Tryptophan

Serotonin Serotonin /ˌsɛrəˈtoʊnɨn/ or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Biochemically derived from tryptophan, serotonin is primarily found in the gastrointestinal tract (GI tract), platelets, and the central nervous system (CNS) of animals, including humans. It is popularly thought to be a contributor to feelings of well-being and happiness.[6] Serotonin secreted from the enterochromaffin cells eventually finds its way out of tissues into the blood. There, it is actively taken up by blood platelets, which store it. When the platelets bind to a clot, they release serotonin, where it serves as a vasoconstrictor and helps to regulate hemostasis and blood clotting. In addition to animals, serotonin is found in fungi and plants.[10] Serotonin's presence in insect venoms and plant spines serves to cause pain, which is a side-effect of serotonin injection. Functions[edit] Receptors[edit] Gauge of food availability (appetite)[edit] Effects of food content[edit] [edit]

Melatonin Melatonin The hormone can be used as a sleep aid and in the treatment of sleep disorders. It can be taken orally as capsules, tablets, or liquid. It is also available in a form to be used sublingually, and there are transdermal patches. There have been few clinical trials, particularly long-term ones, in the use of melatonin in humans. Discovery[edit] Biosynthesis[edit] Melatonin biosynthesis involves four enzymatic steps from the essential dietary amino acid tryptophan, which follows a serotonin pathway. In bacteria, protists, fungi, and plants melatonin is synthesized indirectly with tryptophan as an intermediate product of the shikimic acid pathway. Regulation[edit] In vertebrates, melatonin secretion is regulated by norepinephrine. It is principally blue light, around 460 to 480 nm, that suppresses melatonin,[24] proportional to the light intensity and length of exposure. Animals[edit] Plants[edit] Functions[edit] Circadian rhythm[edit] Antioxidant[edit] Immune system[edit] Medical uses[edit]

Lysergic acid diethylamide Lysergic acid diethylamide, abbreviated LSD or LSD-25, also known as lysergide (INN) and colloquially as acid, is a semisynthetic psychedelic drug of the ergoline family, well known for its psychological effects which can include altered thinking processes, closed- and open-eye visuals, synesthesia, an altered sense of time and spiritual experiences, as well as for its key role in 1960s counterculture. It is used mainly as an entheogen, recreational drug, and as an agent in psychedelic therapy. LSD is non-addictive, is not known to cause brain damage, and has extremely low toxicity relative to dose.[3] However, acute adverse psychiatric reactions such as anxiety, paranoia, and delusions are possible.[4] LSD was first synthesized by Albert Hofmann in 1938 from ergotamine, a chemical derived by Arthur Stoll from ergot, a grain fungus that typically grows on rye. Effects Physical LSD can cause pupil dilation, reduced or increased appetite, and wakefulness. Psychological Sensory Potential uses

Psilocybin Psilocybin[nb 1] (/ˌsɪləˈsaɪbɪn/ SIL-ə-SY-bin) is a naturally occurring psychedelic compound produced by more than 200 species of mushrooms, collectively known as psilocybin mushrooms. The most potent are members of the genus Psilocybe, such as P. azurescens, P. semilanceata, and P. cyanescens, but psilocybin has also been isolated from about a dozen other genera. As a prodrug, psilocybin is quickly converted by the body to psilocin, which has mind-altering effects similar (in some aspects) to those of LSD, mescaline, and DMT. In general, the effects include euphoria, visual and mental hallucinations, changes in perception, a distorted sense of time, and spiritual experiences, and can include possible adverse reactions such as nausea and panic attacks. History[edit] Early[edit] Modern[edit] Albert Hofmann (shown here in 1993) purified psilocybin and psilocin from Psilocybe mexicana in the late 1950s. Occurrence[edit]

Tetrahydrocannabinol Tetrahydrocannabinol (THC), or more precisely its main isomer (−)-trans-Δ9-tetrahydrocannabinol ( (6aR,10aR)-delta-9-tetrahydrocannabinol), is the principal psychoactive constituent (or cannabinoid) of the cannabis plant. First isolated in 1964, in its pure form, by Israeli scientists Raphael Mechoulam and Yechiel Gaoni at the Weizmann Institute of Science,[8][9][10] it is a glassy solid when cold, and becomes viscous and sticky if warmed. A pharmaceutical formulation of (−)-trans-Δ9-tetrahydrocannabinol, known by its INN dronabinol, is available by prescription in the U.S. and Canada under the brand name Marinol. An aromatic terpenoid, THC has a very low solubility in water, but good solubility in most organic solvents, specifically lipids and alcohols.[6] Tetrahydrocannabinol with double bond isomers and their stereoisomers is one of only three cannabinoids scheduled by Convention on Psychotropic Substances (the other two are dimethylheptylpyran and parahexyl). Pharmacology[edit]

Dimethyltryptamine History[edit] Another historical milestone is the discovery of DMT in plants frequently used by Amazonian natives as additive to the vine Banisteriopsis caapi to make ayahuasca decoctions. Biosynthesis[edit] Biosynthetic pathway for N,N-dimethyltryptamine This transmethylation mechanism has been repeatedly and consistently proven by radiolabeling of SAM methyl group with carbon-14 (14C-CH3)SAM).[22][20][24][25][26] Evidence in mammals[edit] In 2013, researchers first reported DMT in the pineal gland microdialysate of rodents.[28] A study published in 2014 reported the biosynthesis of N,N-dimethyltryptamine (DMT) in the human melanoma cell line SK-Mel-147 including details on its metabolism by peroxidases. [29] In a 2014 paper, a group first demonstrated the immunomodulatory potential of DMT and 5-MeO-DMT through the Sigma-1_receptor of human immune cells. INMT[edit] Endogenous DMT[edit] The first claimed detection of mammalian endogenous DMT was published in June 1965: German researchers F.

Harmine Harmine is a fluorescent harmala alkaloid belonging to the beta-carboline family of compounds. It occurs in a number of different plants, most notably the Middle Eastern plant harmal or Syrian rue (Peganum harmala) and the South American vine Banisteriopsis caapi (also known as "yage" or "ayahuasca"). Harmine reversibly inhibits monoamine oxidase A (MAO-A), an enzyme which breaks down monoamines, making it a RIMA. Harmine selectively binds to MAO-A but does not inhibit the variant MAO-B.[5] Uses[edit] Monoamines include neurotransmitters (serotonin, dopamine), hormones (melatonin, epinephrine, norepinephrine) and psychedelic drugs (psilocybin, DMT and mescaline). P. harmala and B. caapi are both traditionally used for their psychoactive effects. Harmine is also a useful fluorescent pH indicator. With the radioisotope carbon-11 harmine is used in positron emission tomography neuroimaging to examine its binding to MAO-A.[6] Anticancer[edit] Adverse effects[edit] Overdosage[edit] See also[edit]

Harmaline Harmaline is a fluorescent psychoactive indole alkaloid from the group of harmala alkaloids and beta-carbolines. It is the reduced hydrogenated form of harmine. Occurrence in nature[edit] Various plants contain harmaline including Peganum harmala (Syrian Rue) as well as the hallucinogenic drink ayahuasca, which is traditionally brewed using Banisteriopsis caapi. Effects[edit] Harmaline is a central nervous system stimulant and a "reversible inhibitor of MAO-A (RIMA)".[2] This means that the risk of a hypertensive crisis, a dangerous high blood pressure crisis from eating tyramine-rich foods such as cheese, is likely lower with harmaline than with irreversible MAOIs such as phenelzine. United States Patent Number 5591738 describes a method for treating various chemical dependencies via the administration of harmaline and or other beta-carbolines.[6] In a study Harmaline has also been found to induce "vasorelaxant effects" in "isolated rat aorta See also[edit] References[edit]

Preferential Biosynthesis and Retention of Endogenous DMT (a progressive thread) - DMT Discussion I have induced endogenous DMT-like experiences on many occasions. I make ZERO claims as to whether it is dimethyltryptamine itself mediating the experience but then I also argue that you probably made this thread to reach the experience itself 1.) Actual psychedelic experience with exact modality of smoked DMT, indistinguishable from the genuine article Technique: Iboga root bark dosed progressively over a few days, 5g total IIRC. Then wait a few weeks for levels of iboga & metabolites to go down enough to feel "normal". During this whole phase, holotropic breathwork (i.e. sustained deep fast pace hyperventilation) is practiced all day every day as often as possible. Result: One day, I lay down in bed while doing the breathwork. 2.) Technique: 3 months of fasting and continual meditation, meditating 24/7 whether asleep or awake. At least 4L water intake per day, probably 8L on a good day or more. Syrian rue + caapi in tea every day, continually. Result: Too long to write about.