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Summary sheet: LSD
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.

Threshold Common Heavy
15 - 25 - 75 - 150 - 300 µg
Light Strong
Bioavailability 71% - 71%[1]
Threshold 15 µg
Light 25 - 75 µg
Common 75 - 150 µg
Strong 150 - 300 µg
Heavy 300 µg +
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 popular semisynthetic psychedelic substance of the lysergamide class that produces "classical" psychedelic effects when administered.[2] LSD has a complex pharmacology involving multiple receptor systems, but primarily acts as a serotonin-2A agonist.

LSD was first synthesized in 1938 by the Swiss chemist Albert Hofmann, although it took until 1943 for its psychoactive properties to be discovered. In 1947, it was introduced as a commercial medication under the name Delysid for use in clinical psychiatry and research.[3]

LSD had a major and immediate 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.[4] During this time, it was investigated by the U.S. Central Intelligence Agency (CIA) as a potential mind control agent in a clandestine project named MK-ULTRA.[5] Its widespread adoption by the Western counterculture in the 1960s eventually resulted in its global prohibition in 1971.[6][7]

LSD has been noted for its elusiveness,[8] impact on various youth subcultures and alternative spiritualities,[9] the arbitrariness of the restrictions on its research,[10] as well as the difficulty of its clandestine production.[11] It is considered by some to be the first modern entheogen, a category which had been limited to traditional plant preparations or extracts.[12]

Unlike most highly prohibited substances, LSD is not considered to be addictive or toxic by the scientific community.[13][14] Nevertheless, unpredictable adverse reactions such as severe anxiety, delusions and psychosis can always occur, particularly among those who are predisposed to mental disorders.[15] It is therefore highly advised to use the proper amount of precaution and 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.[16] 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.[17] This event would come to be known as "Bicycle Day", and is celebrated to this day.

The first intentional ingestion of LSD occurred on April 19, 1943.[18] Hofmann ingested 250 micrograms (µg) of LSD, believing it would be a threshold dose based on the dosages of other ergot alkaloids. Hofmann found the effects to be much stronger than he anticipated and was impressed and puzzled by its radical mind-altering effects. It was introduced into the medical community in 1947 by Sandoz as an experimental tool to induce temporary psychotic-like states in normals (“model-psychosis”) and later to enhance psychotherapeutic treatments (“psycholytic” or “psychedelic” therapy)[19]

Beginning in the 1950s, the U.S. Central Intelligence Agency began a research program code named MK-ULTRA that would go on to investigate LSD for potential applications in mind control, chemical warfare, and the development of a 'truth serum.' Experiments included administering LSD to CIA employees, military personnel, doctors, other government agents, prostitutes, mentally ill patients, and members of the general public in order to study their reactions, usually without the subjects' knowledge. This resulted in at least one death. The project was revealed in the U.S. congressional commission on CIA activities in 1975.[20]

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[21][22] and according to L. R. Veysey, they profoundly influenced the thinking of the new generation of youth.[23]

On October 24, 1968, possession of LSD was made illegal in the United States.[24] 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.[25]


LSD, or d-lysergic acid diethylamide, is a semisynthetic alkaloid of the lysergamide family. LSD contains a core structure of lysergic acid, with an N,N-diethylamide functional group bound to RN of the chemical structure. This core polycyclic structure of LSD is an indole derivative and has tryptamine and phenethylamine groups embedded within it.

LSD's structure contains 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.[26]

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 is sensitive to oxygen, ultraviolet light, and chlorine (especially in solution).[27] 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). In one study, there was a 10% loss of potency after LSD was kept at room temperature for one month.[28] However, there are many anecdotal reports from users who claim to have successfully stored LSD at room temperature for years without noticeable loss in potency.


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.[29]

LSD acts as a 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C and 5-HT6 receptor partial agonist.[30][31] 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.[32] The psychedelic effects are thought to come from LSD's efficacy at the 5-HT2A receptors.[33]

LSD also possesses efficacy at all dopamine and all adrenoreceptors. Most serotonergic psychedelics are not significantly dopaminergic, so LSD is therefore rather unique in this regard. LSD's agonism of D2 receptors has been shown to contribute to its psychoactivity.[34][35]

However, the role of these interactions and how they result in the psychedelic experience continues to remain the subject of ongoing scientific inquiry.

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 receptors for dopamine and norepinephrine.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed 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 and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Visual effects

Cognitive effects

Multi-sensory effects

Combinational effects

  • Cannabis - Cannabis is known to strongly intensify the sensory and cognitive effects of LSD. This combination should be used with extreme caution as there are many reports that indicate that it can significantly increase the risk of anxiety, confusion and psychosis of both cannabis and LSD. Those who choose to use this combination are advised to start off with only a fraction of their usual cannabis dose and take at least 20-minute breaks between hits in order to avoid spiralling negative reactions.
  • Dissociatives - When used in combination with dissociatives, the dissociative, cognitive, visuals and general hallucinatory effects become greatly enhanced. Dissociative-induced holes, spaces, and voids while under the influence of LSD have significantly more vivid visuals than dissociatives alone, as well as more intense internal hallucinations, and corresponding confusion which can spontaneously manifest as delusions and psychosis.
  • MDMA - When combined with MDMA, the physical, cognitive, and euphoric effects of MDMA become amplified. The visual, physical and cognitive effects of LSD can also be intensified to the point of overwhelming euphoric pleasure manifested through pleasurable body highs, headspaces, and uniquely colorful and intricate visuals. The synergy between these substances is unpredictable, and it is advised to start with markedly lower dosages than one would take for each substance individually. There is some evidence that suggests this combination can increase the neurotoxic effects of MDMA.[39][40][41]
  • Alcohol - This combination is not typically recommended due to alcohol’s ability to cause dehydration and nausea and physical fatigue which can negatively affect a trip if taken in moderate to high dosages. This combination is, however, reasonably safe in low doses and can often "take the edge off" a trip as well as dull its psychedelic effects in a fashion somewhat similar to benzodiazepines, albeit in a more physically draining way.
  • Benzodiazepines - When used in combination with benzodiazepines, benzodiazepines can, depending on the dosage, slightly to completely reduce the intensity of the cognitive, physical and visual effects of an LSD trip. They are very efficient at stopping "bad trips" at the cost of amnesia and reduced trip intensity. Caution is advised when acquiring them for this purpose due to the very high addictive potential that benzodiazepines possess.
  • Psychedelics - When used in combination with other psychedelics, each substance's physical, cognitive and visual effects intensify and synergize strongly. The synergy between those substances is unpredictable, and for this reason generally not advised. If choosing to combine psychedelics, it is recommended to start with significantly lower dosages than one would take for either substance individually.

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,"[42] 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 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.[43]
  • 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.

Mimics ("Bunk acid")

LSD has been noted for being unusually potent among psychedelic substances, active at just 15-30 micrograms (µg).[44] 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, ease of synthesis, and black-market connections required to produce these compounds as well as the general inability of inexperienced users to tell the difference.

It should be noted that 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 distinct, 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 vital as mimics are considerably less predictable and can pose severe health risks (including possible death) that LSD does not.[citation needed]

Common mimics

25I-NBOMe, which has been attributed to several deaths,[45][46][47][48] may commonly be mistaken for LSD by sellers and users.[49]



Some studies in the 1960s that used LSD to treat alcoholism resulted in reduced levels of alcohol misuse in almost 60% of those treated, an effect which lasted six months but disappeared after a year.[38][50][51][52][53] 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.[38]

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.[54]

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. Researcher Peter Goadsby describes the headaches as "worse than natural childbirth or even amputation without anesthetic."[citation needed]

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.[55]

Unlike the use of LSD or MDMA in psychotherapy, this research involves non-psychological effects and often sub-psychedelic dosages.[56][57]

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.[58][59]

Toxicity and harm potential

Radar plot showing relative physical harm, social harm, and dependence of LSD[60]

LSD is considered to be non-addictive and has an extremely low toxicity relative to dose.[61]

As with most other psychedelic substances, there are very few physical side effects associated with acute LSD exposure. Various studies have shown that in reasonable doses in a sufficiently prepared context, it is very unlike to present negative physical, cognitive, psychiatric or other toxic consequences.

However, as with psychedelics in general, it is possible that LSD can act as a potential trigger for those with underlying psychiatric conditions. Those with a personal or family history of mental illness are generally advised not to use this substance, particularly when outside of a supervised medical setting.

Lethal dosage

The median lethal dose or dosage at which 50% of participants die (LD50) for human beings has never been reached in any setting and is predicted to be roughly 12,000 micrograms, based on studies involving rats whereas the active dosage is between 100 and 500 micrograms.[citation needed]

This means that assuming a person has unusually potent tabs, each of which is 200 micrograms in strength, they would have to consume at least 60 of them to reach a potentially lethal dosage. Today, the average tab of LSD found through street dealers is perhaps 75 micrograms or less in strength.[citation needed]

Nevertheless, despite its lack of physical toxicity, it is strongly recommended that one uses harm reduction practices when using this substance.

Tolerance and addiction potential

LSD is not habit-forming and the desire to use it can actually decrease with use, although rare cases of addiction and abuse have been documented.[citation needed] Notably, there is virtually no withdrawal syndrome when the chronic use of this substance is ceased.[62]

Tolerance to the effects of LSD is built almost immediately after ingestion. After that, it takes about 5-7 days for the tolerance to be reduced to half and 14 days to be back at baseline (in the absence of further consumption). LSD presents cross-tolerance with all psychedelics, meaning that after the use of LSD all psychedelics will have a reduced effect.

Anecdotal reports further suggest that extremely high dosages of LSD may develop a tolerance which can last subsequently longer anywhere from weeks to months. High dosages of LSD, along with high tolerances, can produce non-typical LSD-like effects that affect change of intensity and duration, but also the profile of physical and cognitive effects.

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can become dangerous or even life-threatening when taken with other substances. The list below contains some potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses but still increase the possibility of injury of death. Independent research should always be conducted to ensure that a combination of two or more substances is safe before consumption.

  • Lithium - Individuals who take lithium for bipolar disorder or other psychiatric conditions should not take LSD. There are numerous anecdotal reports of seizures and or psychosis from this combination.[63][64][65][66]
  • Stimulants - Combining stimulants with psychedelics may induce states of uncontrollable anxiety, over-stimulation, thought loops, and increase the risk of psychosis.[67]
  • Tramadol - Tramadol lowers the seizure threshold[68] and psychedelics may act as potential triggers for seizures in susceptible individuals.[69][70][71]

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 do in practice.[72]

  • 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.[73]
  • Latvia: LSD is a Schedule I drug in Latvia.[74]
  • United Kingdom: LSD is a Class A drug in the UK.[75]
  • 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).[76]

See also

External links


  • 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.
  • 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.
  • Hoffman, A. (1980). LSD - My Problem Child. New York: McGraw-Hill.


  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.
  2. Nichols, D. E. (2016). Psychedelics, (April), 264–355.
  3. Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  4. 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.
  5. Project MK-ULTRA - The CIA's Program of Research in Behavioral Modification, Washington, DC, Government Printing Office, August 31, 1977.
  6. "LSD: cultural revolution and medical advances". Royal Society of Chemistry. Retrieved September 27, 2007.
  7. UN General Assembly, 1971 Convention on Psychotropic Substances, 9 December 1975, A/RES/3443
  8. Thompson, H. S. (2012). Fear and Loathing: On the Campaign Trail '72. New York: Simon & Schuster Paperbacks. “Jesus man! You don't look for acid! Acid finds you when *it* thinks you're ready.”
  9. 09) Henderson and Glass, Introduction, p. 4; Goodman and Gilman, p. 554; Daniel X. Freedman, A Psychiatrist Looks at LSD, Federal Probation, June 1968, pp. 20, 22.
  10. Nutt, D. J., King, L. A., & Nichols, D. E. (2013). Effects of Schedule One Drug Laws on Neuroscience Research and Treatment Innovation. Nature Reviews Neuroscience, 14(8), 577-585.
  11. Rhodium. Discussions on the Synthesis of LSD. Retrieved April 15, 2017, from
  12. 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.
  13. Lüscher, C., & Ungless, M. A. (2006). The Mechanistic Classification of Addictive Drugs, 3(11).
  14. Nichols, D. E. (2016). "Psychedelics." Pharmacological Reviews, 68(2), 264-355.
  15. 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
  16. Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  17. Nichols, David. "Hypothesis on Albert Hofmann's Famous 1943 'Bicycle Day'" Adapted from a presentation given at Mindstates IV. May 24, 2002.
  18. Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  19. Hofmann, A., & Ott, J. (1980). LSD: My Problem Child. McGraw-Hill.
  20. Project MK-ULTRA - The CIA's Program of Research in Behavioral Modification, Washington, DC, Government Printing Office, August 31, 1977.
  21. "LSD: cultural revolution and medical advances". Royal Society of Chemistry. Retrieved September 27, 2007.
  22. |Out-Of-Sight! SMiLE Timeline
  23. 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.
  24. Erowid F. "U.S. Drug Control Timeline". Erowid Extracts. Jun 2004;6:4-5.
  25. Gasser, Peter. "Psycholytic Therapy with MDMA and LSD in Switzerland." MAPS Newsletter 5.3 (1994): 3-7
  27. Entry #26 LSD-25 from TiHKAL by Alexander & Ann Shulgin |
  28. Stability Study of LSD Under Various Storage Conditions |
  29. 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.
  30. 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
  32. Nelson, D. L. (2004). 5-HT5 receptors. Current Drug Targets-CNS & Neurological Disorders, 3(1), 53-58. PMID: 14965244
  33. 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.
  34. 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.
  35. Hanna J, Manning T. "The End of a Chemistry Era.... Dave Nichols Closes Shop". Erowid Extracts. November 2012;23:2-7.
  36. 36.0 36.1 36.2 36.3 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.
  37. Friedman, S. A., & Hirsch, S. E. (1971). Extreme hyperthermia after LSD ingestion. JAMA, 217(11), 1549-1550.
  38. 38.0 38.1 38.2 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.
  39. 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 receptior 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.
  40. Potentiation of MDMA-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists |
  41. Ecstasy induces apoptosis via 5-HT(2A)-receptor stimulation in cortical neurons. |
  42. 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.
  43. Long LSD Prison Terms--It's All in the Packaging |
  44. 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.
  45. Erowid. "25I-NBOMe (2C-I-NBOMe) Fatalities / Deaths". Drug Website. Erowid. Retrieved February 28, 2016. 
  46. Hastings, Deborah (May 6, 2013). "New drug N-bomb hits the street, terrifying parents, troubling cops". New York Daily News. Retrieved May 7, 2013. 
  47. 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. 
  48. 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. 
  49. 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. 
  50. 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.
  51. Ditman, K.S.; Bailey, J.J., "Evaluating LSD as a psychotherapeutic agent," pp.74–80.
  52. Hoffer, A., "A program for the treatment of alcoholism: LSD, malvaria, and nicotinic acid," pp. 353–402.
  53. Mangini, M. (1998). Treatment of alcoholism using psychedelic drugs: a review of the program of research. Journal of Psychoactive Drugs, 30(4), 381-418.
  54. Kast, E. (1967). Attenuation of anticipation: a therapeutic use of lysergic acid diethylamide. Psychiatric Quarterly, 41(4), 646-657.
  55. Sewell, R. A., Halpern, J. H., & Pope, H. G. (2006). Response of cluster headache to psilocybin and LSD. Neurology, 66(12), 1920-1922.
  56. Summarized from "Research into psilocin and LSD as cluster headache treatment" and the Clusterbusters website. Pages accessed 2007-01-31.
  57. Sewell, R. A., Halpern, J. H., & Pope, H. G. (2006). Response of cluster headache to psilocybin and LSD. Neurology, 66(12), 1920-1922.
  58. Psychiater Gasser bricht sein Schweigen |
  59. Landmark Clinical LSD Study Nears Completion |
  60. 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.
  61. 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.
  62. Diaz, Jaime (1996). How Drugs Influence Behavior: A Neurobehavioral Approach. Englewood Cliffs: Prentice Hall. ISBN 9780023287640
  63. | LSD Interactions by Erowid
  64. Wanderli. "A Nice Little Trip to the Hospital: An Experience with Lithium & LSD (ID 83935)". Oct 3, 2010.
  65. MissDja1a. "Having a Seizure and Passing Out: An Experience with Lithium & LSD (ID 75153)". Dec 16, 2008.
  66. Reddit account of seizure on LSD + Lithium |
  67. Tripsit Factsheets - LSD |
  68. 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.
  69. Tripsit Factsheets - LSD |
  70. Fisher, D. D., & Ungerleider, J. T. (1967). Grand mal seizures following ingestion of LSD. California Medicine, 106(3), 210. PMCID: PMC1502729
  71. Question ID: 2837 (Ask Erowid) |
  72. UN General Assembly, 1971 Convention on Psychotropic Substances, 9 December 1975, A/RES/3443.|
  73. Controlled Drugs and Substances Act of Canada
  74. Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (I saraksta 2.2.1.punkts) |
  75. Misuse of Drugs Act 1971 ( |
  76. DEA / Drug Scheduling |