LSD Lysergic acid diethylamide, LSD, LSD-25, or acid, is a semisynthetic psychedelic drug of the tryptamine family.

Arguably the most regarded of all psychedelics, it is considered mainly as a recreational drug, an entheogen, and a tool in use to supplement various types of exercises for transcendence including in meditation, psychonautics, and illegal psychedelic psychotherapy whether self administered or not. LSDs psychological effects (colloquially called a trip) vary greatly from person to person, depending on factors such as previous experiences, state of mind and environment, as well as dose strength. LSD LSD is one of the strongest hallucinogenic drugs. It can disrupt the normal functioning of your brain, possibly for the short term, or possibly for life.

AKA
Acid, blotter, cubes, microdot, yellow sunshine, blue heaven, Cid

What is it?
LSD (or its full name: lysergic acid diethylamide) is a potent hallucinogen that dramatically alters your thoughts and your perception of reality.37 It was discovered in 1938 in a fungus that grows on rye and other grains. LSD has a high potential for abuse.

The Risks
LSD disrupts how your nerve cells and the neurotransmitter serotonin interact throughout the brain and spinal cord.37 By disturbing the normal functioning of the brain, LSD distorts visual judgment, sensations, moods and feelings. And these changes can quickly become frightening. Some users experience terrifying thoughts, feelings of despair, fear of losing control, fear of insanity or even death.37 When you're completely unable to get a grip on reality, it becomes very easy for an unexpected, fatal accident to happen.

LONG-TERM EFFECTS

Flashbacks are a strange but relatively common experience of LSD use. Suddenly and without warning, a few days or even a year later, the brain can produce feelings and thoughts that replay the effects of being on the drug. In some people, these flashbacks can occur over and over, causing a debilitating condition known as Hallucinogen-Induced Persisting Perceptual Disorder (HPPD).37 Flashbacks or not, LSD users can also experience long-lasting psychoses (a complete loss of contact with reality) or severe depression.

THE BOTTOM LINE

LSD disrupts the normal functioning of the brain, making you see images, hear sounds and feel sensations that seem real but aren't.37 As one of the most important organs of your body, your brain works tirelessly to oversee all of the feelings, actions and operations of your body. When you think about it, LSD seems like a cruel and dangerous hoax to play on your brain. Serotonin receptors located in the cortex and deep brain structures are over stimulated
LSD in the body

half life 110 min in humans 35 micrograms can cause measurable effects never been linked to one human overdose death in rats 400 times the effective dose is lethal absorbed in GI tract metabolized in liver secreted through digestive system as inactive 2-oxy-lysergic acid diethylamide effects begin 30-90 min after ingestion 1% reaches the brain- not selectively taken up by brain tolerance develops rapidly in humans. If taken repeatedely effects disappear in 2 or 3 days, therefore no amount of drug will be effective at this time recovery also rapid, same dose as effective week after week no withdrawal symptoms have been found in laboratory studies most animals will not self-administer LSD, most will work to avoid administration taken episodically

Side Effects

may stimulate sympathetic nervous system few physical side effects pupils dialate increase pulse rate increase blood pressure increase salivation increase body temperature

Drugs are made of chemicals, many similar to the chemicals already in our system. Drugs alter the way nerve cells normally send, receive, and process information. They do this by (1) imitating the brains natural chemical messengers, (2) by over-stimulating the reward circuit of the brain, (3) flooding the brain with excess chemicals, and (4) binding to receptors in the brain.

Certain neural structures, called the reward system, are critically involved mediating the effects of reinforcement. A reward is an appetitive stimulus given to a human or some other animal to alter its behavior. Rewards typically serve as reinforcers. A reinforcer is something that, when presented after a behavior, causes the probability of that behavior's occurrence to increase. Note that just because something is labelled a reward does not necessitate it as a reinforcer. A reward can only be said to be a reinforcer if its delivery has increased the probability of a behavior.[1]

When the cortex has received and processed a sensory stimulus indicating a reward, it sends a signal announcing this reward to a particular part of the midbrainthe ventral tegmental area (VTA) whose activity then increases. The VTA then releases dopamine not only into the nucleus accumbens, but also into the septum, the amygdala, and the prefrontal cortex. The nucleus accumbens then activates the individuals motor functions, while the prefrontal cortex focuses his or her attention.

These regions are connected by what is called the pleasure or reward bundle. In neuroanatomical terms, this bundle is part of the medial forebrain bundle (MFB), whose activation leads to the repetition of the gratifying action to strengthen the associated pathways in the brain. First described by James Olds and Peter Milner in the early 1960s, the MFB is a bundle of axons that originates in the reticular formation, crosses the ventral tegmental area, passes through the lateral hypothalamus, and continues into the nucleus accumbens as well as the amygdala, the septum, and the prefrontal cortex. The MFB is composed of ascending and descending pathways, including most of the pathways that use monoamines as a neurotransmitter. The mesocorticolimbic dopaminergic system is one of its main components. Consequently, the reward circuit and the punishment circuit can be said to supply most of the necessary motivation for most of our behaviours.

WHEN THE REWARD CIRCUIT GETS OVERHEATED

All psychoactive drugs seem to increase the amount of dopamine in the reward circuit, either directly or indirectly. In addition to exerting their effects through molecular mechanisms, these drugs intervene at various points in the brains central reward circuit (see diagram).

These drugs also affect several other areas of the brain. It is through this combination of effects on the reward circuit and on other brain structures that a drug induces the behaviours and subjective sensations that are specific to it.

Because neural communication is so plastic, a new equilibrium will gradually be established that incorporates this input of a psychoactive substance from outside the body. It is this adaptability of the brain that is the source of phenomena such as tolerance, dependency, and withdrawal (see boxes).
LSD shuts down filters in your brain. You get info-overload. Your brain tries to make the best of it. Fits things into shapes it can handle. You see things. Voila.

Magic mushrooms

Psilocybin mushrooms (also called psilocybian mushrooms) are fungi that contain the psychedelic substances psilocybin and psilocin, and occasionally other psychoactive tryptamines. There are multiple colloquial terms for psilocybin mushrooms, the most common being magic mushrooms or shrooms. When psilocybin is ingested, it is broken down to produce psilocin, which is responsible for the hallucinogenic effects. The intoxicating effects of psilocybincontaining mushrooms typically last anywhere from 3 to 7 hours depending on dosage, preparation method and personal metabolism. The experience is typically inwardly oriented, with strong visual and auditory components. Visions and revelations may be experienced, and the effect can range from exhilarating to distressing. There can be also a total absence of effects, even with large doses. Psilocybin (4-phosphoryloxy-N,N-dimethyltryptamine), which is the active
ingredient in psychedelic mushrooms, has been in use for thousands of years by the indigenous peoples of the Americas; in fact, the Aztec called these mushrooms teonanacatl, or flesh of the gods. Mescaline (the psychoactive ingredient in peyote cactus) is another type of hallucinogen that was widely used by the Native Americans living in what are now parts of Southwest America and Mexico; even today the peyote cactus figures prominently in religious rituals celebrated by the Navajo and other Indian tribes. LSD (d-lysergic acid diethylamide), another type of hallucinogen, was more recently discovered by Dr. Albert Hofmann in 1943 and then popularized by the counterculture movement of the 1960s.

The study of hallucinogens and their mode of action on the brain have been conducted since the late 1800s (1). By the 1960s, studies of hallucinogens and their effects on consciousness had accelerated dramatically (24). Unfortunately, due in part to the antics of drug enthusiasts such as Dr. Timothy Leary, public and scientific interest in and support of hallucinogen research essentially stopped. It was not until the mid to late 1990s, when better study controls could be implemented, that researchers resumed their investigation of hallucinogenic substances and the effects of these agents on the mind and body. Nowadays, researchers and doctors have renewed their interest in psychedelic substances such as psilocybin because these substances have been found to be effective in the treatment of several challenging behavioral and mental issues like repressed memories (5), alcohol, tobacco and narcotic drug addiction (6), headaches (7) and depression as a result of advanced and/or terminal cancer (8, 9). After first prescreening potential study candidates for mental stability and no prior hallucinogen use, these researchers and doctors administer controlled amounts of the hallucinogenic drug psilocybin. Study participant reactions are then meticulously logged and charted. In many cases, functional MRI (fMRI) and/or PET scans are administered during the psychedelic experience in order to evaluate brain activity. Some rather intriguing results have already been collected from these studies, including the following 10 surprise findings:

1. Lack of addiction. Narcotic drugs like cocaine prevent the reuptake of pleasure/learning-associated neurotransmitters such as dopamine, eventually leading to addiction due to the strong reward feedback loop that narcotics create. Alternately, the hallucinogen psilocybin acts as an agonist (activator) of the 5-hydroxytryptamine (5-HT) receptors 5HT1A, 5-HT2A and 5-HT2C, much like the natural 5-HT receptor agonist serotonin. Serotonin, unlike

dopamine, is associated more with general well-being and memory and less so with short-term pleasure, a key difference that is thought to remove it from the addiction pathway. 2. Anxiety reduction. Dr. Stephen Ross has studied psilocybin-assisted psychotherapy as a treatment method for patients who are suffering from feelings of anxiety and depression as a result of being diagnosed with advanced/terminal cancer. The findings of the NYU Psilocybin Cancer Project, of which he is the principal investigator, indicate that patients with advanced/terminal cancer benefit from the administration of psilocybin in terms of their spiritual and mental well-being and reduced levels of anxiety, depression and pain. This is not surprising in light of the discoveries made by Dr. Franz X. Vollenweider, who has found that psilocybin reduces prefrontal cortex control over the amygdala, the so-called fear center of the brain. Incidentally, Dr. Vollenweider has also published reports on the reduction of depression in patients who regularly partake of psilocybin. 3. Quantum behavioral change. Societys overall perception of individuals who partake in psychedelic substances is that they are anti-social and anti-establishment misfits, burnouts and dope heads. However, research that is being conducted by Dr. Roland Griffiths at the Johns Hopkins University indicates that taking psilocybin can produce positive changes in the personality, attitudes and behavior of participants (10). Individuals who have taken psilocybin report having renewed or stronger feelings of societal responsibility, empathy towards others and a fundamental understanding of the interconnection between all living things. The perceptual and cognitive changes incurred during the psilocybin encounter are partly to credit for these quantum behavioral changes.

4. Mystical-type experience. The Institute of Noetic Sciences, of which Dr. Roland Griffiths is a part, is actively studying the mystical experiences that are

encountered by study participants who take psilocybin or other hallucinogens. In many cases, neuronal responses and brain wave patterns of individuals who are administered psilocybin are akin to those measured during states of fasting, prayer, meditation or other religious/spiritual ecstasy (11). There is also a planned collaborative study between Drs. Roland Griffiths and Richard Davidson (University of Wisconsin-Madison) to find out if hallucinogens can aid individuals who are regular and experienced practitioners of meditation in terms of their overall focus, session length, and spiritual progress. The participants of this study will be screened at Johns Hopkins University and then tested via fMRI at the University of Wisconsin-Madison.

PcP

PCP (Phencyclidine) is a dissociative drug formerly used as an anesthetic agent, exhibiting hallucinogenic and neurotoxic effects. It is commonly known as Angel Dust, but is also known as Wet, Sherm, Sherman Hemsley, Rocket Fuel, Ashy Larry, Shermans Tank, Wack, Halk Hogan, Ozone, HannaH, Hog, Manitoba Shlimbo, and Embalming Fluid, among other names. Although the primary psychoactive effects of the drug only last hours, total elimination from the body is prolonged, typically extending over weeks. PCP is consumed in a recreational manner by drug users, mainly in the United States, where the demand is met by illegal production. It comes in both powder and liquid forms (PCP base dissolved most often in ether), but typically it is sprayed onto leafy material such as marijuana, mint, oregano, parsley or Ginger Leaves, and smoked. PCP has potent effects on the nervous system altering perceptual functions (hallucinations, delusional ideas, delirium or confused thinking), motor functions (unsteady gait, loss of coordination, and disrupted eye movement or nystagmus), and autonomic nervous system regulation (rapid heart rate, altered temperature regulation). The drug has been known to alter mood states in an unpredictable fashion causing some individuals to become detached and others to become animated. When I was taking the drug, I used very small amounts. The effect was incredibly pleasant and social, so much so that me and my friends all used it instead of booze for almost a year. I couldnt dance for shit on the stuff (Id get stumbly and actually fell on my ass on the dancefloor once) but the physical sensations and mental pictures were really fun. It is quite different from any psychedelic visuals or even Ketamine visualsmore like rolling through old film footage. To be honest, I liked it more than my experiences on Ketamine. PCP can make one nearly impervious to pain at high doses. Because of this, PCP can make things seem like a good idea that otherwise wouldnt (leading to the stories of people leaping out of windows, etc.) I experienced very confusing physical reality when really high on it, like being unable to discern the difference between walking up stairs and down them, or standing still and walking. This could lead to very unusual behaviour.

25I

25I-NBOMe acts as a highly potent full agonist for the human 5-HT2A receptor,[5][7] with a Ki of 0.044 nM, making it some sixteen times the potency of 2C-I itself, and a radiolabelled form of 25I-NBOMe can be used for mapping the distribution of 5-HT2A receptors in the brain.[6] In vitro tests showed this compound acted as an agonist but animal studies have not been reported. While the N-benzyl derivatives of 2C-I were significantly increased in potency compared to 2C-I, the N-benzyl derivatives of DOI were inactive.[8] Ki values of the following targets were greater than 500 nM: 5-HT1A, D3, H2, 5-HT1D, 1A adrenergic, opioid, serotonin uptake transporter, 5-HT5A, 5-HT1B, D2, 5-HT7, D1, 5-HT3, 5HT1E, D5, muscarinic M1-M5, H3, and the dopamine uptake transporter.[6]
25I-NBOMe is usually synthesised from 2C-I and 2-methoxybenzaldehyde, in a reductive alkylation. It can be done stepwise by first making the imine and then reducing the formed imine with sodium borohydride, or by direct reaction with sodium triacetoxyborohydride.[1]

25I is a drug that we've become aware of in recent months as an increasing number of patients in our rehab are reporting that they have experimented with it. We're still gathering information on 25i and we are sorting out the confusion between 25i and some other hallucinogenic drugs that have been hitting the market but here is what we know for sure:

it is a hallucinogenic drug that is usually snorted as a powder, but has the risk for overdose as several teens were rushed to the hospital in Richmond Virgina earlierthis year

Here is what we're trying to confirm:

25i appears to be "legal" as it is a new drug (but may be no safer than other "legal" highs like bath salts)

25i may be also referred to as:

Dime 25C NBOME DOB

(but some of those names might be for different although similar hallucinogenic drugs) More Information on The New Drug 25i

25i is a derivative of the phenethylamine hallucinogen 2C-I, discovered at the Free University of Berlin in 2003 by Ralf Heim. We've been told anecdotally that 25i is not active orally and must be smoked or snorted. There's some conflicting information out there with regard to this as there are many pictures on the web of 25i that look like LSD tabs (which may be an inaccurate labeling of LSD blotter paper, but

also may indicate that 25i can be taken orally). The research we've done appears to show it as a powder that is darkly colored- possibly distributed in capsules. The picture to the right of 25i is from Erowid,org, which is a pretty reliable source of information about new drugs. 25i has been in the news sporadically this year and throughout the world as well. A man got in trouble with the authorities in New Zealand for selling a drug which he marketed as Dime. That drug contained 25C-NBOMe, which is an analog (a modified version) of a Class Ad Drug called "DOB" According to the wikipedia article about 25i, the result

Strong open-eye/closed-eye hallucinations Feelings of profoundness similar to other psychedelics Increased sexual desire Feelings of euphoria Intensified emotions Vasoconstriction Nausea

DMT

N,N-Dimethyltryptamine (DMT or N,N-DMT) is a psychedelic compound of the tryptamine family. Its presence is widespread throughout the plant kingdom.[3][4] DMT occurs in trace amounts in mammals, including humans, where it putatively functions as a trace amine neurotransmitter/neuromodulator.[5] It is originally derived from the essential amino acid tryptophan and ultimately produced by the enzyme INMT during normal metabolism.[6] The significance of its widespread natural presence remains undetermined. Structurally, DMT is analogous to the neurotransmitter serotonin (5-HT), the hormone melatonin, and other psychedelic tryptamines, such as 5-MeO-DMT, bufotenin, psilocin and psilocybin. When ingested, DMT acts as a psychedelic drug.[7] Depending on the dose and method of administration, its subjective effects can range from short-lived milder psychedelic states to powerful immersive experiences; these are often described as a total loss of connection to conventional reality with the encounter of ineffable spiritual/alien realms.[8] Indigenous Amazonian Amerindian cultures consume DMT as the primary psychoactive in ayahuasca, a shamanistic brew used for divinatory and healing purposes. Pharmacologically, ayahuasca combines DMT with an MAOI, an enzyme inhibitor that allows DMT to be orally active.[9] Dimethyltryptamine is an indole alkaloid derived from the shikimate pathway. Its biosynthesis is relatively simple and summarized in the picture to the left. In plants, the parent amino acid Ltryptophan is produced endogenously where in animals L-tryptophan is an essential amino acid coming from diet. No matter the source of L-tryptophan, the biosynthesis begins with its decarboxylation by an aromatic amino acid decarboxylase (AADC) enzyme (step 1). The resulting decarboxylated tryptophan analog is tryptamine. Tryptamine then undergoes a transmethylation (step 2): the enzyme indolethylamine-N-methyltransferase (INMT) catalyzes

the transfer of a methyl group from cofactor S-adenosyl-methionine (SAM), via nucleophilic attack, to tryptamine. This reaction transforms SAM into S-adenosylhomocysteine (SAH), and gives the intermediate product N-methyltryptamine (NMT).[22][23] NMT is in turn transmethylated by the same process (step 3) to form the end product N,N-dimethyltryptamine. Tryptamine transmethylation is regulated by two products of the reaction: SAH,[6][24][25] and DMT[6][25] were shown ex vivo to be among the most potent inhibitors of rabbit INMT activity. This transmethylation mechanism has been repeatedly and consistently proven by radiolabeling of SAM methyl group with carbon-14 (14C-CH3)SAM).[

The brain stem controls basic functions critical to life, such as heart rate, breathing, and sleeping.