LSD

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Summary sheet: LSD
LSD
LSD.svg
Chemical Nomenclature
Common names LSD, LSD-25, Lucy, L, Acid, Tabs, Blotter
Substitutive name d-Lysergic acid diethylamide
Systematic name (6aR,9R)-N,N-Diethyl-7-methyl-4,6,6a,7,8,9-hexahydroindolo-[4,3-fg]quinoline-9-carboxamide
Class Membership
Psychoactive class Psychedelic
Chemical class Lysergamide
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.





Sublingual
Dosage
Bioavailability 71% - 71%[1]
Threshold 15 µg
Light 25 - 75 µg
Common 75 - 150 µg
Strong 150 - 300 µg
Heavy 300 µg +
Duration
Total 8 - 12 hours
Onset 15 - 30 minutes
Come up 45 - 90 minutes
Peak 3 - 5 hours
Offset 3 - 5 hours
After effects 12 - 48 hours







DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Lysergic acid diethylamide (also known as Lysergide, LSD-25, LSD, L, lucy, and acid) is a semisynthetic psychedelic substance of the lysergamide class.[2] LSD is one of the most potent, well-known and widely used psychedelic substances. The pharmacology of LSD is complex, but it acts primarily by stimulating serotonin receptors in the brain.[citation needed]

The psychoactive effects of LSD were first discovered in 1943 by the Swiss chemist Albert Hofmann. In the 1950s, LSD was marketed under the trade name Delysid and used in psychotherapy and for experimental purposes.[3] LSD garnered widespread interest from clinicians and researchers and was secretly investigated by the U.S. Central Intelligence Agency (CIA) as a potential mind control agent.[4] During the mid-1960s, use of LSD spread widely in the emerging counterculture, leading to its prohibition in 1971.[5][6]

Following a 40 year hiatus, research into LSD's potential therapeutic uses has been revived. LSD is currently under investigation for the treatment of a number of ailments including alcoholism, addiction, cluster headache, and anxiety associated with terminal illness.[3] LSD remains in widespread illicit use for recreational and spiritual purposes. The lifetime prevalence of LSD use among adults is in the range of 6-8%.[3]

Characteristic effects of LSD include geometric visual hallucinations, time distortion, enhanced introspection, and ego loss. LSD is commonly described by users to evoke entheogenic and mystical-type experiences that can facilitate self-reflection and personal growth. It is considered by some to be the first modern entheogen, a category which had been limited to traditional plant preparations or extracts.[7]

Unlike other highly prohibited substances, LSD is not considered to be addictive or physiologically toxic.[8][9] Nevertheless, adverse psychological reactions such as severe anxiety, paranoia and psychosis are always possible, particularly among those predisposed to mental illness.[10] It is highly advised to use harm reduction practices if using this substance.

History and culture

LSD was first synthesized on November 16, 1938, by the Swiss chemist Albert Hofmann at the Sandoz Laboratories in Basel, Switzerland. It was part of a large research program searching for medically useful derivatives of ergot, a fungus that grows on rye. The abbreviated form of LSD comes from its early research code name LSD-25 which is an abbreviation for the German spelling "Lysergsäure-diethylamid" followed by a sequential number.[11] However, its psychoactive properties were not discovered until five years later when Hofmann claimed to accidentally ingest an unknown quantity of the chemical before proceeding to ride his bike home.[12]

The first intentional ingestion of LSD occurred on April 19, 1943.[13] Hofmann ingested 250 micrograms (µg) of LSD, believing it would be a threshold dose based on the doses of other ergot alkaloids. Hofmann found the effects to be much stronger than he anticipated and was impressed by its profound mind-altering effects. In 1947, Sandoz introduced LSD to the medical community under the name Delysid as an experimental tool to induce temporary psychotic-like states in normals (“model-psychosis”) and later to enhance psychotherapeutic treatments (“psycholytic” or “psychedelic” therapy)[14] LSD had a major impact in the areas of scientific research and psychiatry. Within 15 years of its release, research on LSD and other hallucinogens generated over 1,000 scientific papers and was prescribed to over 40,000 patients.[15]

Beginning in the 1950s, the U.S. Central Intelligence Agency began a research program code named MK-ULTRA that would conduct clandestine research investigating LSD for applications in mind control and chemical warfare. Experiments included administering LSD to CIA employees, military personnel, doctors, prostitutes, mentally ill patients, and members of the general public without their knowledge or consent, which resulted in at least one death.[16]

In 1963, the Sandoz patents for LSD expired. Several prominent intellectuals, including Aldous Huxley, Timothy Leary, and Al Hubbard, began to advocate for the consumption of LSD. LSD became central to the counterculture of the 1960s. Along with other hallucinogens, it was advocated by new proponents of consciousness expansion such as Leary, Huxley, Alan Watts and Arthur Koestler[17][18] and according to L. R. Veysey, they profoundly influenced the thinking of the new generation of youth.[19]

On October 24, 1968, possession of LSD was made illegal in the United States.[20] The last FDA approved study of LSD in patients ended in 1980, while a study in healthy volunteers was made in the late 1980s. Legally approved and regulated psychiatric use of LSD continued in Switzerland until 1993.[21]

Chemistry

Binding affinities of LSD for various receptors. The lower the dissociation constant (Ki), the more strongly LSD binds to that receptor (i.e. with higher affinity). The horizontal line represents an approximate value for human plasma concentrations of LSD, and hence, receptor affinities that are above the line are unlikely to be involved in LSD's effect. Data averaged from data from the Ki Database.

LSD, or d-lysergic acid diethylamide, is a semisynthetic substance of the lysergamide family. LSD's chemical structure consists of a bicyclic hexahydroindole ring fused to a bicyclic quinoline group (lysergic acid). At carbon 8 of the quinoline an N, generally N-diethyl carboxamide is bound, LSD is additionally substituted at carbon 6 with a methyl group.

LSD is a chiral compound with two stereocenters at R5 and R8. LSD, also called (+)-D-LSD, has an absolute configuration of (5R, 8R). The three other stereoisomers of LSD do not have psychoactive properties.[22]

In its pure form, LSD occurs as a colorless, odorless crystal.[citation needed] LSD is sensitive to oxygen, ultraviolet light, and chlorine (especially in solution).[23] Its potency may last for years if it is stored away from light and moisture at cold temperatures around 0°C or below, but will slowly degrade at normal room temperature (25°C).[citation needed]

Pharmacology

Further information: Serotonergic psychedelic
This image shows how, with eyes-closed, much more of the brain contributes to the visual experience under LSD (right image) than under placebo (left image). The magnitude of this effect correlates with participants’ reports of complex, dreamlike visions.[24]

LSD acts as a partial agonist for the 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C and 5-HT6 receptors.[25][26] LSD binds to most serotonin receptor subtypes except for 5-HT3 and 5-HT4. 5-HT5B receptors, which have not been found in humans, also have a high affinity for LSD.[27] The psychedelic effects LSD are thought to be mediated by agonist action 5-HT2A receptors.[28]

LSD also possesses efficacy at all dopamine and all norepinephrine receptors. Most serotonergic psychedelics are not significantly dopaminergic, so LSD is unique in this respect. LSD's agonism of D2 receptors has been shown to contribute to its psychoactive effects.[29][30]

Subjective effects

The subjective effects of LSD can be broken down into several components which progressively intensify proportional to dosage in a nonlinear manner. In comparison to other psychedelics such as psilocybin mushrooms, LSA and ayahuasca, LSD is significantly more stimulating and fast-paced in both its physical and cognitive effects and produces a large number of effects that can potentially be attributed to its binding activity at a wide range of CNS receptors other than serotonin, such as dopamine and norepinephrine.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects
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    • Stimulation - In terms of its effects on physical energy levels, LSD is usually regarded as being very energetic and stimulating without being forced. For example, when taken in any environment it will usually encourage physical activities such as running, walking, climbing or dancing. In comparison, other more commonly used psychedelics such as psilocybin are generally sedating and sedentary.
    • Spontaneous bodily sensations - The "body high" of LSD can be described as prominent in comparison to its accompanying visual and cognitive effects. It behaves as a euphoric, fast-moving, sharp and location specific or generalized tingling sensation. For some, it is manifested spontaneously at different, unpredictable points throughout the trip, but for most, it maintains a steady presence that rises with the onset and hits its limit once the peak has been reached. At moderate to high doses of LSD, many users report that if this sensation hits its highest level it can become so pleasurable so as to immobilize the user.
      • Physical euphoria - This effect is not as reliably induceable as it is with substances like stimulants or entactogens, and can just as easily manifest as physical discomfort without any apparent reason.
      • Perception of bodily lightness - The stimulation and energy LSD produces can often lead one to feel as if they are moving weightlessly.
    • Tactile enhancement - Feelings of enhanced tactile sensations are consistently present at moderate levels throughout most LSD trips. If level 8A geometry is reached, an intense sensation of suddenly becoming aware of and being able to feel every single nerve ending across a person's entire body all at once is consistently present.
    • Changes in felt bodily form - This effect is often accompanied by a sense of warmth or unity and usually occurs during and up to the peak of the experience or directly afterward. Users can feel as if they are physically part of or conjoined with other objects. This is usually reported as feeling comfortable in its sensations and even peaceful, compared to other substances that induce this effect like salvia.
    • Temperature regulation suppression[31]
    • Increased bodily temperature[32] - Potentially dangerous states of overheating have been reported to occur in certain conditions, particularly with higher doses. Users are advised to monitor their core temperature and be cautious if taking LSD in hot or overcrowded outdoor environments.
    • Nausea - Mild nausea is occasionally reported when consumed in moderate to high dosages and either passes instantly soon after the user has vomited or gradually fades by itself as the peak sets in.
    • Bodily control enhancement
    • Stamina enhancement - This is generally mild in comparison to traditional stimulants.
    • Appetite suppression
    • Dehydration
    • Difficulty urinating
    • Increased blood pressure[31]
    • Increased heart rate[31]
    • Increased perspiration
    • Muscle contractions
    • Muscle spasms
    • Excessive yawning - This effect is significantly less pronounced than it is with psilocybin and its related compounds, the four-position substituted tryptamines.
    • Pupil dilation[31]
    • Increased salivation
    • Seizure[citation needed] - This is a rarely observed effect but is thought to occur in those who are predisposed to them, especially while in physically taxing conditions such as being dehydrated, undernourished, overheated, or generally fatigued.[citation needed]

Visual effects
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Cognitive effects
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Auditory effects
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Multi-sensory effects
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    • Synaesthesia - In its fullest manifestation, this is a very rare and non-reproducible effect. Increasing the dosage can increase the likelihood of this occurring, but seems to only be a prominent part of the experience among those who are already predisposed to synaesthetic states.

Transpersonal effects
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Combination effects

  • Alcohol - Alcohol's central depressant effects can be used to reduce some of the anxiety and tension produced by LSD. However, alcohol can cause dehydration, nausea and physical fatigue which can negatively impact the direction of the trip. Users are advised to pace themselves and drink a portion of their usual amount.
  • Benzodiazepines - Benzodiazepines are highly effective at reducing the intensity of LSD's effects through the general suppression of brain activity.
  • Cannabis - Cannabis strongly intensifies the sensory and cognitive effects of LSD. Extreme caution is advised when using this combination as it can significantly increase the chances of a negative psychological reaction like anxiety, confusion and psychosis. Users are advised to start off with only a fraction of their usual cannabis dose and take long breaks between hits to avoid over intake.
  • Dissociatives - LSD enhances the cognitive, visual and general hallucinatory effects of dissociatives. Dissociative-induced holes, spaces, and voids and internal hallucinations become more vivid and intense on LSD. These effects correspond with an increased risk of confusion, delusions, and psychosis.
  • MDMA - LSD and MDMA are highly synergistic and mutually enhance each other's physical, cognitive, and visual effects. The synergy between these substances is unpredictable, and it is advised to start with markedly lower doses than one would take for each individually. There is some evidence that suggests LSD increases the neurotoxicity of MDMA.[34][35][36]

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:


Additional experience reports can be found here:

Forms and mimics

LSD is typically distributed in various forms for oral or sublingual administration. It is one of the few psychedelic substances potent enough to fit onto small squares of "blotter paper,"[37] and has a history of being counterfeited by similarly potent psychedelics that do not have its favorable safety profile.

LSD can be found in a number of forms, with blotter paper being the most common:

  • Blotters are typically small squares pulled off sheets of perforated blotting paper that are dipped into an LSD/alcohol solution which are then either swallowed or chewed, or held sublingually. There should not be a bitter metallic taste which numbs the mouth when chewing the blotters as this likely indicates the presence of a 25x-NBOMe compound.
  • Liquid solutions are often found in vials with a pipette. It is often dropped directly into the mouth or tongue. It may also be dropped onto individual sugar cubes or candy before consumption.[38]
  • Tablets & Microdots are very small tablets which can be chewed or swallowed.
  • Powder can, in theory, be administered orally, sublingually, or via insufflation or injection. However, LSD is rarely encountered or taken in this way in practice due to its incredible potency. It is almost always diluted into a liquid solution or 'laid' onto blotter paper to allow for more accurate and consistent dosing.
  • Gel tabs can be taken orally and are small pieces of gelatin which contain LSD. These are less common now than in the past, but are still occasionally present in some areas of the world.

  • Blotters

  • Liquid solution

  • Microdots

  • Gel tabs

Mimics ("Fake acid")

LSD is unusually potent among psychedelic substances, active at just 15-30 micrograms (µg).[39] It has a long history of being counterfeited by a few other psychedelics potent enough to be laid onto blotter paper (colloquially known as "fake acid" or "bunk acid"). This may be attributed to the major differences in cost and ease of synthesis as well as the general inability of inexperienced users to tell the difference.

While pure LSD is theoretically almost completely tasteless,[citation needed] the blotter paper it is laid on can impart a mildly bitter taste if it contains any ink. Mimics are often described as having a marked "metallic", "numbing", "chemical-like" or "extremely bitter or sour" taste. It is advised to immediately spit out any blotters of acid if they are found to have a strong, persisting taste. However, the taste test alone is not enough to maximize user safety. One should always test each tab of purported LSD that they plan to take using a reagent test kit. This is necessary as mimics are considerably less predictable and more dangerous than LSD.[citation needed] Common mimics include the 25x-NBOMe/25x-NBOH series and the DOx series (less common).

25I-NBOMe, which has been attributed to several deaths,[40][41][42][43] may commonly be mistaken for LSD by sellers and users.[44]

Research

Alcoholism

Some studies in the 1960s that used LSD to treat alcoholism reported reduced levels of alcohol misuse in almost 60% of those treated, an effect which lasted six months but disappeared after a year.[33][45][46][47][48] However, a 2012 meta-analysis of six randomized controlled trials found evidence that a single dose of LSD in conjunction with various alcoholism treatment programs was associated with a decrease in alcohol abuse, lasting for several months.[33]

Trauma-related pain

LSD was studied in the 1960s by Eric Kast as an analgesic for acute and chronic pain caused by cancer or other major trauma.[49] Even at low (i.e. sub-psychedelic) dosages, it was found to be at least as effective as traditional opiates, while being much longer lasting in pain reduction (lasting as long as a week after peak effects had subsided). Kast attributed this effect to a decrease in anxiety; that is to say that patients were not experiencing less pain, but rather were less distressed by the pain they experienced. This reported effect is being tested using a similar psychedelic substance, in an ongoing (as of 2006) study of the effects of psilocin on anxiety in terminal cancer patients.[citation needed]

Cluster headaches

LSD has been used as a treatment for cluster headaches, an uncommon but extremely painful disorder. Although the phenomenon has not been formally investigated, case reports indicate that LSD and psilocin can reduce cluster pain and also interrupt the cluster-headache cycle, preventing future headaches from occurring. Currently existing treatments include various ergolines among other chemicals, so LSD's efficacy in this regard may not be surprising. A dose-response study testing the effectiveness of both LSD and psilocin was planned at McLean Hospital, although the current status of this project is unclear. A 2006 study by McLean researchers interviewed 53 cluster headache sufferers who treated themselves with either LSD or psilocin, finding that a majority of users of either drug reported beneficial effects.[50]

Unlike the use of LSD or MDMA in psychotherapy, this research involves non-psychological effects and often sub-psychedelic dosages.[51][52]

End-of-life anxiety

From 2008 to 2011 there was ongoing research in Switzerland into using LSD to alleviate anxiety for terminally ill cancer patients coping with their impending deaths. Preliminary results of the study are promising, and no negative effects have been reported.[53][54]

Toxicity and harm potential

Further information: Responsible use § Hallucinogens
Radar plot showing relative physical harm, social harm, and dependence of LSD[55]

LSD is physiologically well-tolerated and has an extremely low toxicity relative to dose. There is no evidence for long-lasting effects on the brain or other parts of the human organism. There are no documented deaths attributed to the direct effects of LSD toxicity.[56]

Although classical psychedelics like LSD have not directly caused any deaths, they are capable of impairing the judgment of users. In extreme cases, users may believe that they are invincible or in a dream and may do things they would not normally consider, such as believing they can fly and jumping off of buildings.[57] This is particularly a concern in non-supervised settings or with excessive doses. While an overdose of LSD is incapable of causing direct bodily harm to the user it can still have serious negative consequences in the form of dangerous, erratic behaviors or psychologically traumatic experiences.

Additionally, LSD may trigger symptoms in those who have or are predisposed to mental illness such as bipolar disorder or schizophrenia.[56] Those with a personal or family history of mental illness should not use LSD without the advice of a qualified medical practitioner.

It is strongly recommended to apply harm reduction practices when using this substance.

Overdose

LSD has no known toxic dose. However, higher doses increase the risk of adverse psychological reactions. These reactions include anxiety, delusions, panic attacks and, more rarely, seizures. Medical attention is usually not needed except in the case of severe psychotic episodes or the ingestion of fake acid (such as 25i-NBOMe or DOB). Administration of benzodiazepines or antipsychotics can help to relieve the acute negative cognitive effects of LSD.

Dependence and abuse potential

Like other serotonergic psychedelics, LSD is considered to be non-addictive with a low abuse potential.[56] There are no literature reports of successful attempts to train animals to self-administer LSD — an animal model predictive of abuse liability — indicating that it does not have the necessary pharmacology to either initiate or maintain dependence.[56] There is virtually no withdrawal syndrome when chronic use is stopped.[citation needed]

Tolerance to the effects of LSD forms almost immediately after ingestion. After that, it takes about 7 days for the tolerance to return to baseline (in the absence of further consumption). LSD produces cross-tolerance with all psychedelics, meaning that after the use of LSD all psychedelics will have a reduced effect.

Some anecdotal reports suggest that extremely high doses of LSD can produce a tolerance which can last subsequently longer anywhere from weeks to months. High doses of LSD, along with high tolerances, can produce variations in intensity, duration, and effects.

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The following lists some known dangerous combinations, but may not include all of them. A combination that appears to be safe in low doses can still increase the risk of injury or death. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume.

Legal status

Internationally, the UN 1971 Convention on Psychotropic Substances requires its parties to prohibit LSD. Hence, it is illegal in all parties to the convention, which includes the United States, Australia, New Zealand, and most of Europe. Medical and scientific research with LSD in humans is permitted under the 1971 UN Convention, although has been reported to be difficult to actually carry out in practice.[59]

  • Austria: LSD is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Canada: LSD is a Schedule III drug in Canada.[60]
  • Latvia: LSD is a Schedule I drug in Latvia.[61]
  • United Kingdom: LSD is a Class A drug in the United Kingdom.[62]
  • United States: LSD is a Schedule I drug under the Controlled Substances Act of 1970. This means it is illegal to manufacture, buy, possess, process, or distribute without a license from the Drug Enforcement Administration (DEA).[63]

See also

External links

Literature

  • Nichols, D. E. (2016). Psychedelics. Pharmacological Reviews, 68(2), 264-355. http://dx.doi.org/10.1124/pr.115.011478
  • Passie, T., Halpern, J. H., Stichtenoth, D. O., Emrich, H. M., & Hintzen, A. (2008). The Pharmacology of Lysergic Acid Diethylamide: A Review, 14, 295–314. https://doi.org/10.1111/j.1755-5949.2008.00059.x
  • Carhart-Harris, R. L., Muthukumaraswamy, S., Roseman, L., Kaelen, M., Droog, W., Murphy, K., … Nutt, D. J. (2016). Neural correlates of the LSD experience revealed by multimodal neuroimaging. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1518377113
  • Schmid, Y., Enzler, F., Gasser, P., Grouzmann, E., Preller, K.H., Vollenweider, F.X., Brenneisen, R., Mueller, F., Borgwardt, S.J., & Liechti, M.E. (2015). Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects. Biological psychiatry, 78 8, 544-53. https://doi.org/10.1016/j.biopsych.2014.11.015
  • Carhart-Harris, R.L., Kaelen, M., Bolstridge, M., Williams, T.M., Williams, L.T., Underwood, R., Feilding, A., & Nutt, D.J. (2016). The paradoxical psychological effects of lysergic acid diethylamide (LSD). Psychological medicine, 46 7, 1379-90. https://doi.org/10.1017/S0033291715002901

Further reading

References

  1. ↑ Dolder, P. C., Schmid, Y., Haschke, M., Rentsch, K. M., & Liechti, M. E. (2016). Pharmacokinetics and concentration-effect relationship of oral LSD in humans. International Journal of Neuropsychopharmacology, 19(1), 1–7. https://doi.org/10.1093/ijnp/pyv072
  2. ↑ Nichols, D. E. (2016). Psychedelics, (April), 264–355. https://doi.org/10.1124/pr.115.011478
  3. ↑ 3.0 3.1 3.2 Yasmin Schmid, Florian Enzler, Peter Gasser, Eric Grouzmann, Katrin H. Preller, Franz X. Vollenweider, Rudolf Brenneisen, Felix Müller, Stefan Borgwardt, Matthias E. Liechti, Acute effects of LSD in healthy subjects, Biological Psychiatry, http://dx.doi.org/10.1016/j.biopsych.2014.11.015
  4. ↑ Project MK-ULTRA - The CIA's Program of Research in Behavioral Modification, Washington, DC, Government Printing Office, August 31, 1977. http://publicintelligence.net/ssci-mkultra-1977
  5. ↑ "LSD: cultural revolution and medical advances". Royal Society of Chemistry. Retrieved September 27, 2007.
  6. ↑ UN General Assembly, 1971 Convention on Psychotropic Substances, 9 December 1975, A/RES/3443
  7. ↑ Grof, Stanislav; Joan Halifax Grof (1979). Realms of the Human Unconscious (Observations from LSD Research). London: Souvenir Press (E & A) Ltd. pp. 13–14. ISBN 0-285-64882-9.
  8. ↑ Lüscher, C., & Ungless, M. A. (2006). The Mechanistic Classification of Addictive Drugs, 3(11). https://doi.org/10.1371/journal.pmed.0030437
  9. ↑ Nichols, D. E. (2016). "Psychedelics." Pharmacological Reviews, 68(2), 264-355. https://doi.org/10.1124/pr.115.011478
  10. ↑ Strassman, R. J. (1984). Adverse Reactions to Psychedelic Drugs: A Review of the Literature. The Journal of Nervous and Mental Disease, 172(10), 577-595. PMID: 6384428
  11. ↑ Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  12. ↑ Nichols, David. "Hypothesis on Albert Hofmann's Famous 1943 'Bicycle Day'" Adapted from a presentation given at Mindstates IV. Erowid.org/general/conferences/conference_mindstates4_nichols.shtml. May 24, 2002.
  13. ↑ Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  14. ↑ Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  15. ↑ Henderson and Glass, “Introduction,” p. 3; Goodman and Gilman, p. 554.8 Joseph L. Zentner, “The Recreational Use of LSD-25 and Drug Prohibition,” Journal of Psychedelic Drugs, Vol. 8 (No. 4), Oct.-Dec. 1976, p. 301.
  16. ↑ Project MK-ULTRA - The CIA's Program of Research in Behavioral Modification, Washington, DC, Government Printing Office, August 31, 1977. http://publicintelligence.net/ssci-mkultra-1977
  17. ↑ "LSD: cultural revolution and medical advances". Royal Society of Chemistry. Retrieved September 27, 2007.
  18. ↑ https://web.archive.org/web/20100201234435/http://pages.cthome.net/tobelman/The_Out-Of-Sight_SMiLE_Site.html |Out-Of-Sight! SMiLE Timeline
  19. ↑ L. R. Veysey, The Communal Experience: Anarchist and Mystical Communities in Twentieth-Century America (Chicago IL, University of Chicago Press, 1978), ISBN 0-226-85458-2, p. 437.
  20. ↑ Erowid F. "U.S. Drug Control Timeline". Erowid Extracts. Jun 2004;6:4-5.
  21. ↑ Gasser, Peter. "Psycholytic Therapy with MDMA and LSD in Switzerland." MAPS Newsletter 5.3 (1994): 3-7
  22. ↑ https://www.erowid.org/library/books_online/tihkal/tihkal26.shtml
  23. ↑ Entry #26 LSD-25 from TiHKAL by Alexander & Ann Shulgin | http://www.erowid.org/library/books_online/tihkal/tihkal26.shtml
  24. ↑ Carhart-Harris, R. L., Muthukumaraswamy, S., Roseman, L., Kaelen, M., Droog, W., Murphy, K., … Nutt, D. J. (2016). Neural correlates of the LSD experience revealed by multimodal neuroimaging. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1518377113
  25. ↑ Aghajanian, G. K., & Bing, O. H. (1964). Persistence of lysergic acid diethylamide in the plasma of human subjects. Clinical Pharmacology & Therapeutics, 5(5), 611-614. PMID: 14209776
  26. ↑ http://www.lycaeum.org/research/researchpdfs/2404.pdf
  27. ↑ Nelson, D. L. (2004). 5-HT5 receptors. Current Drug Targets-CNS & Neurological Disorders, 3(1), 53-58. PMID: 14965244
  28. ↑ Moreno, J. L., Holloway, T., Albizu, L., Sealfon, S. C., & González-Maeso, J. (2011). Metabotropic glutamate mGlu2 receptor is necessary for the pharmacological and behavioral effects induced by hallucinogenic 5-HT2A receptor agonists. Neuroscience Letters, 493(3), 76-79. https://www.doi.org/10.1016/j.neulet.2011.01.046
  29. ↑ Marona-Lewicka, D., Thisted, R. A., & Nichols, D. E. (2005). Distinct temporal phases in the behavioral pharmacology of LSD: dopamine D2 receptor-mediated effects in the rat and implications for psychosis. Psychopharmacology, 180(3), 427-435. https://www.doi.org/10.1007/s00213-005-2183-9
  30. ↑ Hanna J, Manning T. "The End of a Chemistry Era.... Dave Nichols Closes Shop". Erowid Extracts. November 2012;23:2-7.
  31. ↑ 31.0 31.1 31.2 31.3 Schmid, Y., Enzler, F., Gasser, P., Grouzmann, E., Preller, K. H., Vollenweider, F. X., ... & Liechti, M. E. (2015). Acute effects of lysergic acid diethylamide in healthy subjects. Biological Psychiatry, 78(8), 544-553. https://doi.org/10.1016/j.biopsych.2014.11.015.
  32. ↑ Friedman, S. A., & Hirsch, S. E. (1971). Extreme hyperthermia after LSD ingestion. JAMA, 217(11), 1549-1550. https://doi.org/10.1001/jama.1971.03190110067020
  33. ↑ 33.0 33.1 33.2 Krebs, T. S., & Johansen, P. Ø. (2012). Lysergic acid diethylamide (LSD) for alcoholism: meta-analysis of randomized controlled trials. Journal of Psychopharmacology, 26(7), 994-1002. https://doi.org/10.1080/02791072.1998.10399714
  34. ↑ Armstrong, B. D., Paik, E., Chhith, S., Lelievre, V., Waschek, J. A., & Howard, S. G. (2004). Potentiation of (DL)‐3, 4‐methylenedioxymethamphetamine (MDMA)‐induced toxicity by the serotonin 2A receptor partial agonist d‐lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939. Neuroscience Research Communications, 35(2), 83-95. https://doi.org/10.1002/nrc.20023
  35. ↑ Potentiation of MDMA-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists | https://indiana.pure.elsevier.com/en/publications/potentiation-of-34-methylenedioxymethamphetamine-induced-dopamine
  36. ↑ Ecstasy induces apoptosis via 5-HT(2A)-receptor stimulation in cortical neurons. | https://www.ncbi.nlm.nih.gov/pubmed/17572501
  37. ↑ Greiner T, Burch NR, Edelberg R (1958). "Psychopathology and psychophysiology of minimal LSD-25 dosage; a preliminary dosage-response spectrum". AMA Arch Neurol Psychiatry. 79 (2): 208–10. PMID 13497365. https://doi.org/10.1001/archneurpsyc.1958.02340020088016
  38. ↑ Long LSD Prison Terms--It's All in the Packaging | http://articles.latimes.com/1992-07-27/news/mn-4335_1_prison-term
  39. ↑ Greiner T, Burch NR, Edelberg R (1958). "Psychopathology and psychophysiology of minimal LSD-25 dosage; a preliminary dosage-response spectrum". AMA Arch Neurol Psychiatry. 79 (2): 208–10. PMID 13497365. https://doi.org/10.1001/archneurpsyc.1958.02340020088016
  40. ↑ Erowid. "25I-NBOMe (2C-I-NBOMe) Fatalities / Deaths". Drug Website. Erowid. Retrieved February 28, 2016. 
  41. ↑ Hastings, Deborah (May 6, 2013). "New drug N-bomb hits the street, terrifying parents, troubling cops". New York Daily News. Retrieved May 7, 2013. 
  42. ↑ Feehan, Conor (January 21, 2016). "Powerful N-Bomb drug - responsible for spate of deaths internationally - responsible for hospitalisation of six in Cork". Irish Independent. Retrieved January 22, 2016. 
  43. ↑ Iversen, Les (May 29, 2013). "Temporary Class Drug Order Report on 5-6APB and NBOMe compounds" (PDF). Advisory Council on the Misuse of Drugs. Gov.Uk. Retrieved June 16, 2013. 
  44. ↑ Iversen, Les (May 29, 2013). "Temporary Class Drug Order Report on 5-6APB and NBOMe compounds" (PDF). Advisory Council on the Misuse of Drugs. Gov.Uk. p. 14. Retrieved June 16, 2013. 
  45. ↑ Maclean, J.R.; Macdonald, D.C.; Ogden, F.; Wilby, E., "LSD-25 and mescaline as therapeutic adjuvants." In: Abramson, H., Ed., The Use of LSD in Psychotherapy and Alcoholism, Bobbs-Merrill: New York, 1967, pp. 407–426.
  46. ↑ Ditman, K.S.; Bailey, J.J., "Evaluating LSD as a psychotherapeutic agent," pp.74–80.
  47. ↑ Hoffer, A., "A program for the treatment of alcoholism: LSD, malvaria, and nicotinic acid," pp. 353–402.
  48. ↑ Mangini, M. (1998). Treatment of alcoholism using psychedelic drugs: a review of the program of research. Journal of Psychoactive Drugs, 30(4), 381-418. https://doi.org/10.1080/02791072.1998.10399714#.UcGZWPk3vMc
  49. ↑ Kast, E. (1967). Attenuation of anticipation: a therapeutic use of lysergic acid diethylamide. Psychiatric Quarterly, 41(4), 646-657. https://doi.org/10.1177/0269881112439253
  50. ↑ Sewell, R. A., Halpern, J. H., & Pope, H. G. (2006). Response of cluster headache to psilocybin and LSD. Neurology, 66(12), 1920-1922. https://doi.org/10.1212/01.wnl.0000219761.05466.43
  51. ↑ Summarized from "Research into psilocin and LSD as cluster headache treatment" and the Clusterbusters website. Pages accessed 2007-01-31.
  52. ↑ Sewell, R. A., Halpern, J. H., & Pope, H. G. (2006). Response of cluster headache to psilocybin and LSD. Neurology, 66(12), 1920-1922. https://doi.org/10.1212/01.wnl.0000219761.05466.43
  53. ↑ Psychiater Gasser bricht sein Schweigen | http://bazonline.ch/wissen/medizin-und-psychologie/Psychiater-Gasser-bricht-sein-Schweigen/story/25732295
  54. ↑ Landmark Clinical LSD Study Nears Completion | http://santacruz.patch.com/articles/landmark-clinical-lsd-study-nears-completion
  55. ↑ Nutt, D., King, L. A., Saulsbury, W., & Blakemore, C. (2007). Development of a Rational Scale to Assess the Harm of Drugs of Potential Misuse, 1047–1053. http://dx.doi.org/10.1016/S0140-6736(07)60464-4
  56. ↑ 56.0 56.1 56.2 56.3 Nichols, D. E. (2004). Hallucinogens. Pharmacology & therapeutics, 101(2), 131-181. https://doi.org/10.1016/j.pharmthera.2003.11.002
  57. ↑ Nichols, D. E. (2016). Psychedelics, (April), 264–355. https://doi.org/10.1124/pr.115.011478
  58. ↑ Talaie, H., Panahandeh, R., Fayaznouri, M. R., Asadi, Z., & Abdollahi, M. (2009). Dose-independent occurrence of seizure with tramadol. Journal of medical toxicology, 5(2), 63-67. doi:10.1007/BF03161089
  59. ↑ UN General Assembly, 1971 Convention on Psychotropic Substances, 9 December 1975, A/RES/3443.|
  60. ↑ Controlled Drugs and Substances Act of Canada
  61. ↑ Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (I saraksta 2.2.1.punkts) | http://likumi.lv/doc.php?id=121086
  62. ↑ Misuse of Drugs Act 1971 (Legislation.gov.uk) |http://www.legislation.gov.uk/ukpga/1971/38/schedule/2/part/I
  63. ↑ DEA / Drug Scheduling | https://www.dea.gov/druginfo/ds.shtml
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