients into a series of doses. Ephedrine can be purchased as
ephedrine sulfate or ephedrine HCL and usually comes in 20-50 mg tablets. Ephedrine sulfate is slightly purer,
but either will work. Caffeine is sold in 200 mg tablets, and baby aspirin tablets contain 81 mg (if you choose
to use it).

Consume ephedrine, caffeine and aspirin doses up to three times a day in equal intervals. Slowly taper the
dose upward as your tolerance increases. Begin at one dose each day, and add in the next dose every two to
four days until you reach the full amount. Take the first dose immediately upon waking. Take each
subsequent dose on an empty stomach, at least four hours after the previous one. Avoid taking too close to
bedtime as it may interfere with sleep.

Repeat this process for up to eight weeks. To maximize the effects of ECA or EC for both fat loss and energy,
it is advised to take one to two days off each week to allow your receptors to recover and avoid adrenal
fatigue.

Side Effects/Risks

The ECA stack combines strong stimulants. It should not be used if you have a pre-existing medical condition
or if you are at risk for heart disease. Consult a doctor before beginning ephedrine use, and monitor blood
pressure and heart rate regularly. Do not use if you are sensitive to stimulants. The athlete may use an
increase in body temperature as a marker that the drug combination is working. This is usually a degree or so
(not an uncomfortable raise).

FAQ

Q: Do I need to cycle ephedrine?

A: Surprisingly, ephedrine does not appear to need cycling for the fat burning aspect of it (it may for
neurological stimulation and appetite suppression). If using an ECA stack, however, Caffeine is still subject to
desensitization. It may be worth cycling the C fragment of the ECA stack, although the E does not need to be.
A break of at least 4-6 weeks is usually taken so that this stack may once again work at an optimal level.

References

1. Astrup A, et al The effect and safety of an ephedrine/caffeine compound compared to ephedrine, caffeine
and placebo in obese subjects on an energy restricted diet. A double blind trial . Int J Obes Relat Metab
Disord. (1992)
2. Toubro S, et al Safety and efficacy of long-term treatment with ephedrine, caffeine and an
ephedrine/caffeine mixture . Int J Obes Relat Metab Disord. (1993)
3. Astrup A, et al Thermogenic synergism between ephedrine and caffeine in healthy volunteers: a double-blind,
placebo-controlled study . Metabolism. (1991)
4. Haller CA, Jacob P 3rd, Benowitz NL Enhanced stimulant and metabolic effects of combined ephedrine and
caffeine . Clin Pharmacol Ther. (2004)

Fulvestrant

Drug Class: SERD

Active Life: 40 days
Fulvestrant (Brand name: Faslodex) is a Selective Estrogen Receptor Down-Regulator (SERD) which functions
by binding to the oestrogen receptor, completely inactivating it (unlike SERMs like tamoxifen) as well as
accelerating its proteasomal degradation.1 It is manly used to treat metastatic breast cancer in post-
menopausal women who have previously undergone anti-estrogen therapay. It is normally made in 50mg/mL
preparations.
Fulvestrant does not interact with AIs and in fact, the two can work together.2 Judging by the fulvestrant's
mechanism, it might be unwise to use it in conjunction with SERMs, as they both bind to the ER and thus
would end up competing. Fulvestrant is metabolized in the liver, which also contains "fulvestrant conjugation
enzymes" that serve to deactivate the drug.4 Fulvestrant does not cross the blood-brain barrier, which should
be taken into consideration when using fulvestrant with highly aromatizing steroids.3
Fulvestrant has no effect on LH or FSH and should not be used for Post-Cycle Therapy.5

Use/Dosing

The clinical method of using fulvestrant is to break the therapy into Loading Phase (LP) and Maintenance
Phase (MP). During the LP, fulvestrant is administered on days 1, 15, and 29 at 500mg. During the MP, the
dose is kept the same but only used once per month.5
Proposed use for athletes, due to its long half-life and that it may be used with AIs, is to carry out the LP and
MP, but at one half or one quarter of the clinical dose as the clinical dose has the same effects as 1mg
Anastrozole per day.2 This should create a sort of "background suppression" of the ER, and flare ups of
estrogen and estrogen related symptoms should be treated with an on-hand AI.

Due to it's long half-life, its use among athletes is limited and might only be suitable for use during long
stretches of highly aromatizing steroids. e.g. high "blast and cruise" cycles

Risks/Side Effects

Fulvestrant has no negative effects on triglycerides or HDL and in fact, it lowers LDL and total
cholestrol.6 Similarly to the AIs and unlike SERMs, fulvestrant leads to bone turnover rates about the same as
letrozole, anastrozole, and exemestane.7,8 High turnover rates are associated with risks for joint and bone
disorders and should always be of concern while running AIs and fulvestrant for long periods of time.
 Fulvestrant will also cause elevated liver enzymes, and is recommended at lower doses for those with hepatic
impairment. Common, notable side effects include nausea, fatigue, hot flashes, headaches, and shortness of
breath.5

References

1. Wikipedia contributors. Fulvestrant. Wikipedia, The Free Encyclopedia. December 11, 2014, 03:43 UTC.
Available at: http://en.wikipedia.org/w/index.php?title=Fulvestrant&oldid=637573674
2. Mehta RS, Barlow WE, Albain KS, et al. Combination anastrozole and fulvestrant in metastatic breast
cancer. N Engl J Med. 2012;367(5):435-44.
3. Vergote I, Abram P. Fulvestrant, a new treatment option for advanced breast cancer: tolerability versus
existing agents. Ann Oncol. 2006;17(2):200-4.
4. Chouinard S, Tessier M, Vernouillet G, et al. Inactivation of the pure antiestrogen fulvestrant and other
synthetic estrogen molecules by UDP-glucuronosyltransferase 1A enzymes expressed in breast tissue. Mol
Pharmacol. 2006;69(3):908-20.
5. Faslodex. Wilmengton, DE: AstraZeneca Pharmaceuticals LP; 2010
6. Camerini A, Rondini M, Garrone O, et al. Fulvestrant treatment is associated with cholesterol plasma level
reduction in hormone-receptor-positive metastatic breast cancer patients. Cancer Biol Ther. 2009;8(15):1450-
5.
7. Mccloskey EV, Hannon RA, Lakner G, et al. Effects of third generation aromatase inhibitors on bone health
and other safety parameters: results of an open, randomised, multi-centre study of letrozole, exemestane
and anastrozole in healthy postmenopausal women. Eur J Cancer. 2007;43(17):2523-31.
8. Agrawal A, Hannon RA, Cheung KL, Eastell R, Robertson JF. Bone turnover markers in postmenopausal breast
cancer treated with fulvestrant--a pilot study. Breast. 2009;18(3):204-7.

Related Posts

Mechanism of action: https://www.youtube.com/watch?v=NVcWdgVBwXY

Human Chorionic Gonadotropin (HCG)

Drug Class:* Leutenizing Hormone (LH) - Gonadotropin **Active Life: 64 hours

Human chorionic gonadotropin (HCG) is a hormone produced in the placenta of the female body during the
early months of pregnancy. It is in fact the pregnancy indicator looked at by the over the counter pregnancy
test kits, as due to its origin it is not found in the body at any other time. Medically, human chorionic
gonadotropin has been used for the treatment of undescended testicles in young males, hypogonadism
(underproduction of testosterone)1 and as a fertility drug used to aid in inducing ovulation in women. In
veterinary practices, it can also be used to rapidly induce ovulation, most often in cows and horses.
For male steroid users, HCG can mimic the action of luteinizing hormone (LH) in the body. Luteinizing
hormone is a pituitary hormone that is released and signals the manufacture of testosterone in the testicles.
It is this ability that enables the compound to help restore the normal function of the testes to respond to
endogenous luteinizing hormone. This ability can be dramatically reduced after a long period of inactivity, as
is the case when administering anabolic steroids. Even when the release of endogenous LH has been
resumed to it's normal levels, testosterone levels may not return to normal because of the extended time of
inaction that the testes were exposed to2 .

Individuals will also often use HCG to combat testicular atrophy, a result of the hypothalamus pituitary testes
axis shut down. While this atrophy is more of a symptom of a side effect of anabolic steroid use rather than
something that can be dangerous to a user, many individuals are concerned about testicular atrophy and turn
to human chorionic gonadotropin to help and alleviate it. For this purpose, HCG is quite effective.

As is fairly obvious by the preceding, human chorionic gonadotropin offers female athletes no performance
enhancing qualities and is useless for this purpose.

Use/Dosing

It is important to note that HCG should only be run while a user is still on cycle and not during PCT. This is due
to human chorionic gonadotropin actually being suppressive to the hypothalamus pituitary testes axis.
Obviously this is something to be avoided when attempting to "re-start" your natural testosterone
production. Ensure that the last shot of HCG is taken within several days of the start time of post-cycle
therapy so that it has cleared the system of the user and the compounds being taken for PCT can function as
intended.

High doses of human chorionic gonadotropin have also been shown to cause a large amount of aromatase
activity. Since a user would obviously want to keep aromatase to the lowest level possible, small and
frequent doses would be most effective while keeping side effects to a minimum. The side effects and risks
associated with HCG will be dealt with later in this profile, however obviously there are several concerns that
a user must take into consideration when choosing a method and dosing with a compound such as this.

Human chorionic gonadotropin can be injected either using intramuscular or subcutaneous injection
methods. There is no evidence showing that either method is more effective or potent than the other. Some
users complain of a sharp sting when injecting the compound. However this pain quickly dissipates.

Once constituted, human chorionic gonadotropin must be refrigerated. Depending on the type/brand of HCG
a user has it could last from approximately four to eight weeks. Constituting the powder of the compound
with bacteriostatic water may add some shelf life but this increase is not dramatic by any means, extending
the life of the constituted compound by only days.
There are numerous effective ways with which a user can administer human chorionic gonadotropin
throughout their cycle. However, one must ensure that they do not run it at such a dose that damage is
caused and that the Leydig's cells are desensitized to luteinizing hormone which could impair an individual's
ability to produce testosterone naturally. Some evidence has shown that doses as low as 800 to 1200ius can
cause at least temporary damage Leydig's cells in some individuals1 . However, the medical literature and
many doctors who specialize in hormone replacement therapy and/or endocrinology still prescribe much
larger doses of HCG despite this. Doses in excess of 3000ius have been recommended and prescribed by
doctors to help stimulate testosterone production in patients suffering from hypogonadism. However, like
many compounds, there is very little research regarding the use of human chorionic gonadotropin for the
reason that most steroid users administer it.

A majority of users have anecdotally reported that frequent small doses are the norm for steroid users
attempting to maintain at least minimal testicular function during their anabolic steroid cycles. However the
timing, doses, frequency and durations of administering the drug vary quite widely amongst users. For the
most part this is due to the lack of credible information available to users about how to go about using the
compound effectively. However, there are some absolutes when using human chorionic gonadotropin.

First, more frequent dosing is nearly always better to use rather than increasing the dose size. Due to the fact
that HCG aromatizes and it is believed that it may be the estrogen, along with other factors, that may cause
testicular desensitization3 large doses would only cause more problems for a user. However, smaller more
frequent doses should enable an individual to use a substantial dose of the drug spread out over several days
while minimizing the risk of damage. Anecdotally users report administering the compound from twice per
week to every other day, with some even choosing to inject everyday at very small doses.

In terms of frequency of injections users often find that it is determined by the length of time that they are
planning on running the compound which influences their decision about dosing length. For example, some
individuals will begin administering HCG during the last few weeks of their cycle prior to beginning their post-
cycle therapy (PCT). The belief is that by doing so you will "shock" the testicles back into functioning just
before PCT begins so that they can start to perform normally. Usually a user will choose to administer the
human chorionic gonadotropin several times per week, even in some cases running it for several consecutive
days at comparitavely high doses.

Another often used method is to run HCG throughout a user's cycle with less frequent injections. The theory
behind this method is that it is much easier to attempt to maintain testicular function throughout a cycle
rather than to try and "re-start" proper functioning. Most often when users are using this method of
administration injections are done at a minimum of twice per week beginning in the first or second week of a
steroid cycle, with them being conducted to a maximum of every three days. Of course a user may vary the
dosing frequency as he sees fit depending on how he reacts to the compound. Usually it is the rate of
testicular atrophy that a user will use as a guide as to when to increase his dosages and/or the frequency of
injections.
Side Effects/Risks

As noted earlier, the primary risk associated with human chorionic gonadotropin is causing testicular
desensitization and damage to the Leydig cells of the testes resulting in permanent impairment to natural
testosterone production4 . It is the aromatase activity that occurs with HCG that some feel is actually toxic to
the Leydig cells of the testes3 . If this sceanrio plays out an individual would be causing permanent damage to
their natural testosterone production (hypogonadism). This is why relatively small doses of the compound
should be administered at a time. If large doses are taken it is likely that some damage may occur.
One way to minimize the risk of permanent damage is to use tamoxifen throughout the administration of
HCG. Studies have shown that human chorionic gonadotropin can, at least partially, block the conversion of
17 alpha-hydroxyprogesterone (17 OHP), which is a testosterone precursor, to testosterone. Obviously this is
something that a user would want to avoid. However tamoxifen has been shown to protect against this effect
quite effectively4 . Therefore, it would appear that by using tamoxifen while running HCG a user could help to
ensure that desensitization of the testes does not occur. However, it should be noted that if a user is not
running large amounts of human chorionic gonadotropin desensitization should not be an issue and
tamoxifen would be unnecessary. Despite this, for those users that administer large amounts of HCG it is
advisable that they also use tamoxifen for this reason.
Due to the fact that there exists luteinizing hormone and human chorionic gonadotropin receptors in various
tissues in the body other then gonadal, this indicates that human chorionic gonadotropin can have an effect
on these tissues resulting in possible negative side effects when administered. Such case of this is the
possible development of gynecomastia in users5 . It appears that the use of human chorionic gonadotropin in
a small number of users has resulted in some men developing gynecomastia that is not related to their
estrogen levels or increased levels of prolactin, the most obvious causes of gynecomastia in steroid users.
Rather, in a very small minority of users it seems that the increased amount of circulating luteinizing
hormone or the human chorionic gonadotropin itself can interact with these receptors in the breast tissue
causing a reaction resulting in the development of gynecomastia5 . It is unknown at this time the actual
mechanism by which this is accomplished, but it does appear to occur frequently in a small number of men.
As well there is no known method to combat this side effect in men who experience it, leaving the only
option to treat this effect the cessation of human chorionic gonadotropin administration altogether.
Fortunately it appears that when this is done the gynecomastia that has developed begins to dissipate rapidly
and becomes unnoticeable within a matter of days or weeks in the majority of cases.
So knowing that the ability of the testes to aromatize androgens could potentially be heightened several
times greater than normal when using HCG2 , it is fairly obvious that it should only be used as a quick stimulus
to the testes and not something that is used to constantly barrage them in an attempt to keep them
functioning6 . If used correctly the compound is capable of aiding in recovery of natural testosterone
production post-cycle, but like all compounds it's use must be tempered with the correct knowledge and
application.
 Related Studies

1. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with
Testosterone-Induced Gonadotropin Suppression

References

1. Acute stimulation of aromatization in Leydig cells by human chorionic gonadotropin in vitro. Proc Natl Acad
Sci USA 76:4460-3, 1979
2. Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp. 272-3
3. Levalle OA, Suescun MO, Fiszlejder L, Aszpis S, Charreau E, Guitelman A, Calandra R. Effect of an antiestrogen
on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic
hypogonadic men: tamoxifen and testicular response to hCG. Andrologia 1991 Mar-Apr, 23(2):109-14
4. Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg PW. Tamoxifen suppresses gonadotropin-
induced 17 alpha-hydroxyprogesterone accumulation in normal men. J Clin Endocrinol Metab 1980 Nov,
51(5):1026-9
5. Carlson HE, Kane P, Lei ZM, Li X, Rao CV. Presence of Luteinizing Hormone/Human Chorionic Gonadotropin
Receptors in Male Breast Tissues. J Clin Endocrinol Metab. 2004 Aug;89(8):4119-23
6. Cantrill JA, Dewis P, Large DM et al. Which testosterone replacement therapy? Clin Endocrinol (oxf) 21 (1984)
97-107

HMG

HMG is typically used to treat infertility . Basically, long term use of HCG at doses of 1000 i.u. 3 or more times
weekly causes suppresion or insensitivity of Luetinizing hormone (LH) and to some degree Follicle stimulating
hormone (FSH).

Body builders who dont respond to the classic PCT schemes of low dose HCG and clomid for a few weeks will
definitley have a hard time with recovery and may encounter depression, a lacking sexual drive, low testicular
weight along with low semen/sperm volume.

HMG is Follicle stimulating hormone (FSH) and luetinizing hormone (LH). This simply stimulates your natural
test production and keeps HCG working optimally. Your sex drive and sense of well being come back more
rapidly then with other treatment as well as your potential for staying or becoming fertile.

Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are called gonadotropins because stimulate
the gonads - in males, the testes, and in females, the ovaries. They are not necessary for life, but are essential
for reproduction. These two hormones are secreted from cells in the anterior pituitary called gonadotrophs.
Most gonadotrophs secrete only LH or FSH, but some appear to secrete both hormones.
As described for thyroid-simulating hormone, LH and FSH are large glycoproteins composed of alpha and beta
subunits. The alpha subunit is identical in all three of these anterior pituitary hormones, while the beta
subunit is unique and endows each hormone with the ability to bind its own receptor.

In both sexes, LH stimulates secretion of sex steroids from the gonads. In the testes, LH binds to receptors on
Leydig cells, stimulating synthesis and secretion of testosterone. Theca cells in the ovary respond to LH
stimulation by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells.

As its name implies, FSH stimulates the maturation of ovarian follicles. Administration of FSH to humans and
animals induces "superovulation", or development of more than the usual number of mature follicles and
hence, an increased number of mature gametes.

FSH is also critical for sperm production. It supports the function of Sertoli cells, which in turn support many
aspects of sperm cell maturation.

Diminished secretion of LH or FSH can result in failure of gonadal function (hypogonadism). This condition is
typically manifest in males as failure in production of normal numbers of sperm. In females, cessation of
reproductive cycles is commonly observed.

Elevated blood levels of gonadotropins usually reflect lack of steroid negative feedback. Removal of the
gonads from either males or females, as is commonly done to animals, leads to persistent elevation in LH and
FSH. In humans, excessive secretion of FSH and/or LH most commonly the result of gonadal failure or
pituitary tumors. In general, elevated levels of gonadotropins per se have no biological effect.

Letrozole, Letro
Pharmaceutical Name: Femara
Formula: C17 H11 N5
Chemical Structure: 4,4'(1 H-1 ,2,4-Triazol-1-ylmethylene) dibenzonitrile.
Molecular Weight Of Base: 285.303
Excretion: Kidneys
Half Life: 2 days
Anabolic/Androgenic Ratio (Range): Oral non-steroidal aromatase inhibitor.

Use/Dosing
The structure and activity of this compound are very similar to that of Arimidex (anastrozole). It is typically
used as a second line of treatment after an estrogen-receptor antagonist like tamoxifen has failed to elicit a
desirable response, although it is sometimes initiated as the first course of therapy depending on the
circumstances. Male bodybuilders and athletes find value in letrozole for its ability to mitigate the estrogenic
 side effects associated with the use of aromatizable anabolic/androgenic steroids, such as gynecomastia, fat
buildup, and visible water.

The dosage of each tablet of Femara is 2.5 milligrams, which according to product information was sufficient
to lower estrogen levels by an average of 780/0 during clinical trails. The drug, however, appears to often
remain quite effective in lower doses. The package insert for the product itself comments that during clinical
studies doses as low as .1 and .5 milligrams produced 75 and 78% estrogen inhibition, respectively in many
patients. The recommended dose, likewise, reflects a level that seems to elicit a desired level of inhibition in
nearly all patients. A large number of people may, therefore, respond well to lower doses of the drug. When
used (off-label) to mitigate the estrogenic side effects of anabolic/androgenic steroid use or increase muscle
definition, male athletes and bodybuilders often take 1.25 mg to 2.5 mg per day. I

Maximum dosage is unknown but it's not suggested to go over 2.5mg a day

Side Effects/Risks (of Aromatase Inhibitors):

• Hotflashes

• Joint pain

• Weakness

• Fatigue

• Mood changes

• Depression

• High blood pressure

• Swelling of arms and legs

• Headache

References:
Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition, pp.521

Melatonin

Chemical Name: N-acetyl-5-methoxytryptamine

Molecular Weight: 232.278 g/mol

Formula: C13H16N2O2

Half-Life: 20-50 minutes

Background Information

Melatonin is a neurohormone secreted by the pineal gland in the brain and it is well known for causing and
regulating sleep. Light suppresses melatonin synthesis. The primary use of melatonin as a supplement is to
normalize abnormal sleep patterns.

It was dubbed 'melatonin' in 1958 by Aaron B. Lerner after he isolated hormone from bovine pineal gland
extracts.

Melatonin was first discovered to be an antioxidant in 1993, and was patented as a low dose sleep aid in
1995.

Effects

Melatonin is used to help reset/establish day-night patterns (circadian rhythm). It was also discovered to be a
powerful antioxidant. Melatonin has been proven to be twice as active as vitamin E, believed to be the most
effective lipophilic antioxidant. Finally, studies show that melatonin has a positive effects on growth hormone
production!

Note: Melatonin will not help with sleep quality, but will drastically improve sleep latency. This means that it
will only help you fall asleep, not stay asleep.

(Potential) Side effects

Melatonin is as side free as it gets (in my opinion). When used in proper protocols, no side effects were
observed. You WILL NOT shut down your natural production of melatonin.

Melatonin is a sedative and will lower body temperature. It is suggested that you do not consume melatonin
before working out.

(Suggested) Dosing Protocol

For regulating the sleep cycle, doses of melatonin between 500mcg (0.5mg) and 5mg seem to work. Start
with 500mcg, and if it doesn’t work, work up to 3-5mg. The benefits of melatonin are not dose-dependent -
taking more will not help you fall asleep faster.

To help with sleep, take roughly 30 minutes before going to bed.

Growth hormone appears to spike slightly better at 5mg than 500mcg, although both doses are fairly
effective.
Sources/Fun reading Material
General Information/Studies on Melatonin
More Gneral Info
Silverhydras Updates on Melatonin
Melatonin Makes Old Bones Stronger
Artificial Light, Biological Clock Disruptions, Increase Breast Cancer Risk, Study Finds

Nolvadex (Tamoxifen Citrate)

Drug Class: Selective Estrogen Receptor Modulator Active Life: 5-7 days
Tamoxifen citrate is a selective estrogen receptor modulator. Selective estrogen receptor modulators can act
as estrogen receptor agonists or antagonists1 . This activity of tamoxifen citrate is tissue selective, effecting
those estrogen receptors located in the liver, breast, and bone. When the tamoxifen molecule binds to this
receptor, the estrogen is blocked and can not have any influence, thereby remaining inactive in that tissue.
By doing so, an "anti-estrogenic" effect is achieved. The drug was developed and still used to treat breast
cancer. It is often used as a first option due to its mild nature in comparison to aromatase inhibitors2 . Of
course one would want to use the mildest compound possible when dealing with estrogen levels in women,
but one could afford to be more aggressive in dealing with male strength athletes or bodybuilders.
In terms of its use in steroid users, tamoxifen citrate can help in two ways. Firstly due to the binding affinity
of the compound it is able to help in the prevention of gynocomastia3 . Tamoxifen will compete with estrogen
for the estrogen receptors in certain tissues, including the breast, and if it can bind to the receptor estrogen
will not have an opportunity to interact with receptor and therefore gynocomastia should not be able to
develop. When using anabolic steroids that can convert to estradiol (estrogen) this protection against
gynocomastia can be invaluable. However it should be noted that tamoxifen citrate will not eliminate the
estrogen or disallow the conversion to occur. Instead it attempts to counteract the effects of circulating
estrogen in the body in those tissues that the drug effects. Therefore there is no evidence that tamoxifen
citrate has any effects counteracting etrogenic side effects that are unrelated to the tissues that are not in
the breast, liver or bone. Namely there is no real causal connection to any reduction in water retention and
acne in users that begin taking tamoxifen citrate as it relates to estrogen.
The second, and possibly more beneficial, aspect of tamoxifen citrate for steroid users is its ability to increase
the production of luteinizing hormone and follicle stimulating hormone, and therefore increasing
testosterone4 . This ability is why it is often used by steroid users during their post-cycle therapy. There are
numerous studies that indicate that tamoxifen citrate can increase the levels of these hormones quite
dramatically. Tamoxifen citrate does this by blocking the negative feedback inhibition caused by estrogen at
the hypothalamus and pituitary, and this in turn will help to increase the production of these hormones.
Unlike clomiphine citrate, tamoxifen citrate has also been shown to increase luteinizing hormone
responsiveness to gonadotropin releasing hormone. Clomiphine citrate can lower this responsiveness over
time.

Use/Dosing

In terms of dosing for combating gynocomastia that has begun to form, there is very little research. The
limited research that does exist does point to the fact that doses of 20-40mgs per day are effective in treating
the existing condition3 . However, anecdotally users have reported sometimes using doses of 60-80mgs per
day. These doses may have more to do with users’ impatience rather than the need for higher doses, as no
research indicates that such doses are needed. It should be noted as well however that tamoxifen citrate may
have no effect on existing gynocomastia in some individuals. Many users have indicated that the compound
will only help alleviate symptoms if the gynocomstia has not been apparent for a long period of time. Of
course, this is all subjective and the effectiveness of the drug can only be determined on a trial and error
basis.
For use during post-cycle therapy users have anecdotally indicated that doses ranging between 20 and 40mgs
per day are average. These doses have been shown to significantly raise levels of testosterone, luteinizing
hormone and follicle stimulating hormone4 . Most users have reported when using tamoxifen citrate for their
post-cycle therapy they will administer the drug for a minimum of three weeks. A maximum length has not
necessarily been established due to the few side effects associated with the compound. In this case, this
compound can be run for as long as wanted with little to no concern being needed to be paid to potential
side effects. See the below section for more details.

Some users have used tamoxifen citrate for the purpose of helping raise their HDL (good) cholesterol values.
In theory it is thought that since the compound is an estrogen agonist in the liver and therefore is capable of
activating the estrogen receptor and mimicking the actions of the hormone in the organ that it may help
improve cholesterol levels as estrogen does. However this effect is rather slight and won’t significantly
improve a user’s HDL levels very noticeably at all. This is especially true when one factors in the dramatic
effect that most anabolic steroids have on these levels. For this reason, tamoxifen citrate should not be relied
upon for this purpose.

Risks/Side Effects

One of the possible side effects associated with use of tamoxifen citrate is the possible reduction of insulin-
like growth factor levels. If these levels are reduced this could suppress the gains an individual can make
slightly. However this reduction, if it actually exists, would not be overly significant with gains in muscle mass
only being marginally reduced for the most part.

Another effect of use of tamoxifen citrate may be vision problems. Recently, there has been some
information from researchers that indicates corneal, retinal and optic nerve abnormalities seen in patients
using the drug could be related to its use5 . Anecdotally a small number of steroid users have reported that
 they have suffered from visual problems while using this drug as well. After discontinuation of the drug these
symptoms seemingly dissipate. However there is simply not enough research on the subject to know whether
permanent damage could occur. More research needs to be conducted.
Other than these concerns, there is little in the way that long-term use of tamoxifen citrate could cause
damage to in the human body. It is seemingly safe in terms of possible effects to the body’s hormonal
production, other than the one relating to insulin-like growth factor, and endocrine system4 . For the vast
majority of users the compound is relatively side effect free and well tolerated.

References

1. Bruning PF, Bonfrer JM, Hart AA, de Jong-Bakker M, Linders D, van Loon J, Nooyen WJ. Tamoxifen, serum
lipoproteins and cardiovascular risk. Br J Cancer. 1988 Oct;58(4):497-9
2. Konig R, Schonberger W, Neumann P, Benes P, Grimm W. [Treatment of marked gynecomastia in puberty
with tamoxifen] Klin Padiatr. 1987 Nov-Dec;199(6):389-91
3. Schopman W, Slager E, Hackeng WH, Mulder H. Stimulation of calcitonin secretory capacity by increased
serum levels of testosterone in men treated with tamoxifen. Int J Androl. 1987 Dec;10(6):747-51
4. van Bergeijk L, Gooren LJ, van der Veen EA, de Vries CP. Effects of short- and long-term administration of
tamoxifen on hCG-induced testicular steroidogenesis in man: no evidence for an oestradiol-induced
steroidogenic lesion. Int J Androl. 1985 Feb;8(1):28-36
5. Isherwood, Dana. Tamoxifen and Your Eyes. Breast Cancer Action. Newsletter #25–August 1994

Toremifene citrate

Drug Class: Selective Estrogen Receptor Modulator

Active Life: 5-7 days
Toremifene citrate is an anti-estrogenic drug, specifically classified as a Selective Estrogen-Receptor
Modulator (SERM) with mixed agonist and antagonist properties. It is a non-steroidal triphenylethylene
derivative, similar in structure and action to both Nolvadex (tamoxifen citrate) and Clomid (clomiphene
citrate). Toremifene citrate is used for the treatment of breast cancer in postmenopausal women with
estrogen-receptor positive or estrogen unknown (unsure if the cancer is estrogen responsive) tumors. It
works by attaching to the estrogen receptor in various tissues in a competitive manner, blocking endogenous
estrogen from exerting biological activity. As an anti-estrogen in many tissues, male bodybuilders and
athletes may use toremifene citrate to counter some of the side effects associated with the use of
aromatizable or estrogenic anabolic/androgenic steroids. This may include gynocomastia, body fat gain, and
increased water retention8 .
The triphenylethylene compounds (toremifene citrate, tamoxifen citrate, clomiphene citrate) tend to be
somewhat estrogenic in the liver. This means that while they can block estrogenic activities in some areas of
the body, they can actually act as estrogens in this other key area. Estrogenic action in the liver is important
in the regulation of serum cholesterol (it tends to support HDL synthesis and LDL reductions). Since steroid-
using bodybuilders are already dealing with the negative cardiovascular effects of these drugs, compounding
the issue with aromatase inhibitors (which will lower total serum estrogen levels) may not always be the best
option. Using a drug that blocks gynocomastia, for example, while at the same time supporting improved
cholestoral values, might be much more ideal. In terms of which triphenylethylene agent is most effective in
this regard, evidence suggests that the positive lipid altering benefits of toremifene are significantly
stronger1,2 than those of tamoxifen, a drug normally favored for this purpose. Toremifene citrate may,
therefore, be the preferred anti-estrogen among those concerned about their lipid profiles8 .

Medically, toremifene citrate was developed and is still used to treat breast cancer and was first approved by
the Food and Drug Administration for this use in the United States in 1995. The difficulty in using toremifene
citrate is the lack of research conducted using human subjects, and specifically male subjects. While it is
possible to apply most of what is known about the other selective estrogen receptor modulators to
toremifene citrate, independent research conducted with the drug itself is invaluable and therefore a risk is
taken when using the drug because of the lack of information. Unfortunately toremifene citrate is possibly
the least researched selective estrogen receptor modulator, with the possible exception of raloxifene.

Despite the lack of human-based research available, in terms of its use in steroid users, toremifene citrate
can help in two ways. Firstly due to the binding affinity of the compound it is able to help in the prevention of
gynocomastia. Toremifene citrate will compete with estrogen for the estrogen receptors in certain tissues,
including the breast, and if it can bind to the receptor estrogen will not have an opportunity to interact with
receptor and therefore gynocomastia should not be able to develop. When using anabolic steroids that can
convert to estradiol (estrogen), this protection against gynocomastia can be invaluable. However it should be
noted that toremifene citrate will not eliminate the estrogen or disallow the conversion to occur. Instead it
attempts to counteract the effects of circulating estrogen in the body in those tissues that the drug effects.
Therefore there is no evidence that toremifene citrate has any effects counteracting estrogenic side effects
that are unrelated to the tissues not affected by the drug. Namely there is no real causal connection to any
reduction in water retention and acne in users that begin taking toremifene citrate as it relates to estrogen.

The second, and possibly more beneficial, aspect of toremifene citrate for steroid users is its ability to
increase the production of luteinizing hormone and follicle stimulating hormone, and therefore increasing
testosterone. This ability is why it is often used by steroid users during their post-cycle therapy. Toremifene
citrate would accomplish this by blocking the negative feedback inhibition caused by estrogen at the
hypothalamus and pituitary, and this in turn will help to increase the production of these hormones.
Currently there is no available research that directly links toremifene citrate to being able to raise
testosterone levels in male users, however due to the nearly identical mechanisms that both tamoxifen and
toremifene citrate use and the reactions that they produce in the body, it would be easy to extrapolate that
both drugs should have similar effects in this respect as well. Anecdotally users have reported good results
with toremifene citrate and say that they are at least comparable that those of tamoxifen citrate.
Use/Dosing

Toremifene citrate is interchangeable with tamoxifen citrate (Nolvadex) while on cycle or in post-cycle
therapy. 20mg of tamoxifen citrate = 60mg of toremifene citrate3 . From this it can be extrapolated that for
treatment and/or prevention of gynocomastia sixty milligrams should be sufficient for treatment. The
recommended dosage for breast cancer treatment is one 60mg tablet administered once per day. During
steroid treatment athletes and bodybuilders may use 30mg to 60mg per day8 .

For use during post-cycle therapy users have anecdotally indicated that doses ranging between 60 and 120
mgs per day are average. Most users have reported when using Toremifene citrate for their post-cycle
therapy they will administer the drug for a minimum of three weeks. A maximum length has not necessarily
been established due to the few side effects associated with the compound. In this case, this compound can
be run for as long as wanted with little to no concern being needed to be paid to potential side effects. See
the below section for more details.

Risks/Side Effects

Toremifene citrate appears to be well tolerated, with a low incidence of serious side effects. In clinical trials,
common side effects associated with its use included hot flashes (35%), sweating (20%), elevated liver
enzymes (19%), nausea (14%), vaginal discharge (13%), dizziness (95%), edema (5%), vomiting (4%), and
vaginal bleeding (2%). Other observed rare adverse effects that may or may not be linked to to toremifene
citrate administration include low white blood cell and platelet counts, skin discoloration or dermatitis,
constipation, difficulty breathing, partial motor paralysis, tremor, vertigo, itching, anorexia, visual
disturbances, loss of strength, hair loss, depression, jaundice, and rigors (stiffening of the muscles).
Antiestrogens may harm the developing fetus and should never be used during pregnancy8 .
In terms of the safety of toremifene citrate, there is some evidence that suggests that it is actually safer and
presents less possible serious side effects than tamoxifen citrate4 . For example the risk of stroke, pulmonary
embolism, and cataract are all lower when using toremifene citrate when compared to that of tamoxifen
citrate5 , although the incident of ocular toxicity is fairly rare with both drugs6 .
There is no toxicity issues directly related to the use of toremifene citrate2,7 . Any issues arising in this area
were seemingly caused by the hormonal effects of the drug, rather then the properties of the drug itself. As
well, most of these complications were connected to the disease, namely breast cancer, that the drug was
being administered to treat. For the purposes of anabolic steroid users, toremifene citrate poses no potential
toxicity issues.

Related Posts

Torem Awareness Torem Superior SERM

 References

1. Saarto T, Blomqvist C, Ehnholm C, Taskinen MR, Elomaa I. Antiatherogenic effects of adjuvant antiestrogens:
a randomized trial comparing the effects of tamoxifen and toremifene on plasma lipid levels in
postmenopausal women with node-positive breast cancer. J Clin Oncol. 1996 Feb;14(2):429-33.
2. Kusama M, Miyauchi K, Aoyama H, Sano M, Kimura M, Mitsuyama S, Komaki K, Doihara H. Effects of
toremifene (TOR) and tamoxifen (TAM) on serum lipids in postmenopausal patients with breast cancer. Breast
Cancer Res Treat. 2004 Nov;88(1):1-8.
3. Valavaara R, Pyrhonen S, Heikkinen M, Rissanen P, Blanco G, Tholix E, Nordman E, Taskinen P, Holsti L, Hajba
A. Toremifene, a new antiestrogenic compound, for treatment of advanced breast cancer. Phase II study. Eur J
Cancer Clin Oncol. 1988 Apr;24(4):785-90.
4. Riggs BL, Hartman L. Selective estrogen-receptor modulators -- mechanism of action and application to
clinical practice. N Engl J Med. 2003;348:618-629.
5. Harvey HA, Kimura M, Hajba A. Toremifene: An evaluation of its safety profile. Breast. 2005 Nov 8
6. Gianni L, Panzini I, Li S, Gelber RD, Collins J, Holmberg SB, Crivellari D, Castiglione-Gertsch M, Goldhirsch A,
Coates AS, Ravaioli A; International Breast Cancer Study Group (IBCSG). Ocular toxicity during adjuvant
chemoendocrine therapy for early breast cancer: results from International Breast Cancer Study Group trials.
Cancer. 2006 Feb 1;106(3):505-13.
7. Gong C, Song E, Jia W, Qin L, Guo J, Jia H, Hu X, Su F. A double-blind randomized controlled trial of toremifen
therapy for mastalgia. Arch Surg. 2006 Jan;141(1):43-7.
8. Llewellyn, William, William Llewellyn’s Anabolics 10th Edition 2011, Molecular Nutrition, pp.472-3
9. Farmakiotis D, Farmakis C, Rousso D, Kourtis A, Katsikis I, Panidis D. The beneficial effects of toremifene
administration on the hypothalamic-pituitary-testicular axis and sperm parameters in men with idiopathic
oligozoospermia. Fertil Steril 2007;88(4):847-53. Elsevier

T3

Intro

Triiodothyronine, or t3, is the main active thyroid hormone of the human body. It affects almost every
physiological process occurring inside your body, which makes it an extremely powerful drug to supplement
exogenously. Now I am not here to give you a full introduction on thyroid hormone, so I would suggest
reading the wikipedia page for triiodothyronine for more about it.

So you all know or have heard of t3 commonly being used by bodybuilders for dieting purposes or in
conjunction with tren or other steroid cycles, and usually in very large doses like 50-100 mcg t3 per day.

I AM WRITING THIS TO TELL YOU THAT THESE DOSAGES OF T3 ARE TREMENDOUS, DANGEROUS, RECKLESS,
AND UNNECESSARY
Now I know this goes against what many of you may have seen or know to be true in terms of t3 dosing, so
let me get into a little bit of science to explain.

Background

A normal thyroid gland produces an average of 100 mcg T4 and 6 mcg T3 daily, although it secretes closer to
10 mcg T3 daily, because some T4 to T3 conversion occurs in the thyroid gland before release. Total daily T3
produced by the body averages 30 mcg, but 80% (24 mcg) of this is from conversion in other tissues.

In other words, roughly 25 mcg of t3 will be made by the human body per day and used.
(http://www.nejm.org/doi/full/10.1056/NEJM199902113400603)

The body really doesn't produce t3 directly, as stated right above. It makes t4 which is converted into t3. By
this unique mechanism, the body can control how much active thyroid hormone it has actively flying around
your bloodstream.

The desire to use t3 on a cut is twofold: it helps increase the rate of lipolysis and glycogen breakdown and
increases the rate of protein synthesis, AND is also to supplement declining t3 levels on a cut or tren cycle.

Cutting for a long time with large caloric deficits and often restriction of dietary fats and carbohydrates is well
proven to lower thyroid hormone levels in the body. (https://www.ncbi.nlm.nih.gov/pubmed/16720655). So
yes, using t3 on a cut could be warranted.
Can using t3 on tren be warranted? This question is very difficult to answer. You need to show proof that tren
does indeed lower t3 levels on its own. Now there are studies (like
this http://tigerprints.clemson.edu/arv_theses/105/) done on COWS that suggest tren doesn't affect thryoid
hormone levels to any significant degree at least requiring exogenous t3 supplementation. Unfortunately,
cows are not MODEL ORGANISMS so these studies are useless and can be quickly dismissed. Anecdotally over
the years, many people have said to have had bloodwork showing decreased t3 levels while blasting tren, so
it has come to be.

The best thing you can do is check your thyroid hormone levels before using tren, and then during, and see if
they have declined, and if you would want to use t3 during your cut.

Muscle Wasting Properties of t3

The meat of my argument is that t3 is dangerous, and will actually cause you to LOSE MUSCLE MASS that you
worked so hard to gain, if you go hyperthyroid (more than normal levels of t3).

Tren is so commonly used on t3 because tren is very anti-catabolic and thought to be muscle sparing enough
to save the muscle waste t3 will cause. This is the only grounds on which my argument breaks, because there
is no actual science on this that I can easily point to in order to refute it. However, I will do my best to refute
this.
Tren is muscle sparing, yes. T3 is very catabolic, very powerful, and breaks down muscle and fat equally
through physiological processes that it influences. HELL, it might even break muscle down faster when you go
hyperthyroid. But caesar?!?! Didn't you just say earlier that t3 increases the rate of protein synthesis?!?!?

Yes, t3 does increase the rate of protein synthesis. However, it also increases the rate of protein degradation,
and in excess (hyperthyroid) the rate of protein degradation exceeds the rate of protein synthesis, meaning
YOU BREAK DOWN MUSCLE. The more hyperthyroid you go, the more likely you are to have more protein
degradation than protein synthesis, meaning the more t3 you take, the more muscle mass you'll lose.
(wikipedia and its sources)

Again, back to the main question: can tren spare the muscle wasting of t3? NO. Look at how powerful thyroid
hormone is in the human body. Look at THYROID STORM. Thyroid hormone is so powerful that you could
overdose on it in a hospital and they wouldn't be able to save your life, barring gastric lavage. Even the best
damn hospital with a million doctors couldn't save you if they wanted to, you would die a hot painful sweaty
cramping overstimulated death.

Thryoid hormone TRUMPS AAS and tren, and tren has no physiological means of stopping the catabolism
excess t3 will bring. Yes, tren will save some of it, sure, but nowhere near all of it.

Final Thoughts

T3 usage can be warranted on a cut with tren, but not in the dosages you typically see all over the internet.
Let's assume tren does lower t3 levels. How much?? 50%?? MAYBE. MAYBE a very large dose of tren, over a
LONG CYCLE could lower your t3 levels 50%. Again, look at how much the body uses t3. You would suffer
hypothyroid effects pretty damn well if tren truly lowered your t3 by 50%. Now the great part of my
argument is that I don't need to guess how much tren lowers your t3, and neither do you.

THE ONLY DOSE OF T3 YOU NEED TO TAKE IS 12.5 MCG PER DAY

Even on tren and a cut, this 12.5 mcg dose is roughly 50% of what your body already makes and uses, and will
bring you back to euthyroid levels (normal). If you have bloodwork showing you need more t3 than this (ie 2
full weeks on 12.5 mcg t3 per day) then this is the only time I would suggest going up to 15 or 20 mcg t3 per
day, which will likely put you slightly hyperthyroid or bring you back to normal status. Taking a full 25 mcg of
t3 in any bodybuilding situation (cutting, tren) is not warranted. There is absolutely no way you will have 0 t3
in your body, trust me. You would know as you would have extreme hypothyroidism from it
The half life of t3 is 2.5 days (http://www.rxlist.com/cytomel-drug.htm) Don't trust any other t3 half life you
ever see on the internet. This means that your t3 dose wont kick in fully for about 10-11 days. FOR THE LOVE
OF SDROL DON'T FRONTLOAD t3. I could write a whole entire new post about this. All this will do is make you
go hyperthyroid and cause you to lose muscle. It's good that t3 has a fairly long half life, that is what makes it
so effective in the body. This is why you need to dose it only once a day.
 Conclusions

• t3 in excess will cause you to lose the muscle you worked so hard for. Don't waste your bulk by cutting your
muscle.

• the only t3 dose you need is 12.5 mcg per day

• t3 usage in a long or extreme cut is warranted, same for being on tren for a long time

• going hyperthyroid is bad for your body and dangerous for your health in general

• Caveat t3 needs to be taken in the morning, on an empty stomach, preferably after an over night fast (ie you
slept for 8 hours and didn't eat anything). (https://online.epocrates.com/u/10a569/Cytomel)

17 HOMEBREW
Steroid homebrew is the process of brewing steroidal compounds on a small scale for personal, non-
commercial purposes. It gives the user total governance over the substance being taken, both positively and
negatively.

Preamble
Everything you see on this subreddit has the potential to be dangerous. If you fuck something up or get bad
gear, you may see effects ranging from nothing, to bitch tits, to dying (and I'll laugh at you for being a
dipshit). Every piece of advice you read here carries with it some risk. Keep that in mind, and research before
putting anything in your body.
I started this as a response to the thread by /u/hypnotoadIRL [+3][2] , so he gets partial credit. I am a firm
believer that everyone should know how to homebrew, so that they are not beholden to UGLs. Of course, not
everyone wants to brew, but if you're here and you're curious, what is outlined below should help you get
started. Links were all valid at time of posting. [...] You don't have to be super clever.
/u/biggerstrongertaller, 'Homebrew on a (smaller) budget', 2014

Essential Reading

Homebrew w/ Pics - 26 Jul 2013 [https://imgur.com/a/1Kie8]

1 Boy, 30 Vials 200mg/ml eq, 200mg/ml deca and 250mg/ml test c. - 02 Jul 2014 [https://imgur.com/a/sqi8p]
Sterilization of Materials. - 29 Sep 2014
Homebrew On A Budget has a lot of good information on how to start. - 16 Feb 2015

Guerrilla Brewing., in which BST brews in his car. - 16 Feb 2015

First Homebrew - 27 Feb 2015
u/RippedGenesBro's Homebrew Supplies and Procedure - 2 October 2017
 Examples Of Things You Shouldn't Do

Filtering with sterile cotton shoved in a syringe

Materials
Absolute Minumum

This is if you plan to make your gear in a pot on the stove like the gym bros on some other forums do. DO
NOT ACTUALLY COOK THE OIL. You're on the stove because heat makes it easier for the hormone to suspend.

• Stove
• Small pot
• Spoon (to stir)
• Sterile syringes
• .22 micron syringe filters
• Sterile needles
• Pre-sterilized vials
Recommended

This is if you want to actually do it right, while still being economical in the materials you need to purchase.

• Glass cylinder, 500ml

• Spoon to stir
• Milligram scale
• Graduated cylinders - 5ml/50ml

If Syringe Filters

• Sterile syringe
• .22 micron syringe filter
• Sterile Needle

If Bottle Top Filters

• Glass media bottle

• .22 micron bottle top filter
• Vacuum pump (options listed in the filtering section)

I did not include vials in the materials list because there would be too many "if" statements and it would end
up a large confusing flow chart. Determine your vial needs by "Vials" section.

What ssjhayes uses

• Glassware
• Funnel for filling vials
• electric vacuum pump You will need 1/4" I.D. tubing to connect vacuum pump to filter
• 12V converter for pump
• leads to connect converter to pump
• Magnetic Stirrer
• Hot Plate
• Vial Crimper
• Glass media bottle
• Bottle top filters
• Pressure cooker

Sterilization Techniques

Sterilization refers to any process that eliminates, removes, kills, or deactivates all forms of life and other
biological agents present in a specified region, such as a surface, a volume of fluid, medication or compound.

Steam (autoclave/pressure cooker)

Using steam is a more effective way of sterilizing your vials as steam transfers heat at a much more efficient
rate. Typically an autoclave is preferred, as it has an automatic dry cycle. I use a pressure cooker, and for
those of you skeptical, here's a study. And another study.
1. Get your pressure cooker/autoclave. If using a pressure cooker, use at least 15psi.
2. Place empty vials AND rubber stoppers into device. Glass media bottles will also need sterilized. (we cannot
dry heat sterilize the rubber stoppers because well... 400* of oven heat)
3. One cycle of an autoclave, 20 minutes once the pressure cooker reaches 15psi.
4. I find there is some condensation on the vials when I pull them from my pressure cooker, I just nuke them in
the microwave for a few minutes to get rid of this. (It's sterile water at that point). If you want, you can bake
them in the oven at 400* until the condensation is gone. (I have moved from the microwave to baking them,
microwave still works fine though)
Dry Heat
1. Collect the vials and the receiver bottle (if using the glass one recommended. If you use the plastic one
included with some filters it is already sterile) you plan to fill, then grab some more. Sometimes something
gets in the vial, you didnt rinse all the alcohol off, etc. Errors happen.
2. Place the vials in a bath of your isopropyl alcohol. If you want to be thorough, get a small brush and go to
town.
3. Transfer one vial at a time to a bath of distilled water, make sure to thoroughly rinse off all alcohol. If there is
still alcohol on the vial when we put it into the oven there will be a film on the vial.
4. Preheat your oven to 350-400*F while you finish preparing the vials.
5. Get a small, flat baking pan and line the bottom with aluminum foil.
6. Place the vials, opening up, onto your foil.
7. Cover the vials with another piece of tin foil. Do not connect the sides, any evaporating water will need
somewhere to go.
8. Set a timer for 30 minutes using 400, 45 minutes for 350. I would not recommend over 400. I have had a vial
or two break at 400, I can only assume that more will break at higher temps.
9. During this time, continue the rest of your brewing process.

The Brew

BA (Benzyl Alcohol) - Used as a sterility agent within the brew itself. This prevents bacteria growth once the
vial has been punctured or stored for an excessive amount of time.
BB (Benzyl Benzoate) - Used as a solvent, this allows higher concentrations of steroid powder to dissolve into
the carrier oil.
EO (Ethyl Oleate) - Also a solvent, but allows for higher concentration brews than using BB alone.
Guaiacol - A solvent used for extremely high concentration brews. Using this typically results in increased
post injection pain.

In order to homebrew your own steroidal compound, you must have, at minimum, the following:

• Carrier Oil
• BA
• BB
• Steroid Raw Powder
The brewing process
1. Grab a clean container (preferably one that can be slightly heated, such as glass)
2. Place your measured steroid raws into the container.
3. Fill the container with the carrier oil you have decided to use.
4. Add the desired amounts of BA/BB/EO/Guaiacol to the container.
5. Stir the brew until the steroid raws dissolve completely. This may take awhile.
6. If after a sufficient amount of stirring the powder has not dissolved, begin to add heat. If brewing Tren, keep
the heat to below 140*F. Others can be heated above that, but you still do not want to cook the oil.
7. If the powder still does not dissolve after some time, you will need to add more solvents.
8. If you heated the brew, let it return to room temperature after the powder has completely dissolved to make
sure the hormone will not fall out of suspension.

Filtering

Filtration is the removal of all microorganisms and particles from liquids without any influence of their
ingredients, due to adsorption or decomposition. There are several methods to achieve this, the 2 most
popular being Bottle Top Filters and Syringe Filters. Bottle Top Filters are recommended for high quantity
brewing (100ml+).
Filter Types
Cellulose acetate (CA) membranes have a very low binding affinity for most macromolecules and are
especially recommended for applications requiring low protein binding, such as filtering culture media
containing sera. However, both cellulose acetate and cellulose nitrate membranes are naturally hydrophobic
and have small amounts (less than 1%) of non-toxic wetting agents added during manufacture to ensure
proper wetting of the membrane. If desired, these agents can be easily removed prior to use by filtering a
small amount of warm purified water through the membrane or filter unit. Surfactant-free cellulose acetate
membranes with very low levels of extractables are available on some Corning® syringe filters.
Cellulose nitrate (CN) membranes are recommended for filtering solutions where protein binding is not a
concern. They are recommended for use in general laboratory applications such as buffer filtration. Corning’s
cellulose nitrate membranes are Triton® X-100-free and noncytotoxic.
Nylon membranes are naturally hydrophilic and are recommended for applications requiring very low
extractables since they do not contain any wetting agents, detergents or surfactants. Their greater chemical
resistance makes them better for filtering more aggressive solutions, such as alcohols and DMSO. However,
like cellulose nitrate membranes, they may bind greater amounts of proteins and other macromolecules than
do the cellulose acetate or PES membranes. They are recommended for filtering protein-free culture media.
Polyethersulfone (PES) membranes are highly recommended for filtering cell culture media. PES has both
very low protein binding and extractables. PES also demonstrates faster flow rates than cellulosic or nylon
membranes.
Regenerated cellulose (RC) membranes are hydrophilic and have very good chemical resistance to solvents,
including DMSO. They are used to ultraclean and de-gas solvents and mobile phases used in HPLC
applications.
Polytetrafluorethylene (PTFE) membranes are naturally and permanently hydrophobic. They are ideal for
filtering gases, including humidified air. The extreme chemical resistance of PTFE membranes makes them
very useful for filtering solvents or other aggressive chemicals for which other membranes are unsuitable.
Because of their hydrophobicity, PTFE membranes must be prewetted with a solvent, such as ethanol, before
aqueous solutions can be filtered.
Polyvinylidene Fluoride (PVDF) membranes are commonly used in a variety of general filtration and sample
preparation applications. It has ultra low binding properties, broad chemical and temperature resistance, and
high flow rates. Hydrophobic and Hydrophilic options are available.
Glass fiber filters are used as a depth filter for prefiltration of solutions. They have very high particle loading
capacity and are ideal for prefiltering dirty solutions and difficult-to-filter biological fluids, such as sera.
Which Filter Type Should I Use?

For sterile filtering of oils use PES, PVDF, Nylon, Cellulose Acetate, Cellulose Nitrate, Regenerated Cellulose,
or MCE (Mixed Cellulose Esters).

Of the list, I recommend either PES or PVDF (They are very commonly found.)
PVDF will have greater filtering capacity, but PES will filter more quickly.

Syringe Filtering

Syringe Filters are luer lock or luer slip compatible filters that connect directly to a syringe. They are available
in a multitude of pore sizes, for our purposes we need .2 or .22 micron. Anything larger and microorganisms
will be able to pass, and sterility will not be achieved. You would draw directly from your brew, connect the
filter and a 20-23g needle to your syringe, and inject into a sterile vial (one you have sterilized, or have
bought pre-sterilized). If you use larger than a 20g needle, you risk cleaving the stopper into the vial and
you'll have pieces of your stopper floating around in your vial.

Also just a quick note that if people are willing to switch out syringe filters every 40ml the oil will flow way
better. I find the whole hand cramping thing is very overrated unless I push 60ml+ through the same filter.
u/3b8bcc64
for small batches use 3-5mL syringes, the bigger ones get MUCH harder due to the wall to bottom ratio being
too high...pressure goes exponentially more to walls instead of the bottom 95% of guys here give up on
syringe filtering because they don't know this
u/Shotmaniac
Bottle Top Filtering

Bottle-top filters are used in research laboratories for sterilization or laboratory fluid clarification. The
asymmetrical hydrophilic membrane styles provide high flow rates. They are available in a multitude of pore
sizes, for our purposes we will need .2 or .22 micron. They are available for purchase of just the filter, or a
complete set with a plastic media bottle. A vacuum pump is required when using a bottle top filter, as the
filter is activated by vacuum pressure.

A warning when using a bottle top filter - the plastic media bottle you can purchase with them tends to break
under moderate vacuum pressure (10+psi). I recommend getting a glass media bottle, most filters will be a
GL45 thread. Be sure to match your media bottle thread with your filter thread. You will need to sterilize your
glass media bottle before each brew, where-as with the plastic one they send is already sterile.

Hand vacuum pump

Electric vacuum pump. You will need a 12V adapter and to run wires from the adapter to the pump.

Vials

There is a lot of debate whether one should buy open vials and crimp them yourselves, or if you should buy
pre-sterilized vials.

If using the syringe filter method, I recommend buying pre-sterilized vials. You will not be brewing large
amounts if you opted for the syringe filters (if you are, good luck), so the extra spent on pre-sterilized vials
will be worth it.
If using the Bottle-Top method, there is a sufficient cost savings in buying open vials, along with rubber seals
and caps. You will need to buy a vial crimper for this, but there are kits that come with 100 vials, seals and
caps for around $90. There is more risk to the sterility of the brew with this method, but if you follow all
procedures correctly it is a non-issue. There is simply more room for user error.

Another option for storage is to keep your filtered brew in the media bottle you filtered into, and seal it with
a septa cap. Using this method you can draw directly from the media bottle as you would a vial. This
eliminates a transfer from the media bottle to another form of storage.

Compound Displacements

Compound 1g Displaces (mL) Notes

Boldenone Undecylenate 0.998 liquid at room temperature

Masterone Propionate 0.935

Metandienone/Methandrostenolone 0.919

Methenolone Enanthate 0.9375

Methyltrienolone/Metribolone 0.846

Nandrolone Decanoate 0.962

Nandrolone Phenylpropionate 0.942

Oxymetholone 0.996

Stanozolol 0.962

Tadalafil 0.995

Testosterone Base 0.893

Testosterone Cypionate 0.909

Testosterone Decanoate 0.962

Testosterone Enanthate 0.943

Testosterone Isocaproate 0.935

Testosterone Phenylpropionate 0.885

Testosterone Propionate 0.909

Trenbolone Acetate 0.848

Trenbolone Enanthate 0.909

 If you have more information to add to this list, please message u/Decatest or u/ssjhayes

Recipes
Testosterone
Test Propionate 100 mg/mL - 100 mL
• 10g Test P powder
• 1 mL BA
• 14 mL BB
• 76 SFO
Test P 100mg/mL - 100mL
• 10.2g Test P powder (9.2mL)
• 1.6g BA (1.5mL) [1.5%]
• 20.7g BB (18.5mL) [18.5%]
• GSO 64.2g OR 66.1g MCT
Test P 120mg/mL - 100mL in MCT
• 10.9mL ~12g powder
• BA 1.52mL ~1.6g
• BB 15.75mL ~17.64g
• MCT 71.8mL ~65.08g

No heat. Took an hour to dissolve.

Test C 200mg/mL - 100mL

• 20.4g Test C powder
• 1.56g BA
• 20.7g BB
• 55.8g GSO OR 57.4g MCT
Test E 200mg/ml - 100ml
• 20.4g Test E powder
• 1.6g BA
• 9.5g-BB [8.5%]
• 64.2g GSO OR 66.1g MCT
Test E 250mg/ml - 100ml
• 25.5g Test E Powder
• 1.6g BA
• 15.1g-BB [13.5%]
• 55.3g-GSO or 57g-MCT
Test E 300mg/ml - 100ml
• 30.6g Test E Powder
• 1.6g BA
• 20.7g-BB [18.5%]
• 46.4g-GSO or 47.8g-MCT
Test E 300mg/ml - 100ml submitted by u/thad54castle
• 30g Test E Powder
• 2ml BA
• 18ml BB
• 34.5ml GSO
• 17.2ml EO
Test U 250mg/ml - 120ml submitted by u/JasonJewnova
• 30g Test U Powder
• 1.8ml BA
• 24ml BB
• 65.7ml Mig840
Test E 500mg/ml - 100ml submitted by u/ssjhayes
• 50g Test E Powder
• 2ml BA
• 10ml BB
• 40.85ml Mig840
Trenbolone
Tren E 250mg/ml - 100ml submitted by u/ssjhayes
• 25g Tren E Powder
• 2ml BA
• 22ml BB
• 53.275ml GSO
Tren E 250mg/ml - 100ml submitted by u/ssjhayes
• 25g Tren E Powder
• 2ml BA
• 75.275ml Mig840
Tren E 250mg/ml - 60ml submitted by u/JasonJewnova
• 15g Tren E Powder
• 0.9ml BA
• 12ml BB
• 33.5ml Mig840
Tren A 120mg/ml - 100ml submitted by u/ssjhayes
• 12g Tren A Powder
• 2ml BA
• 20ml BB
• 67.824ml GSO
Tren A 125mg/ml - 100ml submitted by u/JasonJewnova
• 12.5g Tren A Powder
• 1.5ml BA
• 20ml BB
• 67.9ml Mig840
Nandrolone
NPP 100mg/ml - 100ml submitted by u/ssjhayes - no displacement was found, used .900.
• 10g NPP Powder
• 2ml BA
• 18ml BB
• 71ml GSO
NPP 150mg/ml - 100ml
• 15.3g NPP Powder
• 1.6g BA
• 23g-BB [20.5%]
• 57.7g-GSO or 59.4g MCT
Deca 250mg/ml - 100ml submitted by u/ssjhayes
• 25g Deca Powder
• 2ml BA
• 20ml BB
• 54ml GSO
Deca 300mg/ml - 100ml submitted by u/thad54castle
• 30g Deca Powder
• 2ml BA
• 18ml BB
• 34.1ml GSO
• 17.1ml EO
Deca 300mg/ml - 60ml submitted by u/JasonJewnova
• 18g Deca Powder
• 0.9ml BA
• 6ml BB
• 35.78ml Mig840
Boldenone
EQ 300mg/ml - 100ml submitted by u/ssjhayes
• 30g EQ Raws
• 2ml BA
• 15ml BB
• 53ml GSO
EQ 300mg/ml - 100ml submitted by u/thad54castle
• 30g EQ Raws
• 2ml BA
• 18ml BB
• 34.3ml GSO
• 17.1ml EO
EQ 300mg/ml - 60ml submitted by u/JasonJewnova
• 18g EQ Raws
• 0.9ml BA
• 6ml BB
• 35.14ml Mig840
EQ 500mg/ml - 100ml submitted by u/HailLordSaban
• 50g EQ Raws
• 1.5ml BA
• 18ml BB
• 30.5ml MCT
Bold Cyp 200mg/ml - 100ml submitted by u/AnabolicAsshole
• 20g Bold C Powder
• 2.5ml BA
• 22ml BB
• 30ml GSO
• 30ml EO
Masteron
Mast E 250mg/ml - 100ml submitted by u/billy_bobs
• 25g Mast E Powder
• 2ml BA
• 18ml BB
• 60ml MCT
Injectible Orals
M1T 30mg/ml - 60ml submitted by u/JasonJewnova
• 1.8g Powder
• 0.9ml BA
• 9ml BB
• 48.5ml Mig840
Methyl Tren 2.5mg/ml - 50ml Submitted by u/JasonJewnova
• 125mg Methyl Tren Powder
• .75ml BA
• 5ml BB
• 44.14ml Mig840

Excipients

Carrier Oils
Solvents
Antimicrobials/Preservatives

Triturations and Aliquots

Trituration Method (Capsules)

Guide from The Pharmaceutics and Compounding Laboratory at UNC

Mixing The Powder

Things you'll need: Milligram scale, small scoop, mortar & pestle, math.

1. Fill one capsule with your active ingredient. weigh on the milligram scale. record weight.
2. Fill one capsule with your filler. weigh on the milligram scale. record weight.
3. Find your ratio of active ingredient/filler (asin/creatine) using the formula -(Desired active dose x total
filler)/total active-. This will give you how much space your active ingredient takes up out of a full capsule of
your filler. I will use aromasin and creatine as an example. (THESE ARE EXAMPLE CAPACITIES, WEIGH YOUR
OWN) One size 1 capsule holds 300mg asin, and 340mg creatine. To find out how much creatine to take out
to account for 12.5mg of asin you follow the formula. (12.5 x 340)/300 = 14.166. 12.5mg of aromasin takes
up the same amount of space as 14.166mg of creatine. You will be filling one capsule with 12.5mg asin,
325.8mg creatine. Multiply to meet your capsule requirements. So for 100 caps you would need 1.25g asin,
32.58g creatine.
4. Place your active ingredient in the mortar and pestle. 1.25g of aromasin. (This is where we use geometric
dilution to achieve a thorough blend.)
5. Weigh out 1.25g of creatine, place in the mortar, and mix.
6. Weigh out 2.5g of creatine, place in mortar, and mix.
7. Weigh out 5g of creatine, place in mortar, and mix.
8. Repeat until desired quantity of powder is achieved.
9. Begin capping process with your newly mixed powder.
Liquid Aliquot Method (Oral solution / suspension)

Guide from The Pharmaceutics and Compounding Laboratory at UNC

Carrier Oils

Cottonseed oil

Application
Cottonseed oil is used as a solvent in formulations of sustained-release intramuscular or subcutaneous
injections of steroids or other oil-soluble drug substances. The typical disappearance of these types of oils
from the injection site, following subcutaneous or intramuscular administration, has been reported to have a
half-life of approximately 20-23 days[1].

Description
A pale yellow or bright golden yellow-coloured, clear liquid. It is nearly odourless with a nutty taste. At
temperatures below 10°C particles of solid fat may separate from the oil, and between –5 to 0°C, the oil
becomes solid.

Properties

Property Data

Autoignition
344°C
Temperature

Density 0.916g/cm3

Flash Point 321°C

Freezing Point -5 to 0°C

slightly soluble in ethanol; miscible with carbon disulphide, chloroform, ether,

Solubility
hexane, petroleum ether

Viscosity 70.4 mPa s at 20°C

Stability/Storage
Cottonseed oil may be sterilized by filtration or dry heat. It has been demonstrated that dry heat sterilization
of cottonseed oil at 150°C for 1 hour is sufficient[2].
Cottonseed oil is stable if stored in an airtight, light-resistant glass container in a cool, dry place, not
exceeding 40°C.

Safety
Observe normal precautions. This oil should not be administered intravenously.

Handling
Observe normal precautions. Spillages of this material are slippery and should be covered with an inert
absorbent material. Oil is a combustible liquid when exposed to heat or flame. If it is allowed to impregnate
rags or oily waste, there is a risk of ignition from heat or flame. Dry chemicals extinguishers (e.g. carbon
dioxide) should be used to fight any fires.

Sesame oil

Application
Sesame oil is used as a solvent in formulations of sustained-release intramuscular or subcutaneous injections
of steroids or other oil-soluble drug substances. The typical disappearance of these types of oils from the
injection site, following subcutaneous or intramuscular administration, has been reported to have a half-life
of approximately 20-23 days[1].

Description
A clear, pale to dark-yellow coloured liquid with a slight odour and a bland taste. It solidifies to a soft mass at
-4°C.

Properties

Property Data

Density 0.916g-0.920/cm3

Flash Point 338°C

Freezing
-5°C
Point

practically insoluble in ethanol; miscible with carbon disulphide, chloroform, ether,

Solubility
hexane, petroleum ether

Viscosity 43 mPa s at 20°C

Stability/Storage
Sesame oil is more stable than most oils and is not readily subject to rancidification, possibly due to the
antioxidant effect of some of its constituents. Sesame oil may be sterilized by filtration or dry heat, it has
been demonstrated that dry heat sterilization of sesame oil at 150°C for 1 hour is sufficient[2].

Sesame oil is stable if stored in an airtight, light-resistant glass container in a cool, dry place, not exceeding
40ºC.

Safety
This oil may cause reactions such as allergic rashes and anaphylactic shock. This oil should not be
administered intravenously.

Handling
Observe normal precautions. Spillages of this material are slippery and should be covered with an inert
absorbent material. Oil is a combustible liquid when exposed to heat or flame. If it is allowed to impregnate
rags or oily waste, there is a risk of ignition from heat or flame. Dry chemicals extinguishers (e.g.. carbon
dioxide) should be used to fight any fires.

Peanut oil

Application
Peanut oil is used as a solvent in formulations of sustained-release intramuscular or subcutaneous injections
of steroids or other oil-soluble drug substances. The typical disappearance of these types of oils from the
injection site, following subcutaneous or intramuscular administration, has been reported to have a half-life
of approximately 20-23 days[1].

Description
Peanut oil is colourless to pale yellow-coloured and has a faint nutty odour and a bland taste. At
approximately -3°C it becomes cloudy and solidifies at lower temperatures.

Properties

Property Data

Autoignition
443°C
Temperature

Density 0.915g/cm3

Flash Point 283°C

 Property Data

Freezing Point -5°C

very slightly soluble in ethanol; miscible with carbon disulphide, chloroform,

Solubility
ether, hexane

Viscosity 35.2 mPa s at 37°C

Stability/Storage
Peanut oil is subject to rancidification and thickening upon exposure to air. Peanut oil may be sterilized by
filtration or dry heat, it has been demonstrated that dry heat sterilization of peanut oil at 150°C for 1 hour is
sufficient[3].

Peanut oil is stable if stored in an airtight, light-resistant glass container in a cool, dry place, not exceeding
40ºC.

Safety
This oil may cause reactions such as allergic rashes and anaphylactic shock. This oil should not be
administered intravenously.

Handling
Observe normal precautions. Spillages of this material are slippery and should be covered with an inert
absorbent material. Oil is a combustible liquid when exposed to heat or flame. If it is allowed to impregnate
rags or oily waste, there is a risk of ignition from heat or flame. Dry chemicals extinguishers (e.g.. carbon
dioxide) should be used to fight any fires.

Grapeseed oil

Application
Grapeseed oil is used as a solvent in formulations of sustained-release intramuscular or subcutaneous
injections of steroids. The typical disappearance of these types of oils from the injection site, following
subcutaneous or intramuscular administration, has been reported to have a half-life of approximately 20-23
days[1].

To our knowledge, grapeseed oil is not used in any pharmaceutical preparations but is used extensively by
the underground community.

Description
Grapeseed oil is pale to deep green/yellow-coloured oily liquid that has a faint odour and a bland taste.
Properties

Property Data

Autoignition Temperature No Data

Density 0.920g/cm3

Flash Point No Data

Freezing Point No Data

Solubility No Data

Viscosity No Data

Stability/Storage
Grapeseed oil may be sterilized by filtration or dry heat at 150°C for 1 hour. Grapeseed oil is stable if stored in
an airtight, light-resistant glass container in a cool, dry place, not exceeding 40ºC.

Safety
This oil should not be administered intravenously.

Handling
Observe normal precautions. Spillages of this material are slippery and should be covered with an inert
absorbent material. Oil is a combustible liquid when exposed to heat or flame. If it is allowed to impregnate
rags or oily waste, there is a risk of ignition from heat or flame. Dry chemicals extinguishers (e.g. carbon
dioxide) should be used to fight any fires.

Ethyl Oleate

Application
Ethyl oleate is used as a vehicle in preparations intended for intramuscular injection. Ethyl oleate is a suitable
solvent for steroids and other lipophilic drugs. Its properties are similar to those of other oils, however, it has
the advantage that it is less viscous than fixed oils and is more rapidly absorbed by body tissues[4] . Ethyl
oleate has also been evaluated in subcutaneous injections[5] .

Description
Ethyl oleate is a pale yellow to almost colourless oily liquid with a slight odour and a taste resembling olive oil
Properties

Property Data

Density 0.869g/cm3

Boiling Point 205°C

Flash Point 175.3°C

Freezing Point -32°C

Solubility miscible with chloroform, ethanol, ether, fixed oils and most other organic solvents

Viscosity 3.9 mPa s at 25°C

Stability/Storage
Ethyl oleate should be stored in a cool, dry place protected from light, air should be replaced by an inert gas
as ethyl oleate oxidizes on exposure to air, resulting in an increase in the peroxide value.

Protection from oxidation for over two (2) years has been achieved by storing ethyl oleate in amber glass
bottles with the addition of propyl gallate, butylated hydroxyanisole, butylated hydroxytoluene.

Ethyl oleate antioxidant mixture

At a concentration of 0.03% w/v, the following mixture has been found to be the best
antioxidant/preservative for ethyl oleate[6] :
Antioxidant % w/w

propyl gallate 37.5%

butylated hydroxytoluene 37.5%

butylated hydroxyanisole 25%

Ethyl oleate may be sterilized by filtration or dry heat at 150°C for 1 hour.

Safety
Ethyl oleate is considered to be of low toxicity, however, ingestion should be avoided. Ethyl oleate has been
found to cause minimal tissue irritation[7] and no reports of intramuscular irritation during use have been
recorded. Ethyl oleate dissolves certain types of rubber/plastics and may cause others to swell.

It should be noted that some individuals may have an allergic reaction to ethyl oleate, and so appropriate
cautions should be observed before administration. This oil should not be administered intravenously.
 Handling
Observe normal precautions. Spillages of this material are slippery and should be covered with an inert
absorbent material. Oil is a combustible liquid when exposed to heat or flame. If it is allowed to impregnate
rags or oily waste, there is a risk of ignition from heat or flame. Dry chemicals extinguishers (e.g. carbon
dioxide) should be used to fight any fires.

Sources/References

1. Larsen SW et al. Determination of the disappearance rate of iodine-125 labelled oils from the injection site
after intramuscular and subcutaneous administration to pigs. Int J Pharm 2001; 230(1–2): 67–75.
2. Kupiec TC et al. Dry-heat sterilisation of parenteral oil vehicles. Int J Pharm Compound 2000; 4(3): 223–224.
3. Pasquale D et al. A study of sterilizing conditions for injectable oils. Bull Parenter Drug Assoc 1964; 18(3): 1–
11.
4. Howard JR, Hadgraft J. The clearance of oily vehicles following intramuscular and subcutaneous injections in
rabbits. Int J Pharm 1983; 16: 31–39.
5. Radwan M. In vivo screening model for excipients and vehicles used in subcutaneous injections. Drug Dev Ind
Pharm 1994; 20: 2753–2762.
6. Nikolaeva NM, Gluzman MK. Conditions for stabilizing ethyl oleate during storage. Farmatsiya 1977; 26: 25–
28
7. Hem SL et al. Tissue irritation evaluation of potential parenteral vehicles. Drug Dev Commun1974–751(5):
471–477.
• Rowe, C. Handbook of Pharmaceutical Excipients. London: RPS Publishing, 2009. Print.
• Food Chemicals Codex. Washington: The National Academies Press, 2004. Print.

Solvents

Benzyl Benzoate

Application
Benzyl benzoate is used as a solvent in intramuscular injections at concentrations of 0.01–46.0% v/v[1] .

Description
A colourless oily liquid with a faint aromatic odour, and a sharp burning taste. At temperatures below 17°C it
exists as colourless crystals.
Properties

Property Data

Autoignition
481°C
Temperature

Boiling Point 324°C

Flash Point 148°C

Freezing Point 17°C

soluble in acetone; miscible in chloroform, ethanol, ether and fatty acids and
Solubility
oils

Stability/Storage
Benzyl alcohol is stable when stored properly. It should be stored in an airtight glass container, protected
from light, in a cool, dry place, not exceeding 40°C.

Safety
Benzyl benzoate is metabolized by rapid hydrolysis to benzoic acid and benzyl alcohol. Adverse reactions to
benzyl benzoate include skin irritation and hypersensitivity reactions. Oral ingestion can cause harmful
stimulation of the CNS and convulsions. Benzyl benzoate should be avoided by people with perfume allergies.

Handling
Observe normal precautions. Benzyl benzoate is an irritant to the skin, eyes, and mucous membranes. Eye
protection, gloves, and protective clothing are recommended. Benzyl benzoate should be handled in a well-
ventilated environment. Benzyl benzoate is flammable.

Dimethyl Sulfoxide

Application
Dimethyl sulfoxide is a polar substance that is aprotic, lacking both acidic and basic properties. It has
exceptional solvent properties for both organic and inorganic compounds. Dimethyl sulfoxide enhances the
topical penetration of drugs, however, much of the enhancement capacity is lost if the solvent is diluted.
Increases in drug penetration have been observed with dimethyl sulfoxide concentrations as low as 15%,
however, significant increases require concentrations higher than 60–80%.
Dimethyl sulfoxide is now incorporated into a number of regulated products for drug delivery applications,
including stabilizing formulations, and formulations for sustained-release applications. Dimethyl sulfoxide has
also been used in the formulation of an injection containing allopurinol[2] .

Description
Dimethyl sulfoxide is a colourless liquid, or frozen crystal that is miscible with water, alcohol, and ether. It has
a bitter taste with a sweet aftertaste and has a slight garlic infused solvent-like odour. Dimethyl sulfoxide is
extremely hygroscopic, absorbing up to 70% of its own weight in water with the application of heat.

Properties

Property Data

Autoignition Temperature 215°C

Density 1.0955g/cm3 at 25°C

Boiling Point 189°C

Flash Point 95°C

Freezing Point 19°C

Viscosity 2.47 mPa s at 20°C

Stability/Storage
Dimethyl sulfoxide is reasonably stable to heat however, when heated to decomposition the fumes are toxic.
At temperatures between 40 and 60°C, it has been suggested that dimethyl sulfoxide may partially
decompose, indicated by changes in density, and viscosity[4]

Dimethyl sulfoxide should be stored in an airtight glass container, protected from light, in a cool, dry place,
not exceeding 40°C. Storage in plastics should be avoided.

Safety
Dimethyl sulfoxide has relatively low toxicity but can cause local toxic effects[5] . It is readily absorbed after
injection or after oral or topical administration. Dimethyl sulfoxide acts as an irritant on skin, causing redness,
burning, itching, and scaling. Systemic symptoms may include nausea, vomiting, chills, cramps, and lethargy.
Administration of dimethyl sulfoxide is generally followed by a garlic-like odour on the breath[6] . One report
describes a massive intracranial hemorrhage associated with dimethyl sulfoxide ingestion[8] , and a
hypersensitivity reaction attributed to dimethyl sulfoxide has also been reported[9]
In 1965 the FDA banned investigation, in humans, of dimethyl sulfoxide; however in 1966, the FDA allowed
the study of dimethyl sulfoxide in serious conditions and by 1968 permitted studies using short-term topical
application of the solvent. By 1980, the FDA no longer strictly regulated investigations of dimethyl sulfoxide.

Handling
Observe normal precautions. Dimethyl sulfoxide may cause irritation to the skin. Gloves and eye protection
are recommended.

Polyethylene Glycol (PEG)

Application
Polyethylene glycols (PEGs) are widely used in a variety of formulations, including parenteral, topical, and
oral preparations.

Polyethylene glycols have some disadvantages in that they are more chemically reactive than fats; the rate of
release of water-soluble medications decreases as molecular weight of the polyethylene glycol increases; and
polyethylene glycols tend to be more irritating to mucous membranes.

Aqueous polyethylene glycol solutions can be used either as suspending agents or to adjust the viscosity of
other suspending agents. Liquid polyethylene glycols are often used as water-miscible solvents.

In concentrations up to approximately 30% v/v, PEG 300/PEG 400 have been used as the vehicle for
parenteral administration. In solid dosage formulations, the higher-molecular-weight polyethylene glycols
can enhance the effectiveness of tablet binders however, they have only limited binding action when used
alone.

Polyethylene glycols can also be used to enhance the aqueous solubility or dissolution characteristics of
poorly soluble compounds by making solid dispersions with an appropriate polyethylene glycol[9]

Description
Polyethylene glycol grades 200–600 are liquids; grades 1000 and above are solids at standard ambient
temperatures.

Liquid grades (PEG 200–600) present as a clear, colourless or slightly yellow coloured liquid. They have a
slightly sweet odour and a slight bitter and/or burning taste. Solid grades are white or off-white in colour, and
range in consistency.
Properties

Type of PEG Density (g/cm3 ) Freezing Point Viscosity (mPa s)

200 1.12 -65°C -

300 1.12 -15°C 80-105

400 1.12 4-8°C 105-130

600 1.08 15-25°C 15-20

Solubility

All grades of polyethylene glycol are soluble in water and are miscible in all proportions with other liquid
polyethylene glycols. Liquid polyethylene glycols are soluble in acetone, alcohols, benzene, glycerin, and
glycols.

Stability/Storage
Liquid polyethylene glycols are chemically stable in air and in solution, and are hygroscopic. Polyethylene
glycols do not support microbial growth, and they do not become rancid. Polyethylene glycols and aqueous
polyethylene glycol solutions can be sterilized by autoclaving, filtration, or gamma irradiation[10]

Polyethylene glycols should be stored in an airtight glass container, protected from light, in a cool, dry place,
not exceeding 40°C.

Safety
Polyethylene glycols are generally regarded as non-toxic and non-irritants although hypersensitivity reactions
to polyethylene glycols applied topically have also been reported, including urticaria and delayed allergic
reactions[11]
Ingestion of large quantities of polyethylene glycols have a laxative effect. Therapeutically, up to 4 L of a
mixture of electrolytes and high-molecular-weight polyethylene glycol is consumed by patients undergoing
bowel cleansing[12]
Liquid polyethylene glycols may be absorbed when taken orally, but higher-molecular-weight polyethylene
glycols are not significantly absorbed. Absorbed polyethylene glycol is excreted unchanged although
polyethylene glycols of low molecular weight may be partially metabolized. The WHO has set an estimated
acceptable daily intake of polyethylene glycols at up to 10 mg/kg body-weight[13]

In parenteral products, the maximum recommended concentration of PEG 300 is approximately 30% as
hemolytic effects have been observed at concentrations greater than approximately 40% v/v.

Handling
Observe normal precautions.
 Sources/References

1. Spiegel AJ, Noseworthy MM. Use of nonaqueous solvents in parenteral products. J Pharm Sci 1963; 52: 917–
927.
2. Lee DKT, Wang D-P. Formulation development of allopurinol suppositories and injectables. Drug Dev Ind
Pharm 1999; 25(11):1205–1208.
3. Komemushi A et al. A new liquid embolic material for liver tumors. Acta Radiol 2002; 43(2): 186–191.
4. Jacob SW et al, ed. Dimethyl Sulfoxide., vol. 1: New York: Marcel Dekker, 1971; 81.
5. Mottu F et al. Organic solvents for pharmaceutical parenterals and embolic liquids: a review of toxicity
data. PDA J Pharm Sci Technol 2000; 54(6): 456–469.
6. Yellowlees P et al. Dimethylsulphoxide-induced toxicity. Lancet 1980; ii: 1004–1006.
7. Topacoglu H et al. Massive intracranial hemorrhage associated with the ingestion of dimethyl sulfoxide. Vet
Hum Toxicol 2004; 46(3): 138– 140.
8. Creus N et al. Toxicity to topical dimethyl sulfoxide (DMSO) when used as an extravasation antidote. Pharm
World Sci 2002; 24(5): 175– 176.
9. Miralles MJ et al. Combined water-soluble carriers for coprecipitates of tolbutamide. J Pharm Sci 1982; 71:
302–304.
10. Bhalla HL et al. Radiation sterilization of polyethylene glycols. Int J Pharm 1983; 17: 351–355.
11. Fisher AA. Immediate and delayed allergic contact reactions to polyethylene glycol. Contact Dermatitis 1978;
4: 135–138.
12. Sweetman SC, ed. Martindale: The Complete Drug Reference, 36th edn. London: Pharmaceutical Press, 2009;
2336.
13. FAO/WHO. Evaluation of certain food additives. Twenty-third report of the Joint FAO/WHO Expert Committee
on Food Additives. World Health Organ Tech Rep Ser 1980; No. 648.
• Rowe, C. Handbook of Pharmaceutical Excipients. London: RPS Publishing, 2009. Print.

Antimicrobials/Preservatives

Benzyl Alcohol

Application
Benzyl alcohol is a bacteriostat and is used as an antimicrobial preservative. It is used in foods, and a wide
range of pharmaceutical formulations, including oral and parenteral preparations, at concentrations up to
2.0% v/v.
Description
A colourless oily liquid with a faint aromatic odour, and a sharp burning taste.

Properties

Property Data

Autoignition
436.5°C
Temperature

Boiling Point 204.7°C

Flash Point 104.5°C

Freezing Point -15°C

soluble in water; miscible in chloroform, ethanol, fixed and volatile oils,

Solubility
ether

Viscosity 6 mPa s
Antimicrobial activity

Benzyl alcohol is bacteriostatic and is used as an antimicrobial preservative against Gram-positive bacteria,
moulds, and fungi; although it is only modestly bactericidal and has little activity above pH 8.

Organism Minimum inhibitory concentration (µg/ml)

Aspergillus niger 5000

Candida albicans 2500

Escherichia coli 2000

Pseudomonas aeruginosa 2000

Staphylococcus aureus 25
Bacteria

Benzyl alcohol is only moderately active against most Gram-positive organisms (typical minimum inhibitory
concentrations are 3–5mg/mL), and in general, benzyl alcohol is less active against Gram-negative organisms.

Fungi

Benzyl alcohol is effective against moulds and yeasts; typical minimum inhibitory concentrations are 3–5
mg/mL.

Spores
Benzyl Alcohol is inactive against spores.

Stability/Storage
Benzyl alcohol slowly oxidizes in air to benzaldehyde and benzoic acid. Solutions may be sterilized by
filtration or autoclaving. Benzyl alcohol may be stored in metal or glass containers, but should not be stored
in plastic containers.

Benzyl alcohol should be stored in an airtight glass container, protected from light, in a cool, dry place, not
exceeding 40°C.

Safety
Ingestion or inhalation of benzyl alcohol may cause headache, nausea, vomiting and diarrhea. Overexposure
can result in CNS depression and respiratory failure, however, the concentrations of benzyl alcohol when
employed as a preservative are generally not associated with adverse effects.

Handling
Observe normal precautions. Benzyl alcohol is an irritant to the skin, eyes, and mucous membranes. Eye
protection, gloves, and protective clothing are recommended. Benzyl alcohol should be handled in a well-
ventilated environment. Benzyl alcohol is flammable.

Chlorobutanol

Application
Chlorobutanol is an antimicrobial preservative. It is especially useful as an antibacterial agent in nonaqueous
formulations. Chlorobutanol has also been used as a mild sedative and local analgesic.

Description
Chlorobutanol is a volatile white crystal with an odour resembling camphor.

Properties

Property Data

Boiling Point 167°C

Melting Point
76-78°C
(hemihydrate)

Melting Point (anhydrous) 95-97°C

 Property Data

freely soluble in acetone, chloroform, ethanol, ether, methanol, volatile

Solubility
oils, hot water
Antimicrobial activity

Chlorobutanol has both antibacterial and antifungal properties. It is effective against Gram-positive and
Gram-negative bacteria. Antimicrobial activity is bacteriostatic, rather than bactericidal, and is considerably
reduced above pH 5.5.

Typical minimum inhibitory concentrations are:

Organism Minimum inhibitory concentration (µg/ml)

Gram-positive bacteria 650

Gram-negative bacteria 1000

Yeasts 2500

Fungi 5000

Stability/Storage
Chlorobutanol is very volatile and readily sublimes. Stability is good at pH 3 but becomes worse as pH
increases[1] . The half-life in solution at pH 7.5, stored at 25°C was determined to be approximately 3
months[2] . A 0.5% w/v aqueous chlorobutanol solution, at room temperature, is almost saturated and can
crystallize out of solution at reduced temperatures.

Losses of chlorobutanol also occur, with significant amounts being lost during autoclaving. Also, at pH 5
approximately 30% of chlorobutanol can be lost. Porous containers result in losses from solutions as well.
There is also significant loss of chlorobutanol through stoppers in parenteral vials.

Bulk material should be stored in airtight containers at 8–15°C.

Safety
Reported adverse reactions to chlorobutanol include hypersensitivity reactions, although these are regarded
as rare[3] .

The lethal human dose of chlorobutanol is estimated to be 50–500 mg/kg

Handling
Observe normal precautions. Chlorobutanol is an irritant to the skin, eyes, and mucous membranes. Eye
protection and gloves are recommended. There is a slight fire hazard on exposure to heat or flame.
Propyl Gallate

Application
Propyl gallate is primarily used to prevent the rancidity of oils and fats. It is used in cosmetics, perfumes,
foods, and pharmaceuticals and was first described in preventing autoxidation of oils and fats in 1943.
Synergistic effects with other antioxidants such as butylated hydroxyanisole and butylated hydroxytoluene
have been reported. Propyl gallate is also said to possess some antimicrobial properties and has also been
investigated for its therapeutic properties, although mainly in animal studies.

Description
Propyl gallate is a white, odourless crystalline powder, with a bitter astringent taste that is not noticeable at
lower concentrations, as when used as an antioxidant.

Properties

Property Data

Melting Point 150°C

Solubility soluble in fixed and volatile oils, ether, ethanol, PEG, water
Antimicrobial activity

Propyl gallate has been reported to possess some antimicrobial activity against Gram-negative bacteria,
Gram-positive bacteria, and fungi.

Organism Minimum inhibitory concentration (mg/ml - ethanol cosolvent @ 4% v/v)

Candida Albicans 1500

Escherichia Coli 330

Staphylococcus Aureas 600

Stability/Storage
Propyl gallate is unstable at high temperatures. The bulk material should be stored in an airtight, non-metallic
container, protected from light in a cool, dry place, not exceeding 40°C.

Safety
There have been few reports of adverse reactions to propyl gallate[5] , those that have been described include
contact dermatitis and allergic contact dermatitis.
Handling
Observe normal precautions. Eye protection and gloves are recommended. When heated to decomposition,
propyl gallate may emit toxic fumes and smoke.

Butylated Hydroxytoluene

Application
Butylated hydroxytoluene is used as an antioxidant in cosmetics, foods, and pharmaceuticals. It is mainly
used to delay or prevent the autoxidation of fats and oils and to prevent loss of activity of oil-soluble
vitamins. Butylated hydroxytoluene has some antiviral activity and has been used therapeutically to treat
herpes simplex labialis.

Antioxidant use Concentration (%)

Edible vegetable oils 0.01

Fats and oils 0.02

IM Injections 0.03

IV Injections 0.0009-0.002

Description
Butylated hydroxytoluene is a white or pale yellow crystalline solid or powder with a faint odour.

Properties

Property Data

Melting
70°C
Point

Boiling Point 265°C

Flash Point 127°C

insoluble in water, glycerine, PEG; freely soluble in acetone, benzene, ethanol, ether fixed
Solubility
and volatile oils

Stability/Storage
Exposure to light, moisture, and heat causes discolouration and a loss of activity. Butylated hydroxytoluene
should be stored in an airtight container, protected from light, in a cool, dry place, not exceeding 40°C.
Safety
Although there have been some reports of adverse skin reactions, butylated hydroxytoluene is generally
regarded as non-toxic and a non-irritant at the levels employed as an antioxidant.[6-7]

Handling
Observe normal precautions. Butylated hydroxytoluene may be irritant to the eyes and skin. It should be
handled in a well-ventilated environment; gloves and eye protection are recommended. Closed containers
may explode when exposed to extreme heat.

Butylated Hydroxyanisole

Application
Butylated hydroxyanisole is an antioxidant used in cosmetics, foods, and pharmaceuticals. It is mainly used to
delay or prevent the autoxidation of fats and oils and to prevent loss of activity of oil-soluble vitamins.
Butylated hydroxyanisole is frequently used in combination with other antioxidants, particularly butylated
hydroxytoluene and alkyl gallates.
Antioxidant use Concentration (%)

Fats and oils 0.02

IM Injections 0.03

IV Injections 0.0002-0.0005

Description
Butylated hydroxyanisole is a white or almost white crystalline powder or a yellowish-white solid, with a faint
odour.

Properties

Property Data

Melting
47°C
Point

Boiling Point 264°C

Flash Point 130°C

practically insoluble in water; freely soluble in ethanol, PEG, ether, chloroform, hexane,
Solubility
fixed and volatile oils
 Stability/Storage
Exposure to light, moisture, and heat causes discolouration and a loss of activity. Butylated hydroxyanisole
should be stored in an airtight container, protected from light, in a cool, dry place, not exceeding 40°C.

Safety
Although there have been some reports of adverse skin reactions, butylated hydroxyanisole is generally
regarded as non-toxic and a non-irritant at the levels employed as an antioxidant.[6]

Handling
Observe normal precautions. Butylated hydroxyanisole may be irritant to the eyes and skin. It should be
handled in a well-ventilated environment; gloves and eye protection are recommended.

Sources/References

1. Patwa NV, Huyck CL. Stability of chlorobutanol. J Am Pharm Assoc 1966; NS6: 372–373.
2. Nair AD, Lach JL. The kinetics of degradation of chlorobutanol. J Am Pharm AssocSci 1959; 48: 390–395.
3. Hofmann H et al. Anaphylactic shock from chlorobutanol-preserved oxytocin. Contact Dermatitis 1986; 15:
241.
4. Gosselin RE et al. Clinical Toxicology of Commercial Products, 4th edn. Baltimore: Williams & Wilkins, 1976; II-
119.
5. Golightly LK et al. Pharmaceutical excipients: adverse effects associated with ‘inactive’ ingredients in drug
products (part II). Med Toxicol 1988; 3: 209–240.
6. Roed-Peterson J, Hjorth N. Contact dermatitis from antioxidants: hidden sensitizers in topical medications and
foods. Br J Dermatol 1976; 94: 233–241.
7. EFSA. Scientific Opinion on the re-evaluation of butylated hydroxytoluene BHT (E 321) as a food
additive. Parma: EFSA Journal, 2012. Print.
• Rowe, C. Handbook of Pharmaceutical Excipients. London: RPS Publishing, 2009. Print.

18 ESTERS
A Primer On Esters And How They Work

One of the most misunderstood subjects in the world of steroids is the ester--the mechanism by which
injectable esterified steroids like testosterone cypionate, testosterone enanthate, and Sustanon work. If you take
a quick look around the Internet you will probably find countless articles that consider one form of a steroid far
more effective than another. Arguments over the superiority of cypionate to enanthate, or Sustanon to all other
testosterones are of course very common. Such arguments are in all practicality, baseless. In this report we'll
take an authoritative look at the ester and what specifically it does to a steroid.

I'm sure that if you have taken an interest in anabolic steroids you have noticed the similarities on the labeling
of many drugs. Let's look at testosterone for example. One can find compounds like testosterone cypionate,
enanthate, propionate, heptylate; caproate, phenylpropionate, isocaproate, decanoate, acetate, the list goes on
and on. In all such cases the parent hormone is testosterone, which had been modified by adding an ester
(enanthate, propionate etc.) to its structure. The following question arises: What is the difference between the
various esterified versions of testosterone in regards to their use in bodybuilding?

An ester is a chain composed primarily of carbon and hydrogen atoms. This chain is typically attached to the
parent steroid hormone at the 17th carbon position (beta orientation), although some compounds do carry
esters at position 3 (for the purposes of this article it is not crucial to understand the exact position of the ester).
Esterification of an injectable anabolic/androgenic steroid basically accomplishes one thing, it slows the
release of the parent steroid from the site of injection. This happens because the ester will notably lower the
water solubility of the steroid, and increase its lipid (fat) solubility. This will cause the drug to form a deposit
in the muscle tissue, from which it will slowly enter into circulation as it is picked up in small quantities by the
blood. Generally, the longer the ester chain, the lower the water solubility of the compound, and the longer it
will take to for the full dosage to reach general circulation.

Slowing the release of the parent steroid is a great benefit in steroid medicine, as free testosterone (or other
steroid hormones) previously would remain active in the body for a very short period of time (typically hours).
This would necessitate an unpleasant daily injection schedule if one wished to maintain a continuous elevation
of testosterone (the goal of testosterone replacement therapy). By adding an ester, the patient can visit the
doctor as infrequently as once per month for his injection, instead of having to constantly re-administer the
drug to achieve a therapeutic effect. Clearly without the use of an ester, therapy with an injectable
anabolic/androgen would be much more difficult.

Esterification temporarily deactivates the steroid molecule. With a chain blocking the 17th beta position,
binding to the androgen receptor is not possible (it can exert no activity in the body). In order for the
compound to become active the ester must therefore first be removed. This automatically occurs once the
compound has filtered into blood circulation, where esterase enzymes quickly cleave off (hydrolyze) the ester
chain. This will restore the necessary hydroxyl (OH) group at the 17th beta position, enabling the drug to
attach to the appropriate receptor. Now and only now will the steroid be able to have an effect on skeletal
muscle tissue. You can start to see why considering testosterone cypionate much more potent than enanthate
makes little sense, as your muscles are seeing only free testosterone no matter what ester was used to deploy it.
Actions Of Different Esters

There are many different esters that are used with anabolic/androgenic steroids, but again, they all do basically
the same thing. Esters vary only in their ability to reduce a steroid's water solubility. An ester like propionate
for example will slow the release of a steroid for a few days, while the duration will be weeks with a decanoate
ester. Esters have no effect on the tendency for the parent steroid to convert to estrogen or DHT
(dihydrotestosterone: a more potent metabolite) nor will it effect the overall muscle-building potency of the
compound. Any differences in results and side effects that may be noted by bodybuilders who have used
various esterified versions of the same base steroid are just issues of timing. Testosterone enanthate causes
estrogen related problems more readily than Sustanon, simply because with enanthate testosterone levels will
peak and trough much sooner (1-2 week release duration as opposed to 3 or 4). Likewise testosterone
suspension is the worst in regards to gyno and water bloat because blood hormone levels peak so quickly with
this drug. Instead of waiting weeks for testosterone levels to rise to their highest point, here we are at most
looking at a couple of days. Given an equal blood level of testosterone, there would be no difference in the rate
of aromatization or DHT conversion between different esters. There is simply no mechanism for this to be
possible.

There is however one way that we can say an ester does technically effect potency; it is calculated in the
steroid weight. The heavier the ester chain, the greater is its percentage of the total weight. In the case of
testosterone enanthate for example, 250mg of esterified steroid (testosterone enanthate) is equal to only 175mg
of actual testosterone. 75mg out of each 250mg injection is the weight of the ester. If we wanted to be really
picky, we could consider enanthate slightly MORE potent than cypionate (I know this goes against popular
thinking) as its ester chain contains one less carbon atom (therefore taking up a slightly smaller percentage of
total weight). Propionate would of course come out on top of the three, releasing a measurable (but not
significant) amount more testosterone per injection than cypionate or enanthate. [See

Esters Active Half-Life Table

Different esters exist for various compounds. Different esters give compounds different clearance times in the
blood. All over the internet, you will find different (unreferenced) information on the half-life of compounds.
A lot of the confusion comes from a lack of understanding on a compound's half-life versus it's biological or
terminal half-life. For our purposes, we really only care about the terminal half-life, defined as:
The biological half-life or elimination half-life of a substance is the time it takes for a substance (for example a
metabolite, drug, signaling molecule, radioactive nuclide, or other substance) to lose half of its pharmacologic,
physiologic, or radiologic activity, as per the MeSH definition.
More information on terminal half-life is available here.
Reference study.
 Ester Half-life Terminal Half-life

Suspension within 1 hour

Acetate 3 days 1 day

Propionate 2 days 0.8 days

Phenylpropionate 4.5 days 1.5 days

Butyrate 2-3 days

Valerate 3 days

Hexanoate 3 days

Caproate 4-5 days

Isocaproate 9 days 4 days

Heptanoate 5-6 days

Enanthate 10.5 days 4.5 days

Cypionate 6-7 days 5 days

Octanoate 6-7 days

Nonanoate 7 days

Decanoate 15 days 7.5 days

Undecylenate 8-9 days 14 days

Undecanoate 16.5 days 20.9 days

IMPORTANT NOTE: These half-lives are approximations, and may vary slightly depending on injection
site, carrier oil, and other factors. There isn't any pharmacokinetics studies done on the majority of AAS. Most
of the above is the theoretical half-lives when we are not presented with real data.

Esters And The Active Dose

It is important for every person to understand that the ester which is attached to any injectable anabolic steroid
possesses a certain percentage amount of the total molecular weight of the molecule. Therefore, for example,
100mg of Testosterone Enanthate is not 100mg of pure Testosterone. The reality is that you are receiving less
Testosterone than most of you think, and once the ester has been removed through the esterase enzyme, the
amount of pure un-esterified Testosterone left over is very different depending on the ester in question that was
previously attached to the hormone.
Long chain esters, such as Cypionate, Decanoate, Enanthate, etc. possess a much heavier molecular weight
than short chain esters. Consequently, on a mg for mg basis, you are receiving far extra mg of steroid in a short
estered compound as opposed to a large estered compound. As an example, there exists a larger amount of mg
of Testosterone in 100mg of Testosterone Propionate than 100mg of Testosterone Enanthate. This is due to the
shorter, and therefore lighter weight of the Propionate ester in comparison to the larger and therefore much
heavier Enanthate ester. Many individuals just do not realize this, and should always consider this factor as one
of the factors involved in the decision making process concerning which ester variant of any given compound
to use during a cycle.

Listed below is the percentages of the actual hormones for each ester:
Testosterone Ester % Of The Actual Hormone

Acetate 87%

Propionate 80%

Phenylpropionate 66-67%

Isocaproate 72%

Enanthate 70%

Cypionate 69%

Decanoate 62%

Undecylenate 61%

Undecanoate 61%
Milligrams below are the estimated amount of active hormone per 100 mg of compound.
Compound Ester Pure Hormone

Boldenone (EQ) base 100 mg

Boldenone (EQ) acetate 83 mg

Boldenone (EQ) Propionate 80 mg

Boldenone (EQ) Cypionate 69 mg

Boldenone (EQ) Undecylenate 61 mg

Clostebol Base 100 mg

Clostebol Acetate 84 mg

Clostebol Enanthate 72 mg
Compound Ester Pure Hormone

Drostanolone (Masteron) Base 100 mg

Drostanolone (Masteron) Propionate 80 mg

Drostanolone (Masteron) Enanthate 71 mg

Methenolone (Primobolan) Base 100 mg

Methenolone (Primobolan) Acetate 82 mg

Methenolone (Primobolan) Enanthate 71 mg

Nandrolone Base 100 mg

Nandrolone Cypionate 69 mg

Nandrolone (NPP) Phenylpropionate 63 mg

Nandrolone (Deca) Decanoate 62 mg

Nandrolone Undecylenate 60 mg

Nandrolone Laurate 56 mg

Stenbolone Base 100 mg

Stenbolone Acetate 84 mg

Testosterone Base 100 mg

Testosterone Acetate 83 mg

Testosterone Propionate 80 mg

Testosterone Isocaproate 72 mg

Testosterone Enanthate 70 mg

Testosterone Cypionate 69 mg

Testosterone Phenylpropionate 67 mg

Testosterone Decanoate 62 mg

Testosterone Undecanoate 61 mg

Trenbolone Base 100 mg

Trenbolone Acetate 83 mg

Trenbolone Enanthate 68 mg
 Compound Ester Pure Hormone

Trenbolone Hexahydrobenzyl Carbonate 65 mg

Trenbolone Cyclohexylmethylcarbonate 65 mg

Sustanon: The "King" Of Testosterone Blends

The four different testosterone esters in this product certainly look appealing to the consumer, there is no
denying that. But for the athlete I think it is all just a matter of marketing (Hell, why buy one ester when you
can get four?). In clinical situations I can see some strong uses for it. If you were undergoing testosterone
replacement therapy for example, you would probably find Sustanon a much more comfortable option than
testosterone enanthate. You would need to visit the doctor less frequently for an injection, and blood levels
should be more steadily maintained between treatments. But for the bodybuilder who is injecting 4 ampules of
Sustanon per week, there is no advantage over other testosterone products. In fact, the high price tag for
Sustanon usually makes it a very poor buy in the face of cheaper testosterone enanthate/cypionate.
Bodybuilders should probably stop looking at the four ester issue, and stick with totals (Sustanon is just a
250mg testosterone ampule). Were enanthate to be available for say $10 per amp of 250mg, and Sustanon
priced nearly double that, buying the Sustanon would be like throwing money away. If you could get nearly
double the milligram amount for the same price with enanthate, this is the better product to go with hands
down. Leave the high priced stuff for the guys who don't know any better.

Ester Profiles
Acetate ( C2 H4 O2 )
Also referred to as Acetic Acid; Ethylic acid; Vinegar acid; vinegar; Methanecarboxylic acid. Acetate esters
delay the release of a steroid for only a couple of days. Contrary to what you may have read, acetate esters do
not increase the tendency for fat removal. Again, there is no known mechanism for it to do so. This ester is
used on oral primobolan tablets (metenolone acetate), Finaplix (trenbolone acetate) implant pellets, and
occasionally testosterone.

Propionate ( C3 H6 O2 )
Also referred to as Carboxyethane; hydroacrylic acid; Methylacetic acid; Ethylformic acid; Ethanecarboxylic
acid; metacetonic acid; pseudoacetic acid; Propionic Acid. Propionate esters will slow the release of a steroid
for several days. To keep blood levels from fluctuating greatly, propionate compounds are usually injected two
to three times weekly. Testosterone propionate and methandriol dipropionate (two separate propionate esters
attached to the parent steroid methandriol) are popular items.
Phenylpropionate ( C9 H10 O2 )
Also referred to as Propionic Acid Phenyl Ester. Phenylpropionate will extend the release of active steroid a
few days longer than propionate. To keep blood levels even, injections are given at least twice weekly.
Durabolin is the drug most commonly seen with a phenylpropionate ester (nandrolone phenylpropionate),
although it is also used with testosterone in Sustanon and Omnadren.

Isocarpoate ( C6 H12 O2 )
Also referred to as Isocaproic Acid; isohexanoate; 4-methylvaleric acid. Isocaproate begins to near enanthate
in terms of release. The duration is still shorter, with a notable hormone level being sustained for
approximately one week. This ester is used with testosterone in the blended products Sustanon and Omnadren.

Caproate ( C6 H12 O2 )
Also referred to as Hexanoic acid; hexanoate; n-Caproic Acid; n-Hexoic acid; butylacetic acid; pentiformic
acid; pentylformic acid; n-hexylic acid; 1-pentanecarboxylic acid; hexoic acid; 1-hexanoic acid; Hexylic acid;
Caproic acid. This ester is identical to isocarpoate in terms of atom count and weight, but is laid out slightly
different (Isocaproate has a split configuration, difficult to explain here but easy to see on paper). Release
duration would be very similar to isocaproate (levels sustained for approximately one weak), perhaps coming
slightly closer to enanthate due to its straight chain. Caproate is the slowest releasing ester used in Omnadren,
which is why most athletes notice more water retention with this compound.

Enanthate ( C7 H14 O2 )
Also referred to as heptanoic acid; enanthic acid; enanthylic acid; heptylic acid; heptoic acid; Oenanthylic acid;
Oenanthic acid. Enanthate is one of the most prominent esters used in steroid manufacture (most commonly
seen with testosterone but is also used in other compounds like Primobolan Depot). Enanthate will release a
steady (yet fluctuating as all esters are) level of hormone due to the length of the ester. Although in medicine
enanthate compounds are often injected on a bi-weekly or monthly basis, athletes will inject at least weekly to
help maintain a uniform blood level.

Cypionate ( C8 H14 O2 )
Also referred to as Cyclopentylpropionic acid, cyclopentylpropionate. Cypionate is a very popular ester here in
the U.S., although it is scarcely found outside this region. Its release duration is almost identical to enanthate,
and the two are likewise thought to be interchangeable in U.S. medicine. Althletes commonly hold the belief
than cypionate is more powerful than enanthate, although realistically there is little difference between the two.
The enanthate ester is in fact slightly smaller than cypionate, and it therefore releases a small (perhaps a few
milligrams) amount of steroid more in comparison.

Decanoate ( C10 H20 O2 )

Also referred to as decanoic acid; capric acid; caprinic acid; decylic acid, Nonanecarboxylic acid. The
Decanoate ester is most commonly used with the hormone nandrolone (as in Deca-Durabolin) and is found in
virtually all corners of the world. Testosterone decanoate is also the longest acting constituent in Sustanon,
greatly extending its release duration. The release time with Decanoate compounds is listed to be as long as
one month, although most recently we are finding that levels seem to drop significantly after two weeks. To
keep blood levels more uniform, athletes (as they have always known to do) will follow a weekly injection
schedule.

Undecylenate ( C11 H20 O2 )

Also referred to as Undecylenic acid; Hendecenoic acid; Undecenoic acid. This ester is very similar to
decanoate, containing only one carbon atom more. Its release duration is likewise very similar (approximately
2-3 weeks), perhaps extending a day or so past that seen with decanoate. Undecylenate seems to be exclusive
to the veterinary preparation Equipoise (boldenone undecylenate), although there is no reason it would not
work well in human-use preparations (Equipoise certainly works fine for athletes). Again, weekly injections
are most common.

Undecanoate ( C11 H22 O2 )

Also referred to as Undecanoic Acid; 1-Decanecarboxylic acid; Hendecanoic acid; Undecylic acid.
Undecanoate is not a commonly found ester, and only appears to be used in the nandrolone preparation
Dynabolan, and oral testosterone undecanoate (Andriol). Since this ester is chemically very similar to
undecylenate (it is only 2 hydrogen atoms larger), it has a similar release duration (approximately 2-3 weeks).
Although this ester is used in the oral preparation Andriol, there is no reason to believe it carries any properties
unique of other esters. Andriol in fact works very poorly at delivering testosterone, bolstering the idea that oral
administration is not the idea use of esterified androgens.

Laurate ( C12 H24 O2 )

Also referred to as Dodecanoic acid, laurostearic acid, duodecyclic acid, 1-undecanecarboxylic acid, and
dodecoic acid. Laurate is the longest releasing ester used in commercial steroid production, although longer
acting esters do exist. Its release duration would be closer to one month than the other esters listed above,
although realistically we are probably to expect a notable drop in hormone level after the third week. Laurate is
exclusively found in the veterinary nandrolone preparation Laurabolin, perhaps seen as slightly advantageous
over a decanoate ester due to a less frequent injection schedule. Again athletes will most commonly inject this
drug weekly, no doubt in part due to its low strength (25mg/ml or 50mg/ml).

Conclusion

While the advent of esters certainly constitutes an invaluable advance in the field of anabolic steroid medicine,
clearly you can see that there is no magic involved here. Esters work in a well-understood and predictable
manner, and do not alter the activity of the parent steroid in any way other than to delay its release. Although
the lure surrounding various steroid products like testosterone cypionate, Sustanon, Omnadren etc. certainly
makes for interesting conversation, realistically it just amounts to misinformation that the athlete would be
 better off ignoring. Testosterone is testosterone and anyone who is going to tell you one ester form of this (or
any) hormone is much better than another one should do a little more research, and a lot less talking.

19 SIDE EFFECTS
General
• Acne
• Erectile Dysfunction
• Estrogen Imbalance
• Gonad Atrophy
• Gynecomastia
• Hair Loss
• Hematocrit Increase
• Hypothalamic–pituitary–gonadal axis (HPTA) Shutdown
• Hypertrophic Cardiomyopathy
• Hypogonadism
• Hypothyroidism
• Increased Hematocrit
• Joint Pain
• Lactation (Galactorrhea) - caused by Hyperprolactinemia
• Liver Stress - caused by Hepatotoxic compounds
• Painful Back / Shin / Calf / etc. Pumps
• Lipid (HDL / LDL) Increases
• Spermatogenesis Changes
• "Test Flu" (See Below)

Trenbolone
• Decreased Respiratory Capacity and Treatment
• Insomnia
• Gynecomastia (caused by Hyperprolactinemia)

Solutions

Acne

Without Accutane
The following was written by /u/JuliuscaesarGG
 Why without Accutane?

Accutane has been connected not only to the short term side effects that we all know of (stomach
discomfort, dry skin/eyes/lips, liver effects, joint pain) but also to severe, potentially permanent side effects
such as: joint pain, Crohn's Disease, Irritable Bowel Syndrome, depression, sexual side effects, dry skin,
nosebleeds, reduced healing ability, etc. Accutane is structurally similar to Vitamin A, and most of these
effects are related to Vitamin A toxicity. Research Accutane side effects, and Vitamin A toxicity before getting
on Accutane. Accutane should be the complete last resort for acne.

Steroids and Acne

Unfortunately, any amount of steroids is most likely going to increase acne especially if you are predisposed
to it. Some hormones will affect people differently, some get more acne on tren, some test, some NPP, etc.
Regardless of E2, you will get acne from steroids.

Estrogen (E2) high or low can both cause acne (usually high, but large fluctuations are no good), and acne
may result even from having normal estrogen levels just due to the androgens in your system. Aim
for consistent E2 levels, this will lower your chance of acne the most.
DHT and Acne

Nizoral and Head & Shoulders are supposedly good for fungal acne, although it may be hard to identify it as
such though.

Ketoconazole or Nizoral are typical anti androgens. Get the benefits of stopping DHT from binding to the
sebaceous gland without ingesting an anti-androgen.

Lifestyle Habits & Washing Habits

Firstly, a great resource is acne.org and it's subsequent forums and this includes much general consensus
from acne groups.

Refrain from using harsh washes or activities that will increase inflammation of the skin (#1 reason for
acne). This means:
• Do not use alcohol, sulfates (soap), acne bead scrubs, overly drying washes. instead use gentle cleansers,
(acne.org has one), sulfate free, and wash your face very lightly and splash water to wash it off. PAT to dry
DO NOT scrub.
• Do not touch, scrape, or pop your acne. Don't run your dirty fingers over your acne. Do not spend time
pushing out plugged comedones, black heads, white heads. Do not excessively press and pop pimples that
are not popping, even if the end result it pops. If it takes more than 15 seconds for it to pop, leave it alone
until its ready instead: if you must, only pop pimples that are easily popped and ready with clean hands
right before you wash it. A warm shower can make it easier to pop but scalding hot water may be negative
to skin moisture. However it is more ideal to never pop pimples
• Do not sleep on dirty bedsheets or pillow cases. Do not re wear dirty shirts, or continue wearing a gym shirt
that you just worked out in. instead, shower/rinse immediately after gym and put on a clean shirt. If you go
home after gym and shower that is usually fine too. Replace bedsheets 2x a week and pillow cases EOD
(flipping the pillow after the day to get double use)
• Do not excessively wash your skin, it leads to over-drying. If possible, wash your back/face with a gentle
wash 1x a day at the max. If you need to take a second shower before bed due to general day sweat,
rinsing with water and wiping with hands is completely fine.
Washing

• As counterintuitive as it sounds, over washing can lead to acne. Your aim should be to maintain a certain level
of stability with your skin. This means over-washing will dry out your skin and cause acne. You must
completely avoid normal soap and sulfates.

• Consider a salicylic acid wash or benzoyl peroxide wash (the OG proactive uses this) and using 1x a day max.
If they dry out your skin stop for a couple days. Some people find success with a benzoyl peroxide wash, but I
think salicylic acid is better as benzoyl peroxide is a generally better treatment for leaving on skin. Others
have the opposite opinion.

• Consider washing your back with no soap at all if you haven't gotten extremely dirty. Your body maintains a
natural ph and good bacteria that lessen the ability for bad bacteria to colonize and from acne. Simply rinsing
off and not washing at all can do wonders due to the reduced inflammation on your skin.

• Wash lightly, do not scrub, do not rub hard. Your objective is to clear the previous medicine from your skin
and remove any layer of acne promoting containment on your skin. (Bacteria from sweat, pollution, clogged
pores, etc.)

Treatment

This is where it gets to the good stuff.

Test all medications first in a small part of skin before dousing yourself with it. Benzoyl Peroxide and
Azaelic Acid tend to be the biggest culprits of redness, as well as Differin to a lesser extent.
• Adapalene (brand name Differin) is a 3rd generation retinoid that specifically targets the mechanisms that
produce acne. It prevents the formation of comedones by 50-60% according to studies. Retinoids are
structurally related to Vitamin A - and Accutane is a retinoid. Adapalene (Differin) is a topical retinoid and
since being applied to the skin it does not absorb through the blood stream (as shown by studies significantly
insignificant amounts get through). So, you're basically taking topical Accutane. Adapalene (Differin) has
always been the most effective acne medication for me in permanently reducing the amount of acne I get,
and after a year of diligent use in my teens I never got pimples anymore. Additionally, Adapalene
(Differin) increases the efficacy of other popular acne treatments such as topical Clindamycin and Benzoyl
Peroxide.
• Benzoyl Peroxide 2.5% (gel version is best) - there is no evidence that stronger concentrations are better,
and they generally just dry out the skin more. Benzoyl Peroxide is the holy grail of treatment because
bacteria never get resistant to it. It provides an oxygen rich environment that is impossible for bacteria to live
in. Issues with BP = sensitivity to sunlight, redness on skin, allergic reaction (under 5% have this) so take
away = start slow when using benzoyl peroxide, EOD at first, then ED. 2x a day if your body can handle it. It
also bleaches clothes, so if you put it on before putting on clothes you need to let it dry, and probably have a
white t shirt/white sheets.
• Topical Clindamycin: Clindamycin is a popular antibiotic, but when used topically for acne treatment it
significantly boosts the efficacy of Adapalene and Benzoyl Peroxide. However, tolerance increases pretty
quickly, and I only recommend using it when a breakout occurs, or for spot treatment of specific pimples. It's
useful l usually sold in combination with Benzoyl Peroxide 5% but it's in your interest to get it separately
because 5% Benzoyl Peroxide is over drying and this way you can regulate your tolerance to it
• Curology (prescription) 4% Azelaic Acid. (precursor to Salicylic Acid) 1% Clindamycin, 4% Nicotinamide. I've
read good things about this from skin care addiction but have not used myself. Studies show Nicotinamide
being as effective as 1% Clindamycin without resistance.
• Salicylic Acid option: a slightly weaker option than Benzoyl Peroxide, but still effective. Be sure the lotion it's
mixed with is quality and you might find something useful. You might be better off finding it in pure gel.
However Benzoyl Peroxide has shown in studies be more effective and the combo treatment with Differin is
promising.
• Jojoba Oil: widely considered the best type of oil to moisturize your skin because it is very similar to the
natural oils that we produce. It's a favorite on /r/skincareaddiction
• Zinc 20-50mg for 3 days after breakout you can't stay on high zinc forever, but doing this has been found to
be effective. Lots of anti inflammatory properties in Zinc. 10-20mg is about a maintenance dose. It's good to
use Zinc-Carnosine complex, because it has the added benefit of restoring stomach lining and reversing
damage from spicy food etc. No heartburn for some.
Side Notes

Adapalene (Differin) used to be prescription only, but is now available over the counter. It also comes in a
mixture formula with Benzoyl Peroxide called Epiduo, but it is still prescription only.

Clindamycin is prescription only. Benzoyl peroxide can be found anywhere. For all of these drugs you should
be aiming to get the gel versions. If you go to your dermatologist and ask for them, you should probably be
able to get everything that you want.

Adapalene (used first) followed by Clindamycin, and Benzoyl Peroxide, is the holy trinity of destroying acne. If
using these 3 medications is causing you to get overly dry skin, you probably want to drop everything but
always continue Adapalene usage as it improves your skin over time and reduces your ability to create new
comedones. If you can only take Adapalene 1x a day is fine. 2x is better. It's better to use a thin layer of it
 everywhere (more just over-dries) if your skin is sensitive from overuse, just spot treat with it for a while but
you really want to throw it on everywhere

Moisturizing

Use a non-comodegenic moisturizer. The oil you should be using on your face is Jojoba Oil. Cetaphil and
CeraVe make great facial moisturizers. Use these after treatment in combination with Jojoba Oil, if Jojoba Oil
is not enough.

Dietary Factors

• Many people swear that cutting out Dairy reduced their acne. Considering the amount of hormone
derivatives pumped into cows, it is a reasonable assumption. Since many of us are putting hormones into our
body anyways, it might not matter, but most people get reduced acne from cutting out Dairy.

• Cutting out Sugar & Fructose can reduce acne. Inconsistent blood sugar levels are related to acne, and high
amounts of sugar provide a good environment for bacteria to proliferate. Try it out.

• Eating more veggies. Try it out, it might help.

Generally diet cannot cure acne on its own, but if it helps, it's worth it. If something you're eating is creating
acne, it's probably not something you want in your body anyway.

Summary
In summary, if you get anything out of it: GET ADAPALENE (DIFFERIN)! it's the most effective treatment for
preventing further acne (and reducing current). It's basically topical accutane.

With Accutane
Introduction

Isotretinoin (Accutane) is primarily used to treat bad cases of cystic acne, and to help the skin more rapidly
renew itself. In addition, it is used in rare cases for certain skin cancers and skin diseases. It is a type of
retinoid, which is naturally found in the body in small amounts. In the USA, it’s a prescription drug, but it is
sold over the counter without a prescription in many countries.

Bodybuilders who use anabolic steroids have utilized Accutane to counteract the negative effects of steroids
on their skin; especially, the acne related side effects.

When other treatments fail, Accutane becomes the last resort to help combat acne issues

How it Works

Accutane works as an isomer of Vitamin A, which reduces the amount of oil released by the oil glands in the
skin; this will make it difficult for acne to form and reduce it significantly. Nearly all patients achieve clearing
 of acne during a course, with 90% reporting ‘excellent’ results with higher dosages. Those that choose to
dose low will have results with diminished side effects, but run the risk of recurrence.

Bodybuilding

Since chances of acne are increased with anabolic steroid use, and bodybuilding requires looking good
(especially physique competitors), many athletes who have failed to conquer their acne with natural
remedies will turn to Accutane.

It is the androgenic increases associated with steroids that will trigger increased acne. This is especially true
for those genetically prone to the condition. Also, the hormonal changes can trigger acne as well, such as
increased testosterone levels.

Side Effects

High doses of Accutane will result in vitamin A toxicity, which will result in both permanent and temporary
side effects.

Permanent and temporary side effects such as :

• Stunted growth: The FDA, in 2010, stated the drug may stop bone growth in teenagers still growing

• Inflammatory bowel disease: Some studies have linked this drug to causing Crohn’s disease

• Eye changes: Decreased night vision and dry eyes have been reported

• Other issues like skin problems, hyperostosis, and birth defects (in pregnant women) have been reported

• Psychological effects, particularly depression, seems to be a common, but that has yet to be proven in studies

Dosage

Among bodybuilders, the dosage should be conservative. Once a day dose of 10-20mg for 6-8 weeks (some
need more, some need less), depending on severity, should work fine, but you can extend it necessary. Some
users suggest using Accutane 10-20mg 2-3 times per week when coming off cycle or dropping to a cruise
dose of Test; to prevent acne sides if you're susceptible to it. Among the general public fighting acne, a
dosage of 50-150mg per day may be prescribed by their physician. It is a good idea to take the drug with a
large meal.

Blood Pressure

Jcaesar369's Original Blood Pressure Medication Post: Here

TL;DR Version
• Blood Pressure (BP) is a complex vital sign, and cannot be easily taught and all encompassed within even
several pages of text. You could take an entire semester long course in college learning the physiology of
blood pressure and still not know everything about it. The point of my post and this section of the wiki is NOT
 to completely educate anyone about BP, but to teach anyone willing to learn how to (fairly) easily manage
their BP on their own without a doctor (although if you feel comfortable going to your doctor to get BP
medication while on AAS, then by all means please do) and know a thing or two about what they are doing.

• Different steroids WILL require different BP medications

• Trenbolone: This is where you will want Nebivolol 5 or 10 mg every day (or higher if need be, 20 mg being
the highest you should ever go). Nebivolol is a selective (the most) beta blocker that will slow down the
increased Heart Rate (HR) you experience on tren. As a beta blocker, Nebivolol is a bit more difficult to use
than other BP medications, as it will require a taper off period.
The taper is SIMPLE.

Example: You are on 10 mg Nebivolol every day.

Week 1 of the taper you will take 10 mg Nebivolol for 4 days, then 7.5 mg for 3 days

Week 2 you will take 7.5 mg every day

Week 3 you will take 5 mg every day

Week 4 you will take 2.5 mg every day

Week 5 you will take 2.5 mg every OTHER day

DONE
This taper guideline is a GENERAL EXAMPLE and can be customized to fit your own needs, but every taper
should look fairly similar to this. Larger dosages will take longer to taper off of.

• All other steroids: Use a simple ACE I such as Lisinopril or an ARB such as Losartan every day to manage BP.
These drugs help the kidneys and liver function better as well. If this does not cut it, you must read my above
post to consider duplicate (2 drugs) or triple therapy to manage your BP.

• But Jcaesar369, what about the amazing drug Telmisartan?!?!?! NO. Telmisartan, though an ARB, has very
powerful potassium increasing effects, which just complicates things. You can use Telmisartan if you want,
but you must manage your potassium and electrolyte intake and get bloodwork to monitor it. Telmisartan is
rarely prescribed alone, often with a diuretic to even out the increased potassium and because Telmisartan is
a second line ARB for people who need extra BP control that Losartan or Lisinopril could not control.

• Disclaimer: all of the above from me are just RECOMMENDATIONS and ADVICE. I am not a doctor nor a
medical professional, and you should trust their judgment (but also use your own) when managing your life
and BP. If you do not feel confident that you know how to take BP meds after all your research, ask in the Ask
anything threads for help, or go to a real doctor. Do not take them blindly.
 More on Blood Pressure
• Taking your BP once a day is not enough, as this is only a time snapshot of what is occurring in your body. You
want to take your BP 2-4 times per day. Ideally once in the morning, once in the afternoon, once before bed.
The more the better.

• When you take your BP, the first reading doesn't count. You could be anxious, nervous, what have you. Take
your BP a total of 3-4 times, with the first time not counting. Write down each reading, and average them.
This is your current BP at that time.

• Take your BP after 5 minutes of sitting and relaxing, doing something that calms you down. Watch a funny TV
show, read a book, meditate, sudoku, whatever tiny little hobby you like. Heck read some reddit. You want to
be seated, straight up, back against support like a good chair, both feet planted flat on the floor. Your arm
should be rested on a table of appropriate height, with your elbow 100% supported and you are giving no
though or energy to keeping your arm up. Use a BP machine on your upper arm (no wrist ones) to take the
readings. Make sure the cuff you are using is large enough.

• BP should be managed FIRST with cardio done 5-7 days per week (the more the better) and an active healthy
lifestyle and diet low in sodium and caffeine and ZERO other drugs of abuse. BP can then be attempted at
management with supplements, such as CoQ10, hibiscus tea, Garlic extract, etc etc the list goes on. These
supplements do very little/basically nothing for MOST people who are natural. Imagine how much they
actually do for people on steroids, with AAS induced HTN. Most people on AAS are likely to encounter some
time period that they need or should be on legitimate BP medications. Do not feel like you are a loser
because you need real BP meds while on AAS. However, definitely try cardio and adding 1-2 supplements to
your daily regimen to see if they help you before admitting defeat and taking real BP meds.

• Hypertension (HTN or high blood pressure) is known as the silent killer, because you may never know you
have it but it is very bad for your heart and body and organs. There is a way to possibly be able to tell your BP
is high without taking it: when you lay down at night and everything is dark and calm and you are rested, and
you can feel your veins pulsing and beating in your head or ears when you're on the pillow, this is a plausible
indicative sign your BP is too high, and you should start using a real machine to monitor it.

Cialis For Blood Pressure

Cialis (Tadalafil) DOES NOT lower BP. AT ALL, EVER. Anyone who tells you otherwise is lying, right to your
face, or otherwise ill informed. Read my submitted post above for a full explanation on this.
Package insert for Cialis, FDA approved.
Taken directly from page 7:
Effects on Blood Pressure
 Tadalafil 20 mg administered to healthy male subjects produced no significant difference compared to
placebo in supine systolic and diastolic blood pressure (difference in the mean maximal decrease of 1.6/0.8
mm Hg, respectively) and in standing systolic and diastolic blood pressure"
Until someone shows you scientific data done on many people showing proof that Cialis lowers blood
pressure, don't believe it. Do not attempt to use Cialis to control BP.

Gynecomastia

See The Estrogen Handbook

Hair Loss

[Under Construction]

Lactation (Galactorrhea)

Preventing
When you're wanting to preventatively take action against prolactin, a Dopamine Agonist may not be the
best choice to start with as they come with many unwanted sides and can be harsh drugs. You should always
have a Dopamine Agonist on hand if you wish to take a 19-Nor, but if you wish to run something
preventatively, you should start with some supplements.

Supplements To Help Control Prolactin:

PLEASE READ: Prolactin-Inhibiting Supplements Wiki Page
• Vitamin B6 (Pyridoxine Hydrochloride & P-5-P) - To lower prolactin levels it's recommend you take 50-
200mg of P-5-P a day, in divided doses. If you want to take regular B6, which can sometimes cause minor side
effects, take 300-1000 mg per day in divided doses.
Read the label before you buy B6 (if you choose not to get P-5-P), because the Pyridoxine Hydrochloride
type of B6 (in most supplements) has been shown to be a prolactin inhibitor, but Pyridoxal Hydrochloride
has been shown to be ineffective at lowering prolactin – make sure you buy the right type!
• Vitamin B6 - Examine Page
• Vitamin E - When using Vitamin E as a prolactin inhibitor, it's recommended that you take 300-400 IU per day
of natural Vitamin E – this can be raised up to dosages such as 1000 IU for greater prolactin control, but be
aware of the possible side effects outline here
Natural Vitamin E is labelled D-Alpha Tocopherol whereas synthetic is labeled DL-Alpha Tocopherol – the
natural form works best. D-Alpha Tocopherol with mixed natural tocopherols or D-Alpha Tocopherol with
mixed natural tocotrienols are the absolute best forms to take.
• Vitamin E - Examine Page
• SAM-e - Take 400-1200 mg a day of SAM-e along with Vitamin B6 and Vitamin E. An added bonus is SAM-E's
ability to detoxify the liver.
• SAM-e - Examine Page
• Other Effective Prolactin-Inhibiting Supplements
Remember, only use your Dopamine Agonist if blood work shows elevated levels or if your nipple(s) leak ON
THEIR OWN. Do NOT squeeze your nips and force liquid out, even natural guys can do this, by doing this you
will stimulate and cause an increase in prolactin.
DO NOT TOUCH YOUR NIPS.

Stopping Lactation
See Estrogen Handbook

Liver Stress

Here are some of the most common signs indicating you may have a serious liver issue. Warning signs usually
appear in the following order, with the later signs being the most serious:

• Reduced appetite
• Nausea and fever
• Excessive Itchiness
• Yellow eyes or skin (jaundice)
• Very dark urine (dark amber colored)
• Bloody stools
Waiting for all these signs to appear means you have waited too long. You want to take action BEFORE these
signs appear.

Preventing
See Liver Protection

Painful Pumps

Sometimes when you use AAS (especially some orals) you can get painful back / shin / calf / etc. pumps.

The first line of action should be:

• Taurine (3-10g pre-workout, you may also add 3-5g AM/PM depending on when you workout)

• Magnesium (200-500mg pre-workout, you may also add 200-500mg AM/PM depending on when you
workout)

• Potassium (200-300mg pre-workout, you may also add 200-300mg AM/PM depending on when you workout)

• Upping your water intake (1-2 gallons ED)

If none of this helps, anecdotally, Cialis (10-15mg ED) has been known to help.
 "Test Flu"

First, what is “Test Flu”? It is not an official diagnosis that a physician would label, but a term that is
associated with the flu because of the similarity of symptoms. The symptoms have a rapid onset. Often starts
with the onset of low grade fever, headache, fatigue, and body aches. Not in that exact order or even all the
symptoms listed may occur. Listed below are a few symptoms you may be experiencing:

• Fever (low grade)

• Severe aches and pains in the joints and muscles
• Generalized weakness
• Fatigue
• Headache
• Dry cough
• Sore throat and watery discharge from your nose

“Test Flu” varies from individual to individual based on their immune system. It’s the inter-correlation
between your immune system and your endocrine. If you overload one then the other responds unfavorably.
It’s your body’s auto immune response to the foreign substance that has entered your body and caused and
influx of hormones. Your body sees the large increase as foreign and tries to get rid of it. Triggering an
inflammatory response and raising you metabolism. Once your body builds its resistance to it, the symptoms
relieve or even resolve. This usually takes a week or so.

Really there isn't much you can do besides wait it out, but here is an OTC remedy:

• Emergen-C (or just Vitamin C) - 4000mg split the dose ½ in the AM, ½ in the PM
AND
• Zinc - 100mg - split the dose ½ in the AM, ½ in the PM
Do this for a week and drop the dosages in half until symptoms subside.
Drink plenty of water to ensure hydration which will also aid in recovery.

Acne vulgaris (Acne)

Acne is a condition that causes red bumps, commonly called pimples, to form on your skin. Acne is generally
caused by the pores of the skin becoming clogged and infected by Propionibacterium acnes. The clogging of
the pores can be due to overproduction of sebum by the Sebaceous glands, and / or dead skin accumulation.

Production of sebum increases with increased levels of androgens in the system. This is why acne regularly
occurs during puberty as well as a side effect of AAS use.

Categorization of Acne
Acne is generally categorized by the size of the pimple and it's location among the layers in the skin.
• Seborrhoeic dermatitis. This is a fungal form of acne caused by Malassezia fungus. It is not caused by the
over-production of sebum. Current research indicates that the Malassezia hydrolyze sebum leaving behind
unsaturated fatty acids that irritate the skin.
• Comedo. A blocked hair follicle in the skin typically seen as a black head or a white head. This blockage may
exist with or without the presence of acne.
• Papule. An elevated area of skin with no visible fluid, ranging in size from the size of a pin head to one
centimeter.
• Pustual. These are formed when the follicle wall breaks down from the pressure of the Papule leaking sebum
into tissue. The visible fluid typically consists of a purulent material of necrotic inflammatory cells.
• Nodule. The same as a Papule except for greater than 5 centimeters in width and depth. These are centered
in the dermis layer of the skin, not the epidermis. No attempt should ever be made to "pop" or lance these as
they will cause severe scarring. This type of acne can be non-responsive to topical treatments due to the
depth of the infection in the skin. This type typically takes a significantly longer time to heal.
• Cystic (Nodulocystic). When an actual cyst -- a ball of fat and connective tissue -- forms under a nodular acne
lesion. The cysts do not go away, even after the acne has subsided and can leave a permanent lump under
the skin that can be felt and moved around manually. All cystic acne is nodular, but not all nodular acne is
cystic. This type of acne can be severe and require immediate dermatological attention.

Avoid Acne
The following advice will ensure that no contribution is being made to the formation of acne.

• Avoid High-Glycemic Index Foods. Simple sugars will spike insulin levels and incite increased sebum
production. This includes most dairy products.(1)
• Mildly Cleanse the Area Twice a Day. Use a mild cleanser with warm (not hot) water, avoid scrubbing hard,
and shower after sweating heavily. The acne.org regimen for cleaning.
• Control Estrogen Levels. Wild fluctuations in estrogen levels will contribute to acne development. Estrogen is
good for the skin (1) (2) and should be maintained in the system at a reasonable level.
• Avoid Comedogenic Ingredients. These are known to be pore clogging. Do not apply any product
with comedogenic ingredients to your skin in acne prone areas.

Treatment
There are many ways to treat acne that have been tried and proven to have some benefit. These treatments
generally break down into two categories.

Commercial Remedies

The following treatments are commercial in nature wether sold over the counter or requiring a prescription.

benzoyl peroxide
 salicylic acid

Azelaic_acid

alpha-hydroxy acid

Retinoids / Isotretinoin (Accutane) / Adapalene (Differin)

Antibiotics / Minocycline / Triclosan / Chloroxylenol / Chlorhexidine / erythromycin / clindamycin /

doxycycline

AcnEase?

Laser Hair Removal?

Home Remedies

The following treatments are ones that have been discovered

Dawn Dish Soap

Diluted Bleach Bath

Tanning

OCM

Vitamin B5 Superdoses

Zinc Gluconate

ghrp2 + mod grf ?

Related Links

Bodybuildnig, Steroids, Acne Glytone Benzoyl Peroxide

Benzacilin

Changes In Estrogen Levels

With the introduction of exogenous testosterone and other AAS, estrogen levels become elevated.
Occasionally, with the use of AI, estrogen levels can crash as well. Here are the sides effects that result from
both high and low levels of estrogen.

High estrogen sides

• Acne
• Loss of libido
• Water retention (Bloat)
• Moon face
• Small testicles
• Scrotum hanging too high
• Soft testicles
• Extreme oiliness all over
• Moodiness (Aggression, depression, increased irritability)
• Lethargy
• Insomnia
• Soft erections
• Extreme cravings for sugar/chocolate
• High BP
• BP spikes
• Enlarged prostate
• Pressure in lower abdomen when urinating
• Thin stream when urinating
• Constipation (from water retention)
• Itchy nipples
• Gynecomastia

Low estrogen sides

• Dry skin/lips
• Feeling of dehydration
• Loss of libido
• Erectile Dysfunction
• Loss of sensitivity
• Dry glans (penis)
• White glans
• Loss of girth
• Irritability/Mood swings
• Crying for no reason
• DHT rage (aggression you take out on others)
• Dull orgasm
• Hesitation just before urinating
• Night sweats
• Loss of appetite
• Constant fatigue
• Lethargy
• Constipation (due to dehydration)
• Diuretic effect (pissing more water than you are consuming)
• Itchy scalp
• Obsessive thoughts

Gynecomastia (Gyno)
Gyno is the benign enlargement of breast tissue in males. Most cases of gynecomastia are caused by
excessive estrogen (aka: estradiol, E2) and are often the result of an increased ratio of estrogen to androgen.
There are two categories of gynecomastia.

Physiologic.
Gyno that is induced during the normal processes of being born, growing up and growing older. This also
includes chronic conditions that can occur naturally. The cause of approximately 25% of physiologic cases
remain unknown.

• Neonatal. 60-90% of newborns of both sexes show breast development at birth or in the first few weeks of
life. General consensus is that the cause is due to placental estrogens. This type of gyno usually clears itself
within two years.
• Puberty. The period is defined by the endogenous pulsing of GnRH which precedes the rise
in LH and FSH between the ages of nine and sixteen. LH pulses double in frequency and excrete 11x more LH
in pubertal boys than prepubertal boys. This type of gyno usually clears itself within two years.
• Advaned Age. Also referred to as senile gynecomastia, this is caused by declining testosterone levels and is
found in men between the ages of sixty and eighty. Testosterone levels begin dropping at thirty-five and fall
approximately 1-2% per year.
• Chronic Conditions. It is fairly rare to have chronic condition induced gynecomastia. There are, however,
many conditions from which it may result.

Non-physiologic.
Gynecomastia that is induced from the use of medications (including AAS). Approximately 10-25% of all
gynecomastia falls into this category. Approximately 1/3rd of all steroid users are, or will be, affected. The
likelihood of having to deal with the prevention or elimination of gynecomastia for AAS users is very high.

Approximately 4% of Testosterone is converted to dihydrotestosterone (DHT) with about 0.2% of that being
converted to estrogen. Supra-physiological doses of testosterone will, inevitably, cause excessive estrogen.
Aromatase catalyzes the three successive hydroxylations of the 19-methyl group of androgens, followed by
simultaneous elimination of the methyl group as formate and aromatization of the A-ring. This chemical
process is called "aromatization" and the step by step chemical process is depicted here. Inhibiting aromatase
from taking part in this process is very effective in controlling estrogen production.

Pseudogynecomastia
In the case of pseudogynecomastia, the reason for breast enlargement is actually fat rather than breast tissue
which in turn, leads to the chubbiness or feminization of the breast.
Signs and Symptoms
Abnormal areola sensitivity and itchiness, especially at the edge, are a primary indicator. This can followed by
areola diameter growth, breast tissue development and chest tissue asymmetry. When feeling the nipple, a
small lump may be found as a clear sign of gyno. As signs and symptoms, as well as a person's sensitivity to
them, vary greatly, it is important to be on watch for any sign or symptom.

With experience, AAS users can often learn to judge their current estrogen levels as being relatively "high" or
"low" according to their libido. Estrogen levels in a low (but not depleted) / low-normal range typically give
AAS users an ample libido. Loss of libido while not on a regime of Aromatase Inhibitors could indicate higher
estrogen levels, depending on the AAS users current cycle.
Treatment by Duration
The treatments vary depending on how long the gyno has existed. The key to all of the treatments is to
eliminate estrogen interaction in the breast cells promoting growth.

Over Two Years

There have been some reports of some of the same standard medicinal treatments working in these cases.
Typically, however, surgical removal is the only thing that will remove gyno this old.

Under Two Years

There are many reports of being able to eliminate gyno that is of this age through extended periods of near
complete estrogen suppression or SERM use.

Acute
If caught quickly, acute gyno can be eliminated without much effort or worry. There is not much time to
waste, therefore getting treatment immediately is paramount. Treatment of acute gynecomastia typically
focuses on immediate suppression of Estrogen as a primary course of action. This, combined with a SERM
proves very effective to eliminate acute gyno presentation.

An aromatase inhibitor should always be on hand for AAS users so as to avoid the complications of allowing
gyno to progress to later stages. It is also strongly advisable to have a SERM on hand as an added precaution.

Drugs Administered
There are two categories of drugs that are administered to help in clearing up gyno.
 1. Aromatase Inhibitors (AIs). These block enzymatic action of aromatase and therefore down regulate the
conversion of testosterone to estrogen.

Non-steroidal Inhibitors.
These drugs inhibit aromatization by reversible competition for the aromatase enzyme. By using up the
aromatase molecules in the system, it is unavailable to participate in aromatization which greatly slows down
the process.

• Testolactone is an older, weaker, and relatively expensive first series AI. At a dose of 250mg, it will block
approximately 25% of aromatization.
• Anastrozole (Arimidex) is a mild AI that, at a dose of .5mg, will block 50% of aromatization.
• Letrozole is a very strong AI that, at a dose of 2.5mg, it will block 99% of aromatization.

Irreversable Steroidal Inhibitors.

These drugs form a permanent and deactivating bond with the aromatase enzyme. This prohibits the
aromatase molecule from participating in the aromatization of testosterone.

• Aminoglutethimide (Cytadren). This also has the affect of being able to lower circulating levels of cortisol at
higher doses. Cortisol is catabolic to protein in muscle and effective blockade of P450scc by
aminogluthethimide at high doses prevents muscle loss.
• Exemestane (Aromasin) is a powerful AI that, at a dose of 25mg, will block 85% to 95% of estrogen
production.
2. Estrogen antagonists. This class of drugs do not lower the amount of estrogen that is in the system. They
act by binding to the estrogen receptor without generating a biological response. These are also
called Selective Estrogen Receptor Modulators (SERMS). Different SERMs can block the estrogen receptors in
different areas of the body. The below ones block them in breast tissue.
• Tamoxifen (Nolvadex) at 20 to 40 mg has been shown to be an effective treatment.
• Cyclofenil at a dose of 200 - 400mg / day is sufficient for gyno prevention or reduction.
• Raloxifene has been shown to have less relapse than tamoxifen. 60mg per day is what is typically prescribed.
• Toremifene has anecdotal information that it will reduce gyno. More information needed.

Protocols discussed in AAS users communities

This is not medical advice. All treatments for gynecomastia should be in full consultation with a licensed
physician. Everything expressed here are simply ideas to discuss with a physician.

• Starting on day #1 with .25 mg of Letrozole, you increase the Letrozole dose every day until you reach 2.5 mg.
Stop increasing the dose and maintain if gyno begins to decrease. If 2.5mg is reached, you maintain it until
the gyno is gone , if reducing or after 20 days if no reduction is noticed. This is a very aggressive protocol.
• Tamoxifen has been shown has been shown to eliminate gynecomastia at 20mg / day, if it is less than two
years old, over a six month period. This regime experienced a 27% relapse rate.

• A combination of 40mg / day of Tamoxifen with .5mg / day of Arimidex has been suggested as a way to halt
acute gyno.

Related Posts

Gynecomastia – evaluation and current treatment options

Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia.
/u/TattooedBacon had success with this protocol.
Clomid and Letro do the job
Cycle Report for treating Gyno
Foo-Dog's Gyno Series-Part 1
Foo-Dog's Gyno Series-Part 2

References

https://www.gynecomastia.org/
http://www.ncbi.nlm.nih.gov/pubmed/920892
http://www.ncbi.nlm.nih.gov/pubmed/19408804
http://www.ncbi.nlm.nih.gov/pubmed/22534349
http://www.mayoclinic.com/health/gynecomastia/DS00850
http://www.nlm.nih.gov/medlineplus/ency/article/003710.htm
http://www.ncbi.nlm.nih.gov/pubmed/2108425
http://www.newliving.com/issues/jun_2004/articles/steroids2.html
http://www.medicinecoach.com/testosterone-basics/
http://www.ncbi.nlm.nih.gov/pubmed/11897260
http://www.ncbi.nlm.nih.gov/pubmed/6887872
http://www.ncbi.nlm.nih.gov/pubmed/14649213
http://www.ncbi.nlm.nih.gov/pubmed/14709804
http://www.ncbi.nlm.nih.gov/pubmed/11014220
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2073000/
http://www.ncbi.nlm.nih.gov/pubmed/18357357
http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=f0b31daa-0792-43d5-af08-8b6a864dc90a
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs+hsdb:@term+@DOCNO+3255
http://jcem.endojournals.org/content/92/6/2197.full
http://www.ncbi.nlm.nih.gov/pubmed/22802308
http://jco.ascopubs.org/content/20/3/751.long
http://www.ncbi.nlm.nih.gov/pubmed/11606380
http://cancerpreventionresearch.aacrjournals.org/content/1/2/135.full
http://www.ncbi.nlm.nih.gov/pubmed/15238910

Hypertrophic Cariomyopathy
Taken
from: http://www.reddit.com/r/steroids/comments/1ggw9a/aas_use_and_hypertrophic_cardiomyopathy/

Over some more recent reading (was curious after I just learned about cardio in one of my classes), I read up
a little bit on cardiac hypertrophy and AAS use.

So there are actually different types of heart enlargement. They can be physiological (normal) or pathological
(bad). Athlete's heart is a type of hypertrophy that's physiological in response to exercise (a lot of elite
endurance and resistance athletes end up with athlete's heart) and your heart actually gets stronger as a
result of it (it can pump blood more efficiently).
Hyertrophic cardiomyopathy is another one where your ventricles get more muscular, without your heart
necessarily getting stronger or pumping out blood more efficiently. This can be bad, and is one of the most
common causes of sudden cardiac death in athletes. It's important to note: most of these people
were born with the potential for this happen. But this is what you hear about when you see a 19 year old
football player dropping dead of a heart attack.

So here's the thing: AAS use/abuse long term can precipitate left ventricular hypertrophy that has the
potential to be pathological. You can have athlete's heart and hypertrophic cardiomyopathy too. Generally
it's not going to fuck your shit up, but it might be potentially dangerous in the very long term.
See here:
The smaller LVDEd in DUs is coupled with a significantly disproportionate septal and posterior wall thickness
in DUs when indexed to body mass compared to DFs. There was no direct evidence of diastolic dysfunction
detected by mitral inflow velocity patterns.

So no abnormalities other than hypertrophy itself.

If you have a pre-existing condition (ie: zyzz), then it could be potentially bad. There's lots of n=1 studies on
the subject, but fuck n=1 studies for the most part.
Working out on it's own seems to have a protective effect

The thing is though, even after cessation of AAS for 1+ years, cardiac hypertrophy doesn't full attenuate
itself. This trial compared resistance athletes, former AAS users, and current AAS users.
Systolic blood pressure was higher in users (mean (SD) 140 (10) mm Hg) than in ex-users (130 (5) mm Hg) (p <
0.05) or weightlifters (125 (10) mm Hg; p < 0.001). Left ventricular muscle mass related to fat-free body mass
and the ratio of mean left ventricular wall thickness to internal diameter were not significantly higher in users
(3.32 (0.48) g/kg and 42.1 (4.4)%) than in ex-users (3.16 (0.53) g/kg and 40.3 (3.8)%), but were lower in
weightlifters (2.43 (0.26) g/kg and 36.5 (4.0)%; p < 0.001).

The maximum late transmitral Doppler flow velocity (Amax) was higher in users (61 (12) cm/s) and ex-users
(60 (12) cm/s) than in weightlifters (50 (9) cm/s; p < 0.05 and p = 0.054).

Doppler testing is used to test heart function (and to differentiate between athlete's heart and myopathy in
athletes). So there is a bit of a discrepancy.

Important to keep in mind: a lot of the current users might have been absolutely swimming in AAS and a
variety of compounds (elite bodybuilders), so the results might not carry over to your average dude just
taking a 500mg/week cycle of Test E, or 125mg/week for TRT.

BUT: in animal studies it's been shown that the T:E ratio might have an influence on cardiac hypertrophy in
animal models (women are also much less likely to have hypertrophy), and there ERB is expressed in the
heart and in normal amounts has an anti-hypertrophy effect on heart muscle.

From this:
These data suggest an important role for estrogen receptor-β in attenuating the hypertrophic response to
pressure overload in females. (mice)
In susceptible humans, there appears to be polymorphisms in the aromatase enzyme, and it seems to be
pretty common in people with cardiomyopathy.

There might also be a role of Vitamin D deficiency in the development of cardiac hypertrophy.

This trial shows an increased expression of VDR in cardiac hypertrophy, and Vitamin D is thought to have an
antihypertrophic effect in heart ventricles. There is some evidence that it might increase conversion of
Testosterone to Estradiol in certain tissues (via acting on the aromatase enzyme), like the bones and in the
balls (promoting spermiogenesis and bone formation). There's also a trial I remember reading showing
improved cytokine profiles in congestive heart failure, which is only tangentially related.
Edit: here's another trial that showed people on dialysis (who suffered from several Vitamin deficiencies,
including Vitamin D) had a reduction in their cardiomyopathy after being given fully active Vitamin D
(calcitriol). Now it's not known how much can be extrapolated from this to healthy people (or AAS users), but
the mechanism definitely seems to be there.
Relevant section on Examine of Vitamin D

Then there's Coenzyme Q10 which has repeatedly been shown to be good for blood vessel and heart health
(among other things). In cardiomyopathy there might actually be a deficiency of CoQ10 as is shown in this
article.
This six year clinical trial showed improvements in cardiomyopathy with supplementation of 100mg/day
This trial showed improvements with 200mg/day and even showed a reduce in septal thickness:
The mean interventricular septal thickness improved significantly from 1.51±0.17 cm to 1.14±0.13 cm, a 24%
reduction (P < 0.002). The mean posterior wall thickness improved significantly from 1.37±0.13 cm to
1.01±0.15 cm, a 26% reduction (P<0.005). Mitral valve inflow slope by pulsed wave Doppler (EF slope)
showed a non-significant trend towards improvement, 1.55±0.49 m/sec2 to 2.58±1.18 m/sec2 (P<0.08).

(13-15mm is the "danger zone" and 15mm+ = pathology)

Relevant section on Examine of CoQ10

So what the hell's the point of all this? Should you stop taking AAS? If you have a heart defect, probably, or
you should definitely run it by your doc. But for the average user, what should you do? Well, maybe some
prophylaxis might not be a bad idea.

You can buy some Vitamin D and Coenzyme Q10 (you should probably be taking Vitamin D already, especially
if you're running any sort of AI) and take it every morning.

http://www.iherb.com/Thorne-Research-Vitamin-D-K2-1-fl-oz-30-ml/23517?at=0&rcode=JIT328
D3 + K2 (synergism), 4 drops/day = 2000IU/d of D, and 0.4mg of MK4, take in the MORNINGS
300 doses for $22.80 = 7.6 cents per dose. This is something almost everyone should be taking anyway, but
that's another story.
http://www.iherb.com/Healthy-Origins-CoQ10-Gels-100-mg-150-Softgels/4131?at=0&rcode=JIT328 or
http://www.iherb.com/Healthy-Origins-CoQ10-200-mg-150-Softgels/10131?at=0&rcode=JIT328
1 pill/dose if you wanna go with 100mg or 200mg
150 doses for $27 or $47 = 18 cents or 31.3 cents per dose.
You can also use my coupon code for some moneys off (JIT328).
Disclaimer: I stand to make a whole $0.40 per purchase or something like that
If you find it cheaper (maybe through amazon prime or on smartpowders?) then go with that, obviously.
Additional References:
http://eurheartj.oxfordjournals.org/content/ehj/17/10/1576.full.pdf

Changes to Spermatogenesis

Spermatogenesis has not been studied much. However, gear usage does have an affect on spermatogenesis.
(Need more information)

Explained

FSH will initiate the sequestration of testosterone into the testes. After sequestered, the testosterone will be
used for spermatogenesis. Without FSH, the testes will not sequester more testosterone. Therefore, once the
testosterone in the testes is used up completely, and in the absence of FSH, the testes sill be unable to engage
in spermatogenesis.

How long does it take for the spermatogenesis to stop in the absence of FSH? Current estimation is
approximately 12 weeks after HPTA shutdown, which generally occurs after 15 weeks of exogenous
testosterone use.

Nonetheless, sperm motility has been noted to be worse in the presence of excess testosterone.
Defects rates of sperm is higher and miscarriage chances are greater.

If you want to continue to produce sperm, for sure, run HCG and HUMOG / Menopur during cycle.

http://www.ncbi.nlm.nih.gov/pubmed/16318399

"When administered to a healthy man, testosterone functions as a contraceptive by suppressing the secretion of
luteinizing hormone and follicle-stimulating hormone from the pituitary, thereby depriving the testes of the
signals required for normal spermatogenesis. After 2-3 months of treatment, low levels of pituitary
gonadotropins lead to markedly decreased sperm counts and effective contraception in the majority of men.
Treatment with exogenous testosterone has proven not to be associated with serious adverse effects and is well
tolerated by men. In addition, sperm counts uniformly normalize when testosterone is discontinued. Thus, male
hormonal contraception is safe, effective, and reversible; however, spermatogenesis is not suppressed to zero
in all men, meaning that some diminished potential for fertility persists"

References
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271653/
http://rstb.royalsocietypublishing.org/content/365/1546/1557.full
http://www.ncbi.nlm.nih.gov/pubmed/19846485
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC370892/
http://www.ncbi.nlm.nih.gov/pubmed/11739331
http://www.ncbi.nlm.nih.gov/pubmed/11750736
http://www.ncbi.nlm.nih.gov/pubmed/9813188
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1496959/
http://www.ncbi.nlm.nih.gov/pubmed/8889701
http://www.ncbi.nlm.nih.gov/pubmed/14989793

HCG and hMG assisting in Spermatogenesis:

http://www.ncbi.nlm.nih.gov/pubmed/1621528

Myostatin, Muscles and Bodyfat

By: Jerry Brainium

Myostatin is a protein discovered by researchers at Johns Hopkins University in 1997. The word myostatin
means 'muscle stopper,' an accurate description of what it does in the body. Scientists aren't sure how
myostatin works, but the leading theory is that it inhibits the involvement of satellite cells, or immature muscle
cells, in muscle growth. That's the opposite of what several anabolic hormones, particularly insulinlike growth
factor 1 (IGF-1), do.

Animals born without the gene that codes for myostatin have two primary characteristics: They have much
larger muscles than usual, and they have less bodyfat than usual. Other than that, they appear normal, with no
obvious physical problems.

Myostatin is a topic of enormous interest to bodybuilders, since, theoretically, if you can somehow block its
effects, your muscles will grow like crazy. As noted previously in this space, weight training is an effective
myostatin blocker, which accounts for some of the growth that comes from regular training. In animals,
blocking myostatin activity or manipulating their genes so that they don't produce myostatin yields not only
increased muscular growth but also a dramatic reduction in bodyfat. The theory is that the lack of myostatin
produces a repartitioning effect, promoting muscle growth at the expense of bodyfat. In short, bodyfat is used
as a source of energy to support muscle growth.

A new study partially illuminates the relationship between myostatin and bodyfat levels.1 It involved six
morbidly obese (a medical euphemism for 'very fat') subjects who underwent surgery to shorten their
stomachs. That limits the amount of food they can eat without feeling full. The surgery is considered extreme
and is a last resort for people with dangerously high bodyfat levels, people who, for some reason or other, will
not or cannot diet and exercise. The side effects of the surgery can include death'but that's another story.

As a result of the surgery, the patients lost 38.9 percent of their bodyweight. The researchers measured their
myostatin levels before and after the weight loss and found a clear and significant decline in myostatin after
the weight loss, which consisted mostly of bodyfat. The scientists suggest that the drop in myostatin was the
body's way of preventing the loss of vital lean mass under rapid and extreme fat-loss conditions. The drop in
myostatin apparently had the effect of preventing muscle loss and may have also helped the body actually
reduce the size of fat cells, as it does in animals.

Even though bodybuilders don't resort to stomach stapling as a fat-loss technique, the study has two
implications for them. As you lose fat, myostatin levels will likely decline, helping you preserve muscle during
a diet. The addition of a weight-training routine will no doubt amplify the effect. The other implication is that
having excess bodyfat probably increases myostatin, making it harder to build muscle. That's been the case in a
few studies of obese people who begin weight-training programs. They often start with considerable amounts
of lean mass under the fat, but, compared to their leaner peers, they seen to have trouble adding muscle mass.
Perhaps the higher levels of myostatin preclude significant muscle gains.
Steroids, HCG and Fertility
One of the more worrisome aspects of using high-dose anabolic steroid regimens is their effect on fertility.
Many commonly used anabolic steroids exert a feedback mechanism on the pituitary gland in the brain, which
responds by stopping the release of two hormones known as gonadotropins: luteinizing hormone and follicle-
stimulating hormone. Interestingly, estrogen is even more potent than testosterone at inhibiting the release of
LH and FSH. (Increased estrogen levels in male steroid users are the result of the conversion of testosterone or
anabolic steroid drugs into estrogen through the activity of the ubiquitous enzyme aromatase.)

The lack of gonadotropins lowers fertility, since those hormones are required for complete sperm development.
Infertility is still often listed as a major side effect of anabolic-steroid use, though permanent infertility is rare
among bodybuilders and other athletes. Cycling, or taking a break from all drug use, enables the body to
bounce back from impaired fertility in most cases. Sometimes, however, that can take a while, depending on
how much was used and the duration of the cycle.

Athletes have well-known ways of offsetting the possible antifertility effects of high-dose anabolic-steroids.
They turn to anti-estrogen drugs to prevent the rise in estrogen that results from aromatization. Such drugs
include Nolvadex, clomiphene and lately, potent anti-aromatase drugs such as Arimidex and others in that
category, which cripple the activity of aromatase, lowering estrogen levels.

While blocking estrogen helps maintain fertility in men (although some estrogen is required for full sperm
development), it doesn't affect the lack of gonadotropin secretion required for sperm development. For that
purpose, bodybuilders and other athletes turn to human chorionic gonadotropin. HCG is the same hormone that
shows up early in pregnancy. Male athletes are interested in the substance because it looks a lot like LH.

Not only is LH needed for sperm development, but it's also the rate-limiting hormone for testosterone synthesis
in the body. Athletes hope HCG will maintain the body's testosterone production, which would normally be
suppressed by anabolic steroids. HCG also maintains the sperm count, offsetting infertility.

Bodybuilders use HCG either during a steroid cycle or during the last two weeks of a cycle, when the drugs are
tapered down to zero. Some have written that it's futile to use HCG during a cycle because the high steroid
doses will overcome any effect of HCG. Others point out that HCG promotes not only testosterone synthesis
but also estrogen. If the athlete doesn't also use an estrogen-blocking drug, estrogen-related side effects, such
as gynecomastia, can quickly become apparent.

A newly published study followed the use of HCG and steroids in 21 men, mostly bodybuilders, aged 24 to 42,
for six years.2 The athletes used their own steroids; none were supplied by the researchers. As a result, the
cycles of the subjects varied in dosages and time but were far higher than any doctor would prescribe. In short,
they used real-world drug regimens. The average-length drug cycle was 138 days, while the average daily dose
was 96 milligrams.
As expected, all the subjects showed a decrease in sperm count while on a cycle. Within six weeks after getting
off the drugs, nearly all had significant increases in sperm count. By the six-month mark most were back to
normal, although one subject showed no sperm production at all at the end of his cycle. Nor did he recover
after the six-month follow-up. Within five years, however, he and his wife had two healthy daughters.

The study proved the long-held contention that injecting HCG (as a protein hormone, it must be injected) while
on a high-dose steroid regimen does maintain sperm production. On the other hand, a novel finding was that
using both high-dose anabolic steroids and HCG leads to abnormalities in sperm.

What caused the abnormalities? Full sperm development requires not only LH, which is provided by the HCG,
but also FSH. The men didn't use any type of FSH drug, although such drugs are available and are used to treat
female infertility. The authors, however, suggest that HCG caused the abnormal sperm production all on its
own.

At first glance, this study appears to be alarming. Abnormal sperm is linked to male infertility and to possible
birth defects. On the other hand, I know of not a single professional bodybuilder who's had a child born with
any birth defect'and some of them used huge steroid cycles off and on for years. My guess is that somehow the
body can tell which sperm are more effective at the job than others, and the superior sperm get to the goal first.

One Reason to Steer Clear of Trucks

Bodybuilders, particularly male bodybuilders, are acutely aware of the negative effects of excess estrogen,
among them gynecomastia, or the development of excess glandular tissue in the breasts of men; increased
subcutaneous fat deposits, or fat just under the skin; and excess water retention. Estrogen also sends potent
feedback signals to the brain, which has the effect of shutting down testosterone synthesis.

Bodybuilders are usually aware of adverse estrogen effects, and those who use drugs turn to aromatase-
inhibiting drugs like Arimidex or Aromasin. There are, however, other sources of estrogen ubiquitous in the
environment. In fact, environmental estrogens have become a major health concern.

Some health authorities predict that if something isn't done about chemicals that produce environmental
estrogens, the male sperm counts of the world are going to drop precipitously. Experimental animals exposed
to environmental estrogens became infertile or were born with abnormal sex organs.

If you're concerned about such estrogens, you may want to maintain a safe distance from trucks on the
highway. That's because of research findings that diesel-fuel exhaust contains chemicals called alkylphenols,
which interact with cellular estrogen receptors to exert potent estrogenic activity.3 Diesel exhaust particles
have previously been linked to lung cancer, allergic rhinitis and asthma.

Since the air around major highways contains tons of the stuff, what the effects are is anyone's guess.
Related Posts

Does Test E make you infertile?

References
1 Milan, G.,et al. (2004). Changes in muscle myostatin expression in obese subjects after weight loss. J Clin
Endocrinol Metab. 89:2724-2727.
2 Karila, T., et al. (2004). Concomitant abuse of anabolic androgenic steroids and human chorionic
gonadotrophin impairs spermatogenesis in power athletes. Int J Sports Med. 25:257-63.
3 Furuta, C., et al. (2004). Estrogenic activities of nitrophenols in diesel exhaust particles. Biol Repr.
70:1527-1533. IM

20 BLOOD WORK
If you want to use AAS safely, blood tests are essential. A pre-course check will warn of any reason not to use
AAS at that time, and will give a baseline for comparison later on. It is also wise to check mid-cycle, when
things should be at their worst from a health point of view. Finally, a test after PCT to ensure things have
returned to normal. For those that Blast & Cruise (B&C), it is important to run blood work at least 3-4 times
per year. It's like getting your pool water checked to make sure there is the right amount of chemicals for it
to stay clear and problem free, or checking the air pressure in your car's tires.

It's also good to have a base knowledge of the what the individual health markers mean, so be sure to check
out our Health Markers page.

How Do I Get Blood Work?

There are two ways to get blood work done. The one way to do so is requesting blood work from your
doctor, give him a list of things you want to get done, and he will send you to the lab. Most do not wish to do
this, as they are afraid of potentially getting marked as a steroid/drug abuser and they don't want it to
potentially affect their health insurance (for mid-cycle and Blast & Cruisers). The safest and most popular
mode of getting blood work is ordering it online, where you independently pay for what you want done, and
then take the forms to the lab.

Where To Get Private Blood Work

There are many services through out the world that provide individuals the capability to get private paid
blood work. These services are invaluable to AAS users to monitor our health and safety.
 In the USA
There are several providers in the USA to choose from.
Note: Unfortunately testing is unavailable in NY, NJ, MA, MD, and RI. If you are a resident of one of these
states you'll have to drive out of state to use Private MD Labs, LabsMD, or any other private lab. Instructions
Below.
MA & MD residents only: You can use Health Tests Direct.
Private MD Labs
Private MD Labs -- A good and trusted lab with many locations.
• Female Hormone Testing is recommended.
• Hormone Panel with F&T Testosterone LC/MS-MS is similar to the Female Hormone Panel but uses LC/MS for
testosterone. This will provide an actual value rather than "> 1500".
• Hormone Panel with Estradiol Sensitive and Testosterone LC/MS-MS Same as above, but with LCMS estrogen
test. Use this to get an accurate estrogen reading while running tren. DO NOT use this to test whether your
tren is bunk, as it will not count it in the estrogen test.
• Anything with Test 070195 will show the actual value for testosterone, rather than "> 1500".
• Thyroid TSH, T4 and T3 Panel
• Liver Panel for you Oral users This is included in the Hormone Panel for Females. You do not need to order it
separately.
• Lipid Test to check Cholesterol levels
• Anything with Test 303756 contains a lipid panel.
• The Hormone Panel Unisex panel includes thyroid, lipids, estrogen and F&T Testosterone LC/MS-MS.
LabsMD
• Hormone Panel for Females will provide the actual number for testosterone rather than "> 1500". The assay
used for testing estradiol will not give a false reading when using tren.
Walgreens
• Cholesterol tests are available at most locations.
Blood Work For NY, NJ, MA, MD, & RI Residents

For Private MD Labs or Labs MD:

1. Add the tests needed to cart.

2. At checkout, select a LabCorp / Quest location to go to that is outside of your state.

3. If applicable, apply coupon code (Google search for a 15% coupon code for Private MD Labs) This should give
the price needed to pay for the tests.

4. In a new browser tab, buy a gift certificate of that amount on the Private MD Labs or Labs MD website. Using
a credit/debit card with a NY, NJ, MA, MD, or RI billing address should work here.
5. Use that gift certificate code to pay for the test. NOTE: Some report being able to skip Step 4 and just pay
using their credit card, even if the billing information is a NY, NJ, MA, MD, & RI address.
6. Leave credit card info blank. Put in both Billing Information and Patient Information with your own name, but
with an address outside of your state. Others put a out-of-state relative's address (with their permission) with
no issues. Nothing should be physically mailed to that address either . . . Billing address shouldn't matter
since you didn't put in credit card info, but they ask for it anyway.

7. Print requisition papers. You may optionally (but recommended) set up an appointment for your desired out-
of-state LabCorp / Quest location.

8. Show up to the LabCorp / Quest location. If asked for ID it's reportedly fine to show your NY, NJ, MA, MD, &
RI Drivers License. Alternatively, others have used Passports, Work or School IDs, etc.

9. Wait to be emailed the lab results.

For Discounted Labs

1. Make an account and order desired labs on discountedlabs.com

2. Print requisition papers. You may optionally (but recommended) set up an appointment for your desired out-
of-state LabCorp / Quest location.

3. Show up to the LabCorp / Quest location. If asked for ID it's reportedly fine to show your NY, NJ, MA, MD, &
RI Drivers License. Alternatively, others have used Passports, Work or School IDs, etc.

4. Wait to be emailed the lab results.

In the UK
Medichecks
Medichecks
Blue Horizon
Blue Horizon Medical

In Canada
Info Taken From This Post
The Following are all anecdotes taken from the thread linked above:

• In Ontario? Go to an Appletree clinic and say you want blood work. That easy. They also run acne clinics and
oversee and prescribe Accutane. Dudes take good care of us.

• Worth saying, just go to a walk-in. Say you're on steroids, don't be embarrassed, literally no one cares. Is
there a chance you encounter a doctor who says SHAME and refuses to give you healthcare? Sure. Less likely
 than them just covering their asses and checking your shit. Maybe you won't get uncapped Test levels but
you'll get your lipids and liver enzymes.

• In New Brunswick. I don't have a family doctor, so I went to a walk in clinic and told the doctor I was planning
to go on steroids, and wanted bloodwork done. He filled out a bloodwork order form that I could take to the
hospital, or to a walk-in blood clinic. After a couple visits, I asked for the order to be made a recurring one. So
now I can just stop in at the walk-in blood clinic (they charge $14 to draw) and they'll use the order they have
on file and send it to the hospital lab. Lab results get sent to the doctor that ordered them. I generally don't
go to the clinic to review results, I go to the personal health records office at the hospital and request a hard
copy of the results. They print it out and hand it over to me.

• In BC but this should go for anywhere in Canada (Naturopaths cannot order blood tests in New Brunswick).
Go to a naturopathic doctor, they can request blood tests. Most benefits packages include visits to
naturopaths, so it's in a way almost free.

• I'm in Montreal, and i just went to a doctor, walk-in clinic and asked for blood test, the reason if I remember
was test booster, feeling moody. He gave me a paper with the test he wanted checked, i checked the rest,
didn't get in trouble.

• In Quebec. I went to my doctor and basically told her I was on and explained why blood work was important
for me to stay safe. If the doc is reasonable they will hook you up, if the doc is hard-headed (the first doc I
tried was like this) then just go to another doc. The thing that sucks is that you can't get bloods as often as
you'd like because the doc probably won't think its necessary.

• I go to a medical clinic in Ottawa (Sandy Hill Clinic) that has large numbers of drug users. Every big town or
city has one. Just look up HIV Prevention on your cities web site. There they practice "Harm Reduction" so
when you ask a doc for any test in order to reduce harm, they will do it eagerly.

• Honestly I just kept asking ... This is in Alberta btw. Ended up finding someone at a walk in clinic (Calgary)
willing to write me up for what I wanted.

• In Alberta i went to a walk in with the whole im tired etc thing to get my first bloods. Eventually i got sick of
making excuses so i just told him what im going to be taking and that i wanted regular bloodwork to monitor
health. Very understanding no lecture nothing he just said ok whatever you need on the panel let me know
and i will give you req sheets for it. When you want more bloodwork just make an appointment. Now i just go
to him when i need bloodwork and he's also my family doc now as well.

• I went to a walk in clinic. Told the doctor I want a sheet for SELF PAID blood work. Tell them your interested
in having your hormones check because you feel rundown and you just want to see for your piece of mind.
Photo copy it and keep re using it. The costs for self paid test vary place to place and Provence to Provence.
In BC a testosterone test from a lab cost $80. In Alberta labs charge $45 and the universities charge $22. Shop
 around and check your local university for pricing . There is single collection fee aswell each time you go, in
Alberta it's $25. If the doctor puts their info on the sheet get a new slip from another doctor or they'll keep
being sent your bloodwork and your history will show up. If your tight with your doctor they won't mind. Be
aware your bloodwork is not private and will be sent to provincial data bases for physicians to access. It may
be possible for self paid bloodwork to be request not to appear in databases. However my self Paid blood
has.

• AB here. I go to a naturopath to avoid getting labeled a drug user on my medical file. Work benefits cover 2
blood tests /yr.

Related Canadian Blood Work Post

Potential Route:

Go to a walk in clinic. When the doc comes in say you are taking a test booster and you feel moody and your
nipples are sensitive. S/he will send you for a blood test. Make sure you say your nipples are sensitive or s/he
wont check the e2 boxes on the form The forms are good for a year, so once you have them, just give blood
when you want.

Blood Work Considerations

Trenbolone
When testing estrogen while running tren, make sure to get the LCMS estrogen reading. Most estrogen tests
are ECLIA or RIA, which will count tren as estrogen. This will give you a false estrogen reading if you are trying
to dial your AI in. The only time you may want ECLIA or RIA method is when you wish to see if there actually
is Trenbolone in the vial you believe to be Trenbolone.

Other
Of importance to look at is: LFT's or Liver Function Tests; fractionated cholesterol (HDL/LDL), and the relevant
hormones. Below is a full list of recommended tests.

Haematology: Measures haemoglobin, red blood cell numbers and size, as well as distribution of white blood
cell types.
Electrolytes and LFT's: gives information on liver and kidney function.
Fractionated cholesterol: HDL/LDL ratio and triglycerides.
Iron studies: Total serum iron, transferrin levels (the carrier protein) and ferritin (the tissue storage protein).
Thyroid Function Tests: Include free T3 and T4 as well as Thyroid Stimulating Hormone (TSH).
Cortisol
Insulin and Glucose
LH/FSH: The gonadotrophins that stimulate the testes to produce testosterone.
Testosterone and SHBG: Free testosterone should be measured not calculated.
Estradiol
IGF-I (if available): Especially useful for those using hGH or hGH releasing peptides to measure effectiveness.
A moderate rise will be seen with AAS use alone.
Redditors in North America can access on-line blood tests at http://www.privatemdlabs.com/ and in
Australasia at http://www.bloodworks.com.au/ Regardless of whether you get your bloods done by your
local doctor or by an online service, you can get expert interpretation of blood tests either re-cycle, mid-
cycle, or after PCT at http://www.bloodworks.com.au/ (Please mention Reddit to receive this service for
AUD$80).
hGH/IGF-1

hGH stands for human Growth Hormone a 171 amino acid polypeptide hormone released from the Anterior
Pituitary gland in the brain. Its release is controlled by at least two hormones from the Hypothalamus...GH
Releasing Factor and Somatostatin. GHRF stimulates GH in a pulsitile manner, while Somatostatin inhibits it's
release. IGF-I, which is released from the liver into the circulation in response to GH release, is also thought
to inhibit GH release in a negative feedback loop.

IGF-I is thought to mediate many of the effects of hGH... and in response to hGH, muscle and many other
tissues, can make their own IGF-I inside the cells. The resultant IGF-I synthesis effects both neighboring cells,
and the cell itself via the Akt pathway (autocrine/paracrine secretion). Some of those neighboring cells in
muscle are satellite cells, which are stem cells present inside the muscle sarcolemma, but outside of the
actual muscle cells. IGF-I has the effect of increasing their number, and to differentiate (change them) into
muscle cells. The satellite cell changes into a myoblast (primitive muscle cell) which then fuses into an
existing fibre (particularly an inured one) and donates its nucleus.

When a muscle has to grow or repair, it requires more DNA which is donated by the satellite cells. This is to
keep the protein/DNA ratio constant as a cell grows. Skeletal muscle is unusual in that it is a multi-nucleated
cell. This is thought necessary as skeletal muscle cells are so relatively large that one nucleus could not
adequately serve the whole cell.

The effects of IGF-I administration for BB purposes are controversial in terms of efficacy of low (microgram)
dosages. In clinical trials it has been used in the range of 8-10 milligrams per day. There seems to be a great
disparity here between anecdotal reports and published studies.

While the effectiveness of direct IGF-I administration is debated, the use of synthetic recombinant hGH is
clear. It has been shown that doses upwards of 4 iu/day confer significant anabolic effects in muscle. Does
this increase in muscle size relate to an increase in strength? Research says yes, but not as much of an
increase in strength as seen with AAS. That is the strength per cross sectional area will increase in response to
androgens, while remaining fairly constant for hGH administration. This has been put down to the synthesis
of non-contractile elements, such as collagen.

GHRP's
GHRP's are peptide hormones (short chain of amino acids) that stimulate either directly or indirectly hGH
release in humans. GRP6 or GHRP2 are relatively short acting, while CJC1295 is longer acting. GHRP6
stimulates Gherelin release, resulting in hunger. GHRP2 does not have the same effect on Gherelin, but like
GHRP6, it elevates cortisol. Ipamorelin stimulates GH release without the increases in Gherelin and cortisol
seen with the others.

Myostatin Inhibitors:

Myostatin is a protein hormone that stops muscle growing too big. It is thought that most organs, including
skeltal muscle, have a specific growth regulating protein. In Skeletal muscle, that is myostatin or GDF8,
Growth and Development Factor 8. So if myostatin stops muscles from growing too big, why not suppress or
inhibit it? There is much research to try and accomplish this in humans without side effects.

There are three viable methods for myostatin inhibition. Firstly, there is the antibody approach. This entails
injecting a monoclonal (very specific) antibody into a subject, which will bind to, and tie up circulating
myostatin levels. (see MYO-029:http://en.wikipedia.org/wiki/Stamulumab)

Secondly, there is the "small molecule approach" that use inhibitors of the myostain receptor, such as SB 431
542 and GW 788 388. These receptor inhibitors act in a similar manner to Nolvadex as a blocker of the
estrogen receptor. It won't reduce the amount of myostatin, but it will block its effects at the receptor level.

Thirdly, there is the use of a soluble portion of the receptor (ActIIb receptor), which mops up myostatin in the
blood and acts essentially as a binding protein for myostatin. Analogous to SHBG, which we are all familiar
with, which mops up (binds) testosterone and its analogues in the blood. ActIIb receptor binds too and
deactivates myostatin. The Activin receptor and the myostatin receptor are essentially the same thing.

http://www.reddit.com/r/steroids/comments/1vysry/so_you_got_your_blood_work_but_what_does_it_all/

Related Posts

If you run Tren you should include bilirubin on your bloodwork.

Blood Values Sorted By Mass and Molar Concentration

View Full
Size
Health Markers

Individual Heath Markers Defined

Alanine amino-transferase (ALT)

An enzyme produced primarily in the liver but also in other tissues. ALT is involved in amino acid and protein
metabolism. Used as a primary marker of hepatic strain. Also called Serum Glutamic Pyruvic Transaminase
(SGPT).

Albumin
The main protein that circulates in the blood. Produced in the liver and has antioxidant properties. Transports
certain hormones, vitamins, and minerals, and plays a role in water balance. Used as an indicator of liver
health. Higher levels are optimal.

Alkaline Phosphatase (ALP)

A family of cholestatic enzymes produced mainly in the liver, but also in the intestines, kidneys, and bone.
Used as a marker of hepatic strain, often relating to disease of the bile ducts.

Apolipoprotein A-I (apoA-I)

A constituent of HDL (good) cholesterol, apoA-I is responsible for initiating beneficial reverse cholesterol
transport. This process pulls cholesterol particles from the artery walls and transport them back to the liver.
Higher levels are optimal.

Apolipoprotein B (apoB)
A constituent of LDL (bad) cholesterol, apoB is responsible for attaching these lipoproteins to artery walls.
ApoB is a promoter of fatty plaque deposits in the arteries. Lower levels are optimal.

Aspartate amino-transferase (AST)

An enzyme produced primarily in the liver but also in muscle tissue. AST is involved in amino acid and protein
metabolism. Used as a marker of hepatic strain, although it is considered less specific than ALT testing. Also
called Serum Glutamic-Oxalocetic Transaminase (SGOT).

Basophils
A type of white blood cell. Action not fully understood, but cells are known to carry histamine, heparin, and
serotonin. Levels are elevated with allergic reaction and parasitic infection.

Bicarbonate
A measure of carbon dioxide content in the blood, and a common marker of the acid-base balance.
Bilirubin
A waste product made from the breakdown of red blood cells. Excreted into the bile. Regarded as an
important indicator of liver health. Elevated levels in the blood indicate liver toxicity.

Blood Urea Nitrogen (BUN)

A waste product from the breakdown of proteins, filtered and excreted through the kidneys. Elevated levels
may indicate a number of problems including excessive protein intake, kidney damage, dehydration, heart
failure, or reduced production of digestive enzymes. Low levels may be indicative of many things including
malnutrition or liver damage.

BUN/Creatinine Ratio
The ratio of Blood Urea Nitrogen to Creatinine, used as a marker of kidney and liver health.

C-reactive Protein (CRP)

A key marker of inflammation in the body. Elevated levels may indicate increased risk of cardiovascular
disease or stroke.

Carbon Dioxide (CO2)

Byproduct of respiration, and a common marker of the acid-base balance. See also Bicarbonate.

Calcium
Electrolyte involved in a myriad of body functions including bone metabolism, protein utilization, muscle and
nervous system functioning, cardiovascular functioning, blood clotting, and nutrient transport.

Chloride
Electrolyte involved in the regulation of water balance. Elevated levels may indicate a number of things
including anemia, dehydration, excess salt consumption, and hyperthyroid. Low levels may indicate heart or
kidney failure, severe vomiting, or a number of other health conditions.

Cholesterol, Total
A measure of all fractions of cholesterol in the blood (LDL, VLDL, and HDL). High total cholesterol is regarded
as a risk factor for cardiovascular disease.

Cholesterol, HDL
A measure of the beneficial high-density lipoprotein (HDL) fraction of cholesterol, which helps remove plaque
deposits from arteries. High levels are optimal. Low levels may be found in cardiovascular disease.
Cholesterol, LDL
A measure of the low-density lipoprotein (LDL) fraction of cholesterol. This is the primary atherogenic
particle, meaning it tends to promote the formation of plaque deposits in the arteries. Low levels are
optimal.

Cholesterol, VLDL
A measure of the very low-density lipoprotein (LDL) fraction of cholesterol. VLDL contains the highest amount
of triglycerides. Considered an atherogenic (“bad”) cholesterol particle. Lower levels are optimal.

Cholesterol, LDL/HDL Ratio

A measure of the primary atherogenic particle (LDL) in relation to the primary antiatherogenic particle (HDL).
This ratio is generally considered the most important cholesterol test value for assessing cardiovascular
disease risk. A low ratio is desirable.

Creatine Kinase
An enzyme found largely in the heart and muscle, and responsible for converting creatine to
phosphocreatine. Elevated levels may be linked to a number of things including heart attack, kidney failure,
or sever muscle damage.

Creatinine
A waste product of muscle metabolism. Low levels may indicate kidney disease, malnutrition, or liver disease.
High levels may indicate a number of things including reduced kidney function or muscle degeneration.
Creatine supplementation may also elevate creatinine levels.

Eosinophils
A type of white blood cell. Similar to basophils, eosinophils are used by the body to protect against allergy
and parasites. Levels are elevated with infection, and are low with good health.

Estradiol
The principle active form of estrogen. High levels can be associated with water retention, fat buildup, and
gynecomastia (men). Also plays a role in prostate hypertrophy. Low levels of estradiol may be associated with
increased heart disease risk.

Follicle Stimulating Hormone (FSH)

A pituitary hormone involved in reproduction. In men, FSH is mainly responsible for supporting
spermatogenesis. In women it supports ovulation.
Gamma-Glutamyl Transpeptidase (GGT)
A cholestatic enzyme produced in the bile ducts. GGT is involved in glutathione metabolism and the transport
of amino acids and peptides. Used as a marker of hepatic strain.

Globulin
A blood protein similar to albumin. Globulin is responsible for transporting certain hormones, lipids, metals,
and antibodies. Levels may be elevated in many conditions including chronic infections, liver disease,
arthritis, cancer, or lupus. Lower levels may be found with a number of conditions including suppressed
immune system, malnutrition, malabsorption, and liver or kidney disease.

Glucose (fasting)
Glucose is the product of carbohydrate metabolism and the primary source of energy for most cells in the
body. Fasting glucose levels are elevated in a number of conditions including diabetes, liver disease,
metabolic syndrome, pancreatitis, dieting, and stress. Low fasted glucose levels may indicate liver disease,
overproduction of insulin, hypothyroidism, or other diseases.

Hematocrit
A measure of the percentage of red cells in the blood. Low levels indicate an anemic condition. High levels
may indicate a number of things including dehydration, increased red cell breakdown in the spleen,
cardiovascular disease, or respiratory disease. Anabolic steroids may also increase hematocrit.

Hemoglobin
A constituent of red blood cells, and the main carrier of oxygen and carbon dioxide in the blood. Levels may
be suppressed with a number of conditions including malnutrition, malabsorption, and anemia. High levels
may indicate many things including dehydration, cardiovascular disease, or respiratory disease. Anabolic
steroids may also increase hemoglobin levels.

Homocysteine
A compound formed from the metabolism of the amino acid methionine. Involved in blood clotting and LDL
cholesterol oxidation. Elevated levels of homocysteine indicate an increased risk of cardiovascular disease
and stroke.

Iron
Mineral necessary for many functions including the formation of hemoglobin and certain proteins, and the
transport of oxygen. Elevated levels may be caused by many conditions including certain forms of anemia,
liver damage, hepatitis, iron poisoning, or vitamin B6 or B12 deficiency. Low levels can indicate a number of
things including gastrointestinal blood loss, heavy menstrual bleeding, iron malabsorption, or dietary iron
deficiency.
Lactic Acid Dehydrogenase (LDH)
An intracellular enzyme found in many tissues including the kidney, heart, skeletal muscle, brain, liver, and
lungs. Used as a marker of tissue damage. High levels are found in many conditions including heart attack,
anemia, low blood pressure, stroke, liver disease, muscle injury, muscular dystrophy, and pancreatitis.

Luteinizing Hormone (LH)

A pituitary hormone responsible for the stimulation of testosterone production in the testes (men). LH
primarily supports ovulation in women.

Lymphocytes
A type of white blood cell. Primary role is to fight viral infection. Levels are elevated with active infection. Low
levels are associated with suppressed immune system or active bacterial infection (noted by elevated
neutrophils).

Mean Corpuscular Volume (MCV)

A measure of the size of red blood cells, determined by measuring the volume of a single red blood cell.
Useful in determining the cause of anemia. Elevated levels may reflect a number of things including a
deficiency of vitamin B6 or folic acid. Low levels may reflect iron deficiency, or other causes.

Mean Corpuscular Hemoglobin (MCH)

A measure of the average weight of the hemoglobin in red blood cells. Useful in determining the cause of
anemia.

Mean Corpuscular Hemoglobin Concentration (MCHC)

A measure of the average concentration of hemoglobin in red blood cells. Useful in evaluating the cause of,
and therapy for, anemia. Low levels may indicate blood loss, B6 or iron deficiency, or other causes.

Monocytes
A type of white blood cell. Primary role is to fight severe infection not sufficiently countered by lymphocytes
and neutrophils. Levels can be elevated with a number of things including chronic infection and certain
cancers. Low levels indicate good health.

Neutrophils
A type of white blood cell, also known as granulocytes. The primary white cell used by the body to fight
bacterial infection. Levels are elevated with infection. May be suppressed with compromised immune system
or bone marrow.
Phosphorous
An abundant electrolyte involved in a number of body functions including the utilization of carbohydrates,
fats, and proteins for cellular maintenance, repair, and growth, the production ATP for the storage of cellular
energy, the transport of calcium, the maintenance of osmotic pressure, and the maintenance of heartbeat
regularity.

Platelet Count
A measure of the concentration of platelets (also known as thrombocytes) in the blood. Platelets are involved
in blood clotting, and protect against excessive bleeding. Elevated levels may be linked with a number of
things including dehydration. Low levels are found in suppressed immune system functioning, drug reactions,
or deficiencies of vitamin B12 or folic acid, or may have other causes.

Potassium
A key electrolyte necessary for nerve and muscle function, and the transport of nutrients and waste products
in and out of cells. Along with sodium it helps maintain the acid base balance and osmotic pressure. High
levels may be caused by a number of things including kidney failure, metabolic or respiratory acidosis, and
red blood cell destruction.

Prolactin
A reproductive hormone involved specifically in lactation. Prolactin is sometimes (but not commonly)
elevated in steroid abusers, and may be linked to estrogen excess or hormone imbalance. Elevated prolactin
may also indicate other issues with the pituitary.

Prostate-specific antigen (PSA)

A protein found in prostate cells. Used as a screening for prostate cancer risk. Elevated levels reflect an
increased risk of developing prostate cancer. Low levels are desirable, although do not assure against
prostate cancer.

Red Blood Cell Count

A measure of the total concentration of red blood cells, responsible for transporting oxygen and carbon
dioxide in the body. High red cell counts are seen with a number of conditions including heart disease,
dehydration, or pulmonary fibrosis. Low levels may be linked to many things including anemia, bone marrow
failure, red blood cell destruction, bleeding, leukemia, and malnutrition.

Red Cell Distribution Width (RDW)

A measure of the variation in size between red blood cells. Useful in evaluating the cause of, and therapy for,
anemia. Increased values may indicate a number of things including vitamin B12, folic acid, or iron deficiency.
Sodium
An abundant electrolyte necessary for many functions including the maintenance of osmotic pressure, acid-
base balance, and nerve impulse activity. Disturbances in the sodium level may be caused by minor things
including excessive sweating, vomiting, diarrhea, water intake, or very serious conditions including heart,
kidney, or liver disease.

T3 Uptake
This test measures the level of unsaturated thyroxine binding globulin (a carrier of thyroid hormones) in the
blood. Increased levels may indicate a number of things including hyperthyroidism (overactive thyroid), liver
disease, cancer, and decreased lung function. Low levels may be indicative of hypothyroidism (under active
thyroid), excess estrogen levels, pregnancy, or other causes.

Testosterone, Total
The measure of both unbound (active) and bound (inactive) portions of testosterone in the blood.

Testosterone, Free
The measure of free (unbound) testosterone in the blood. This represents the total amount of testosterone
immediately available to tissues.

Thyroid-Stimulating Hormone (TSH)

A pituitary hormone responsible for stimulating the release of thyroid hormones.

Thyroxine (T4)
The more abundant of the two major thyroid hormones (T3 and T4). T4 serves mainly as a reservoir for the
more active thyroid hormone (T3), which helps to stabilize and regulate thyroid supply. This is a key marker
of the state of thyroid health (low, normal, or overactive).

Thyroxine, Free Index

This measure is a calculation of the amount of unbound (free) T4 in the blood. This is a key marker of the
state of thyroid activity (low, normal, or overactive).

Total Protein
A measure of the total serum protein concentration, mainly albumin and globulin. Serum proteins are
important to the function and supply of enzymes, hormones, nutrients, and antibodies, and also play a role in
maintaining the water and pH balance. Low levels may indicate a number of things including malnutrition,
liver disease, malabsorption, diarrhea, or severe burn injury. Elevated levels may indicate infection, liver
damage, or other disease.
Triglycerides
The main storage form of fatty acids in the body. May be metabolized and used for energy. Elevated
triglyceride levels may contribute to hardening of the arteries (atherosclerosis), and increase the risk of heart
disease or stroke. Low levels are optimal.

Urea
see Blood Urea Nitrogen (BUN)

Uric Acid
The waste product of purine metabolism, which is filtered and excreted through the kidneys. Elevated levels
may indicate a number of things including gout, infection, kidney damage, and excessive protein intake. Low
levels may indicate kidney damage, malnutrition, liver damage, or other causes.

White Blood Cell Count

A measure of the total concentration of white blood cells (also known as leukocytes), responsible for fighting
infection and protecting the body from pathogens. A differential measure of white blood cells is usually also
taken including neutrophils, eosinophils, basophils, lymphocytes, and monocytes. Levels may be elevated
with certain infections or allergic conditions.
This pdf version of the /r/steroids wiki was compiled by u/Big_Papa_Bear_ on 11/9/2020