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46 An exciting update on both pregnenolone and coconut oil

jeffbo777777 Aug 28, 2013

Here's an update i sent to all my readers ... .for some reason the exhibits won't
paste here but you will get the idea .....

UPDATE-Some Interesting new ideas and experimental results:

Hi thanks to all who helped me down vote that reviewoit now dwells in the
reviewer sewer!

Most of you on the update list contacted me after reading the Vitamin D3
book. Sorry to say this update is more related to the Alzheimer's and ALS
books-but should be interesting to all who are concerned with good health.

Update 1: Around Christmas of 2012 I was contacted by a person who had

been recently diagnosed with ALS and wondered about D3. I remembered in
my D3 book I bragged that anyone could find a cure for any disease in 30
days or less using the top down research technique with Pub Med (it's like
working a jigsaw puzzle and learning just enough to get by).

So I felt obligated to try and make good on my boast and began reading from
Abstract #1, all 12,000 abstracts of science journal reports and studies
concerning ALS.

Well after I had finished about 5,000 of them or so, one little fact that had kept
hitting me in the faceofinally PUNCHED me in the face. The key puzzle piece
it seemed to me was this:

Men get ALS at a much higher rate than women except around age 60 or so
when the ratio of men and women getting ALS reverts to 1 to 1. it seemed
relevant but I don't know why I didn't see it right awayoWomen have a much
higher lifetime level of progesterone levels than men until menopause when
progesterone drops to the same level as men. From working on Alzheimer's I
had learned that progesterone is the most neuroprotective substance on
earth! It is the reason why women recover from brain injuries much faster and
better than men. I knew it wasn't estrogen because that keeps rising in men
all their lives even though it crashes in women at menopause.

So that was it! I suggested the ALS patient start taking large doses of
progesterone and melatonin which also causes you to produce progesterone
(more on this later). I'm not sure how much the patient followed my advice as
the patient seemed to be trying all sorts of things from acupuncture to faith
healing, but it was claimed the patient was using progesterone cream and
taking melatonin.

Now keep in mind that there is no effective treatment for ALS at all except
one drug called Rilutek (which looks kind of similar in structure to melatonin
chemically). All it does is extend their life span by at most 5 months . People
diagnosed with ALS tend to live only 2 to 4 years from diagnosis. So finding
an effective treatment would be quite exciting.

Well once I came up with the progesterone idea I searched progesterone vs.
ALSDNOTHING!!! No one had ever studied it ! Talk about criminal
negligence.

So that is where it stayed for about six months until I was contacted by
someone from a family that had a genetic form of ALS (about 10% of the
cases are genetic). And they asked if I had seen the recent study with mice
that get ALS- the genetic type ... I said no looked it up and with a 4mg/kg of
progesterone injection they got about a 15% increase in average lifespan in
the mice which in human terms would mean about 9 years of extra survival
instead of just the 5 months one gets from Rilutek: And keep in mind this

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genetic form of ALS might be more difficulty to treat then the sporadic kind
that most people get because the genetic kind is caused by a bad gene
spitting out poison right onto your DNA where sporadic might be less
aggressive and maybe more treatable with progesterone. Here is the
headline and article.

Autophagy activation and neuroprotection by progesterone in the G93A-

SOD1 transgenic mouse model of amyotrophic lateral sclerosis
o Jean Kima, 1,
o Tae-Youn Kima, 1,
D Kyung-Sook Choa,
o Ha Na Kima,
o Jae-Young Koha, b,,
o a Neural Injury Research Lab, University of Ulsan College of Medicine,
Seoul 138-736, Republic of Korea
D b Department of Neurology, University of Ulsan College of Medicine, Seoul
138-736, Republic of Korea

Highlights
D
PG activates functional autophagy in cells and mice.
D
PG increases survival of motoneurons in G93A-SOD1 slice cultures and
mice.
D
PG reduces hSOD1 level in G93A-SOD1 Tg cultures and mice.

Abstract
Progesterone (PG) exerts neuroprotective effects under conditions such as
brain ischemia, traumatic brain injury, and spinal cord injury. Previously, we
reported that PG activates autophagy, a potential neuroprotective
mechanism, in cortical astrocytes. In the present study, we explored the
possibility that PG, by activating autophagy in spinal cord cells, protects
against motoneuron degeneration in transgenic (Tg) mice expressing the
human G93A-SOD1 (superoxide dismutase 1) mutant, a model of
amyotrophic lateral sclerosis.
PG treatment increased autophagic flux in G93A-SOD1 Tg spinal cord
astrocyte cultures and mice. In addition, PG treatment reduced mutant SOD1
protein levels and motoneuronal death. Inhibition of autophagy with 3-
methyladenine (3MA) reversed these PG effects, indicating that activation of
autophagy contributed to the PG neuroprotection. PG effects in vivo were
tested by intraperitoneally injecting male G93A-SOD1 Tg mice with different
doses of PG (2, 4, or 8 mg/kg) or vehicle from 70 days of age until death.
Measurements of motor functions using rota-rod tests showed that the onset
of symptoms was not different among groups, but the progression of motor
dysfunction was significantly delayed in the PG-treated group compared with
the vehicle control group. The average lifespan was also prolonged in the
PG-injected group. Histological examinations revealed that PG treatment
substantially reduced the death of spinal motoneurons at 14 weeks of age
with a concomitant decrease in mutant SOD1 levels.
Our results demonstrated that PG delays neurodegenerative progress in
G93A-SOD1 transgenic mice, possibly through activation of autophagy in the
spinal cord.
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D
Keywords
o Steroid hormone;
D Spinal cord;
D hSOD1;
D LC3;
D ALS

Figures and tables from this article:

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Fig. 1. Increased autophagic flux by PG in G93A-SOD1 Tg spinal astrocyte

cultures and mice.A) Western blot analysis of LC3-ll in samples prepared
from Tg astrocytes, sham-treated (CTL) or treated for 3 h with 50 nM Baf A 1,
100 nM PG, or Baf A1 plus PG. In the presence of Baf A1, PG further
increased LC3-ll levels compared with PG and Baf A1 alone. Bars denote fold
increases in densitometric values of the LC3-ll band, normalized to the
density of the corresponding j3-actin band and expressed as means ± SEM
(*P < 0.05; n = 406).B) Samples of lumbar spinal cords of G93A-SOD1 Tg
mice that had been prepared at 15016 weeks of age were processed for p62
immunoblotting. In the PG (4 mg/kg)-treated group, there was a substantial
reduction in p62 levels as compared with vehicle controls. Bars denote fold
increases in densitometric values of the p62 bands, normalized to the density
of the corresponding 13-actin bands and expressed as means ± SEM (*P <
0.05; n = 304). These results indicate that PG increased autophagic flux.
Figure options

Fig. 2. Increased survival of motoneurons in PG-treated G93A-SOD1 slice

cultures.Slice cultures prepared from spinal cords of WT and G93A-SOD1 Tg
mice. AoH) Fluorescence photomicrographs of slices stained with anti-SMl32
antibody to identify motoneurons. Slices at DIV 507 were exposed for an
additional 16 days to sham wash (CTL, A, E), 100 nM PG (B, F), PG plus 1
mM 3MA (C, G), or 3MA alone (D, H).I) Bars represent the number of
motoneurons in each group in the above experiments. Compared with the
control group, the number of motoneurons was significantly greater in the PG-
treated group of ALS Tg mice. The autophagy inhibitor 3MA abrogated PG-
induced increases in motoneuron survival of Tg slices (means ± SEM, #P <
0.005, tt#P < 0.001 ). In non-TG slices, although a suggestion of increased
survival was seen in PG-treated culture, no significant difference was noted.
Scale bar, 200 µm.
Figure options

Fig. 3. Delayed disease progression in and increased survival of PG-treated

ALS Tg mice.G93A-SOD1 Tg mice were given intraperitoneal injections of PG
(2, 4, or 8 mg/kg/day) or vehicle from 10 weeks of age until death. A) PG-
treated mice remained on a rota-rod apparatus for longer than vehicle-treated
mice (means ± SEM, *P < 0.05, **P < 0.01 ). B) Lifespan was significantly
longer in mice treated with 4 mg/kg PG (n = 15) than in vehicle-treated mice
(n = 12) (P < 0.05, ManteloCox log-rank test).C) Lumbar spinal cords from
vehicle- or PG (4 mg/kg)-treated mice were stained with cresyl violet.
Motoneurons are large and stain densely with cresyl violet (arrows).D) Bars
denote the number of motoneurons at 14 and 17 weeks of age (means±
=
SEM, *P < 0.05; n 405). At 17 weeks of age, the number of motoneurons
was significantly greater in the PG-treated group than in the control group.
Scale bar, 200 µm.
Figure options

Fig. 4. Reduction of hSOD1 accumulation by PG in G93A-SOD1 Tg cultures

and mice.A) lmmunoblots for human SOD1 in samples collected from G93A-
SOD1 Tg astrocytes and slices. Astrocytes or slices were treated for 7 days
or 16 days with sham wash (CTL), 100 nM PG alone, or PG plus 1 mM 3MA.
hSOD1 levels were reduced by PG treatment, an effect that was blocked by
the addition of 3MA. Bars denote fold increases in densitometric values of the
hSOD1 band, normalized to the density of the corresponding 13-actin band
and expressed as means ± SEM (*P < 0.05, **P < 0.01, tt#P < 0.001; n =
6012).B) Samples of lumbar spinal cords of G93A-SOD1 Tg mice prepared
at 15016 weeks of age were processed for hSOD1 immunoblotting. In the PG
(4 mg/kg)-treated group, there was a substantial reduction in hSOD1 levels
compared with vehicle controls. Bars denote fold increases in densitometric
values of the SOD1 band, normalized to the density of the corresponding 13-
actin band and expressed as means± SEM (**P < 0.01; n 304). =
Figure options

Corresponding author at: Department of Neurology, University of Ulsan

College of Medicine, 388-1 Poongnap-Dong, Songpa-Gu, Seoul 138-736,
Republic of Korea. Fax: + 82 2 483 5446.
1
J.K. and T.Y.K contributed equally to the manuscript.
Copyright© 2013 Published by Elsevier Inc.

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So what a coincidence that all of the sudden someone decided to try

progesterone to treat ALS. The scientists claim they were researching
autophagy (self eating during repair) which had mixed results in ALS. I'm sure
it had nothing to do with the publication of my unfinished book " The ALS
Puzzle Solved?" in January of 2013. It is also a coincidence that these
scientists just happened to notice the big clue of changing sex ratios of ALS
at menopause in their conclusion. Oh well they say imitation is the sincerest
form of flattery.

UPDATE 2-

Now this is really cool. Vitamin D3 research was just a detour for me ram
about 25 years of studying aging and aging related diseases and how
hormones are involved.

In the Alzheimer's book I describe how I have come to believe and facts
suggest that aging is driven by changes in your hormones..just like puberty
and menopause.. not a big mental jump right.

It is caused by declines in your "good" antioxidant like hormones like

melatonin, DHEA, testosterone, growth hormone, progesterone etc. AND by a
rise in your "bad" free radical like hormones such as cortisol, FSH, LH, hCG,
DHTetc.

And when do the dramatic changes in these hormones occur? Around age 50
in most people. In fact melatonin drops 90% along with DHEA and the bad
hormones go up sometimes 1,000's of percent!!

I've always thought that melatonin was the #1 anti aging hormone as it
controls all your other hormones. So when I experimented with taking high
dose melatonin (300mg +per night) over a one year period I noticed my hair
grew back nice and thick where it was thin. My skin got real soft like a baby's.
The first four months I slept like a baby 14 hours a dayoand then was able to
get back to about 8 hours a day after the 4 months.

I finally had a hormone test done after a year of melatonin and found as
expected it suppressed my LH and FSH up to 30%, but I also noticed it
dropped my bad form of testosterone called DHT to almost undetectable-this
was the same effect when I earlier took propecia, proscar, and avodart.. all
expensive drugs to shrink your prostate and to grow your hair!

And I noticed that my progesterone level was 2.1 !! Which was 2X the highest
level of the reference range for men who are supposed to be between .1 and
1.0.

That was a prediction I had made in the Alzheimer's book that melatonin
prevents the progression of Alzheimer's by boosting your progesterone levels.
After the test I knew it was true.

So here are some recent findings of mine.

Propecia , Proscar, and Avodart aka as finesteride and dutasteride are

nothing more than slightly altered versions of progesterone which Big Pharma
sells for enormous profits when progesterone would likely be healthier and
way cheaper!

Progesterone alone suppresses FSH and LH (and DHT)D ..so maybe

melatonin doesn't do all that much except to make your body make m ore
progesterone AND IT TURNS OUT THE REAL ANTI AGING HORMONE IS
PROGESTERONE!! Melatonin just calls for its production.

And finally- and this is the bestD D

I've always thought that the "health benefits of coconut oil" like good skin hair
heart health etc And more recently that it cures Alzheimer's disease was all a
bunch of new age baloney.

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And anyway all the doctors and mainstream health industry was telling us all
to stay away from tropical oils like coconut oil since it was a saturated fat and
was thought to cause heart disease.

Imagine my surprise when I looked at the chemical structure of coconut oil

and found this:

And compared it to progesterone:

It turns auto.the exact progesterone molecule sits right inside the coconut oil
and only needs some very easy organic cleaving of the 4 carbon ring chain
attached only by a single oxygen bond .. and the movement of a double bond
or tow which is quite easy

and cleave a little carbon tail on the other side oand you have progesterone!

We now know why it is likely true that coconut oil can be used to treat
Alzheimer's, ifs the same as using progesterone!!!

And if you go to Amazon.com and search for books on coconut oil you will
now know the reason there are so many of them.

Coconut oil works!!!= progesterone!!

So I will now be working with a friend who is an organic chemist to see if there
are any easy ways to cleave coconut oil into progesterone by mixing with
household food items. Or to see if maybe your body turns coconut oil into
progesterone when you digest it.

Anyway that's it..I love it when all the puzzle pieces fit together!!

Thanks again for the support Jeff

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