LSD - PsychonautWiki
Summary sheet: LSD
Chemical Nomenclature
Common names LSD, LSD-25, Lucy, L, Acid, Cid, 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.

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.

Tricyclic antidepressants

Lysergic acid diethylamide (also known as Lysergide, LSD-25, LSD, L, Lucy, and Acid) is a classical psychedelic substance of the lysergamide class.[2] It is considered to be the best known, most researched, and culturally influential psychedelic substance. It is thought to produce its psychedelic effects by binding to serotonin receptors in the brain, although the precise mechanism is not fully understood.

The psychoactive effects of LSD were first discovered in 1943 by Albert Hofmann, a Swiss chemist at Sandoz Laboratories.[3] In the 1950s, it was distributed by Sandoz under the name Delysid and intended for use as an experimental drug in psychotherapy and scientific research.[4] During this period, LSD generated widespread interest from clinicians, researchers, and intellectuals and was notoriously the subject of a secret investigation by the U.S. Central Intelligence Agency (CIA) for potential applications in "mind control".[5] Recreational LSD use became a central part of the 1960s youth counterculture movement which eventually led to its prohibition in 1971.[6][7]

Following a 40 year hiatus, research into the therapeutic applications of LSD has experienced a revival.[citation needed] It is currently being investigated for the treatment of a number of ailments including alcoholism, addiction, cluster headache, and anxiety associated with terminal illness.[4] 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%.[4]

Subjective effects include open and closed-eye visuals, time distortion, enhanced introspection, conceptual thinking, euphoria, and ego loss. LSD is commonly reported to be able to evoke mystical-type experiences that can facilitate self-reflection and personal growth.[8] It is considered by some to be the first modern entheogen, a category which is otherwise limited to traditional plant preparations or extracts.[9]

Unlike other highly prohibited substances, LSD has not been proven to be physiologically toxic or addictive.[10][2] However, adverse psychological reactions such as severe anxiety, paranoia, delusions, psychosis and HPPD are always possible, particularly for those predisposed to psychiatric disorders.[11] As a result, it is highly advised to use harm reduction practices if using this substance.

History and culture

The original synthesis of LSD was recorded on November 16, 1938, by the Swiss chemist Albert Hofmann while employed at the Sandoz Laboratories in Basel, Switzerland. It was synthesized as part of a large research program searching for medically useful derivatives of ergot, a fungus that grows on rye and other grains. However, its psychoactive properties were not discovered until five years later when Hofmann claimed to have accidentally ingested an unknown quantity of the chemical before proceeding to ride his bike home.[12]

The first intentional ingestion of LSD was recorded 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, LSD was introduced by Sandoz 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).[13]

LSD had a major impact in the areas of scientific research and psychiatry upon its release — within 15 years, research on LSD and other hallucinogens generated over 1,000 scientific papers and was prescribed to over 40,000 patients.[14] In the 1950s, the U.S. Central Intelligence Agency created 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.[5]

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 a central part of the youth-driven counterculture of the 1960s. Along with other hallucinogens, LSD was advocated by new proponents of consciousness expansion such as Leary, Huxley, Alan Watts and Arthur Koestler[6] who, according to L. R. Veysey, profoundly influenced the thinking of the new generation of youth.[15]

On October 24, 1968, possession of LSD was made illegal in the United States.[16] 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.[17]


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.[13] LSD has numerous street names including: acid, lucy, L, cid/sid. It is also referred to as blotter or tabs, a reference to their typical form of distribution.


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 compound that belongs to the lysergamide (or ergoline) family. It is the parent compound of the lysergamides, meaning it serves as the prototype for a series of compounds derived from its structure. These compounds include: 1P-LSD, ALD-52, AL-LAD, ETH-LAD, PRO-LAD, and LSZ.

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,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.[18]

LSD in its pure form occurs as colorless, odorless, prismatic crystals.[19] It is sensitive to oxygen, ultraviolet light, and chlorine (especially in solution).[18] Its potency may last for years if it is stored away from light and moisture at cold temperatures around 0°C or below, but slowly degrades at normal room temperature (25°C).[citation needed]


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.[20]

LSD is a partial agonist for the 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C and 5-HT6 receptors.[21] 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.[22] The psychedelic effects of LSD are thought to be mediated by agonist action 5-HT2A receptors.[23]

LSD also shows 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.[24][25]

Subjective effects

The subjective effects of LSD can be broken down into several components which progressively intensify proportional to dosage in a nonlinear manner.

Compared to other common psychedelics such as psilocybin mushrooms, LSA and ayahuasca, LSD is reported to be significantly more stimulating and fast-paced in both physical and cognitive dimensions and produces a wide variety of effects that might be attributed to its binding activity at a range of CNS receptors other than serotonin, such as those of dopamine and norepinephrine.

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), a research literature based on collected anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be regarded with a healthy degree of skepticism. It is worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce a full spectrum of effects. Likewise, adverse effects become much more likely with higher doses and may include addiction, serious injury, or death ☠.

Physical effects

Visual effects

Cognitive effects

Multi-sensory effects

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 influence the trip. Users are advised to pace themselves and drink a portion of their usual amount if making the decision to drink on LSD.
  • Benzodiazepines - Benzodiazepines are highly effective at reducing the intensity of LSD's effects through the general suppression of brain activity.
  • 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.[29][30][31]
  • Antidepressant and antipsychotic drugs may block the effect of LSD by acting on the same receptors and outcompeting their ability to bind. Antidepressants mirtazapine and trazodone act on the 5-HT2A and 5-HT2C receptors where they block serotonin and other molecules from binding[32]. Atypical antipsychotics also act on these receptors in order to decrease hallucinations and cognitive distortion.

Experience reports

There are currently 41 experience reports which describe the effects of this substance in our experience index.

Additional experience reports can be found here:


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",[33] 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.[34]
  • 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.



Some studies in the 1960s that investigated LSD as a treatment for alcoholism found reduced levels of alcohol misuse in almost 60% of those treated, an effect which lasted six months but disappeared after a year.[28][35][28][36][37] 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.[28]

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.[38] 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 purported 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 tryptamines 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.[39] Unlike the use of LSD or MDMA in psychotherapy, this research involves non-psychological effects and often sub-psychedelic dosages.[40][39]

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.[41][42]


A 2018 study demonstrated neuroplasticity induced by LSD and other psychedelics through TrkB, mTOR, and 5-HT2A signaling.[43]

Reagent Results

Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.

Marquis Mecke Mandelin Liebermann Froehde Robadope Ehrlich Hofmann Simon's
No reaction No reaction No reaction No reaction No reaction No reaction Pink - Purple - Blueish (slow) Blue No reaction

Toxicity and harm potential

Radar plot showing relative physical harm, social harm, and dependence of LSD[44]

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 organs and there are no documented deaths attributed to the direct effects of LSD toxicity.[45]

However, while LSD may not be capable of causing direct bodily toxicity or death, its use can still have serious negative consequences. For example, it is capable of impairing the user's judgment and attention, which may promote erratic or dangerous behaviors. In extreme cases, users may experience delusions such as that they are currently inside a dream and therefore physically invincible, prompting them to jump off of a building or run into oncoming traffic.[2]

Additionally, intense negative experiences and psychotic episodes (i.e. "bad trips") can cause lasting psychological trauma if not properly managed or treated afterward. This is particularly a concern in non-supervised settings or when heavy doses are used.

LSD may trigger or exacerbate symptoms (e.g. delusions, mania, psychosis) in those who have or are predisposed to mental illness such as bipolar disorder or schizophrenia.[45] Those with a personal or family history of mental illness (including anxiety and depression) should not use LSD without the advice of a qualified medical professional.

Finally, it should be noted that evidence of LSD's effectiveness as a mental health treatment only applies to the controlled procedures used in clinical studies, in which professional psychotherapists help guide the patient’s experience. LSD alone is not considered the treatment because the evidence suggests it must be combined with professional psychotherapy to produce enduring effects. Without the appropriate safeguards, attempts at self-medicating with LSD may actually worsen conditions like anxiety and other mental health issues.[46]

It is strongly recommended to use harm reduction practices if using this substance. This includes practices such as:

  • Taking the substance under the supervision of a tripsitter for one's first time or while experimenting with a higher dose
  • Using a reagent testing kit to verifying the substance is genuine LSD and not some other substance
  • Keeping a supply of benzodiazepines or antipsychotics like Seroquel to abort the trip in the case of overwhelming anxiety or psychosis

Hallucinogen-perception persisting disorder (HPPD)

LSD may trigger hallucinogen persisting perception disorder (HPPD) in some individuals.[47]

Dependence and abuse potential

Like other serotonergic psychedelics, LSD is considered to be non-addictive with a low abuse potential.[45] 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.[45] Likewise, there is no human clinical evidence that LSD causes addiction. Finally, there is virtually no withdrawal syndrome when chronic use of LSD 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 unusual variations in intensity, duration, and effects.


Unlike many psychoactive substances, LSD has no known toxic dose and is essentially impossible to physiologically overdose on. However, higher doses increase the risk of adverse psychological reactions. These reactions include anxiety, paranoia, panic attacks, delusions, psychosis, and in rare cases, seizures.

Medical attention is usually not needed except in the case of severe psychotic episodes or the suspected ingestion of so-called "fake acid", substances that partially mimic LSD's psychedelic effects but carry the risk of physiological toxicity and overdose (e.g. 25x-NBOMe or DOx). Administration of benzodiazepines (e.g. diazepam, alprazolam) can help to relieve the acute negative psychological effects of LSD. Antipsychotics such as quetiapine (Seroquel) may also be used in extreme cases, although they may be less reliable for this purpose.

Mimics ("Fake acid")

LSD's high chemical potency gives it the unique property of being able to infuse it onto paper for distribution. It has a long history of being counterfeited by select other psychedelics that are also potent enough to be laid onto blotter paper (colloquially known as "fake acid" or "bunk acid"). These include the DOx series and, more commonly, the 25x-NBOMe series.

Unlike pure LSD blotters, which are usually only mildly bitter due to any ink the paper contains (pure LSD is almost completely tasteless), mimics are usually described as having an obvious "metallic", "numbing", "chemical-like" or "extremely bitter or sour" taste. As a result, it is commonly advised to immediately spit out any blotters of acid that are found to have a strong, persisting taste.

However, the taste test can only partially ensure user safety. Users should always test their LSD using a reagent test kit. Testing kits are considered important because mimics (such as 25x-NBOMe and DOx) have significantly worse safety profiles than LSD which includes the risk of death.[citation needed]

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can suddenly become dangerous or even life-threatening when combined with other substances. The following list includes some known dangerous combinations (although it is not guaranteed to include all of them). Independent research (e.g. Google, DuckDuckGo) should always be conducted to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • Lithium:[48][49] Lithium is commonly prescribed in the treatment of bipolar disorder; however, there is a large body of anecdotal evidence that suggests taking it with psychedelics can significantly increase the risk of psychosis and seizures.[50][51][52] As a result, this combination should be strictly avoided.
  • Tricyclic antidepressants:[48] Tricyclic antidepressants increase physical, hallucinatory and psychological responses to LSD.[53] Anecdotal evidence suggests that TCAs increase the risk of bad trips and psychosis when combined with LSD. Since the symptoms are similar to those induced by lithium and LSD, seizures cannot be excluded. Therefore, this combination should be avoided.
  • Tramadol:[54] Tramadol is well documented to lower the seizure threshold in individuals[55] and LSD also has the potential to induce seizures in susceptible individuals.[27]
  • Ritonavir:[48] Severe vascular constriction has happened when taking ergolines in combination with ritonavir. Because it is not known if this extends to LSD, utmost caution is advised.
  • Cannabis:[54] Cannabis can have an unexpectedly strong and unpredictable synergy with LSD. While it is commonly used to intensify or prolong LSD's effects, caution is highly advised as mixing these substances can significantly increase the risk of negative psychological effects like anxiety, paranoia, panic attacks, and psychosis. Anecdotal reports often describe the ingestion of cannabis as the triggering event for a bad trip or psychosis. It is advised to start off with only a fraction (e.g. 1/4th - 1/3rd) of their typical cannabis dose and space out hits to avoid accidental over intake.
  • Stimulants (e.g. amphetamine, cocaine, methylphenidate):[54] While capable of intensifying LSD's euphoric effects, stimulants elevate anxiety levels and increase the risk of paranoia, thought loops, and psychosis, particularly during the comedown phase. This risk may be higher than with other psychedelics due to LSD's direct effect on dopamine pathways. Caution is highly advised.

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.[7]

  • Australia: LSD is considered a Schedule 9 prohibited substance in Australia under the Poisons Standard.[56] A Schedule 9 substance is a substance which may be abused or misused and the manufacture, possession, sale or use of is prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities.[56]
  • Austria: LSD is illegal to possess, produce and sell under the Addictive Substances Act (Suchtmittelgesetz).[57][7]
  • Brazil: Possession, production and sale is illegal as it is listed on Portaria SVS/MS nº 344.[58]
  • Canada: LSD is a Schedule III controlled substance in Canada.[59]
  • Croatia: LSD is a controlled substance.[60]
  • Czech Republic: In 2010, the possession of 5 tabs of LSD has been decriminalized. Anybody possessing less than this amount may be charged for a misdemeanor or receive a warning from police.[61]
  • Denmark: LSD is a Category A controlled substance in Denmark.[62]
  • Germany: LSD is controlled under Schedule I of the Narcotics Act (Anlage I BtMG)[63], former Opium Act (Opiumgesetz) as of February 25, 1967.[64] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[65]
  • Italy: LSD is a Schedule I (Tabella I) controlled substance.[66]
  • Japan: LSD is classified as a narcotic under the Narcotic and Psychotropic Drugs Control Act (麻薬及び向精神薬取締法).[67]
  • Latvia: LSD is a Schedule I controlled substance in Latvia.[68]
  • Luxembourg: LSD is a prohibited substance. [69]
  • The Netherlands: LSD is classified as a List I (Lijst 1) controlled substance under the Opium Law (Opiumwet).[70]
  • Norway: LSD is classified as a narcotic.[71]
  • Portugal: LSD is illegal to produce, sell or trade in Portugal. However since 2001, individuals found in possession of small quantities (up to 500 µg) are considered sick individuals instead of criminals. The substance is confiscated and the suspects may be forced to attend a dissuasion session at the nearest CDT (Commission for the Dissuasion of Drug Addiction) or pay a fine, in most cases.[72]
  • Russia: LSD is a List I (список I) contolled substance. It is illegal to possess, produce and sell.[73]
  • Switzerland: LSD is a controlled substance specifically named under Verzeichnis D.[74]
  • Sweden: LSD is a Schedule I (Förteckning I) controlled substance.[75] The Swedish supreme court concluded in 2018 that possession of processed plant material containing a significant amount of DMT is illegal. However, possession of unprocessed such plant material was ruled legal.[citation needed]
  • United Kingdom: LSD is a Class A controlled substance in the United Kingdom.[76]
  • United States: LSD is a Schedule I controlled substance 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).[77]
  • Poland: LSD is illegal to own, produce and sell under "Wykaz środków odurzających i substancji psychotropowych" and is grouped in "I-P" [78]

See also

External links



  • Nichols, D. E. (2016). Psychedelics. Pharmacological Reviews, 68(2), 264-355.
  • 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.
  • 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.
  • 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.
  • Daniel Wacker, Sheng Wang, John D. McCorvy, Robin M. Betz, A.J. Venkatakrishnan, Anat Levit, Katherine Lansu, Zachary L. Schools, Tao Che, David E. Nichols, Brian K. Shoichet, Ron O. Dror, Bryan L. Roth (2020). Crystal Structure of an LSD-Bound Human Serotonin Receptor. Cell, Volume 168, Issue 3, 377-389.

Further reading


  • Hoffman, Albert. LSD — My Problem Child. McGraw-Hill, 1980.
  • Lee, Martin A., and Bruce Shlain. Acid Dreams: The Complete Social History of LSD: The CIA, the Sixties, and Beyond. Grove Press, 1992.



  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. 2.0 2.1 2.2 Nichols, David E. (2016). Barker, Eric L., ed. "Psychedelics". Pharmacological Reviews. 68 (2): 264–355. doi:10.1124/pr.115.011478. eISSN 1521-0081. ISSN 0031-6997. 
  3. Passie, T.; Halpern, J. H.; Stichtenoth, D. O.; Emrich, H. M.; Hintzen, A. "The Pharmacology of Lysergic Acid Diethylamide: A Review" (PDF). CNS Neuroscience & Therapeutics. 14: 295–314. doi:10.1111/j.1755-5949.2008.00059.x. eISSN 1755-5949. ISSN 1755-5930. Archived from the original (PDF) on May 1, 2013. Retrieved January 1, 2020. 
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Schmid, Y.; Enzler, F.; Gasser, P.; Grouzmann, E.; Preller, K. H.; Vollenweider, F. X.; Brenneisen, R.; Müller, F.; Borgwardt, S.; Liechti, M. E. (2015). "Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects". Biological Psychiatry. 78 (8): 544–553. doi:10.1016/j.biopsych.2014.11.015. eISSN 1873-2402. ISSN 0006-3223. 
  5. 5.0 5.1 "Joint Hearing before the Select Committee On Intelligence and the Subcommitte On Health And Scientific Research of the Committee On Human Resources: Ninety-fifth congress: First Session" (PDF). U.S. Government Printing Office. August 3, 1977. Retrieved January 3, 2020. 
  6. 6.0 6.1 David Nichols (December 22, 2005). "LSD: cultural revolution and medical advances". Chemistry World. Royal Society of Chemistry. Retrieved September 27, 2007. 
  7. 7.0 7.1 7.2 "Convention On Psychotropic Substances, 1971" (PDF). United Nations Office on Drugs and Crime. Retrieved January 3, 2020. 
  8. Lyvers, Michael; Meester, Molly (2012). "Illicit Use of LSD or Psilocybin, but not MDMA or Nonpsychedelic Drugs, is Associated with Mystical Experiences in a Dose-Dependent Manner". Journal of Psychoactive Drugs. 44 (5): 410–417. doi:10.1080/02791072.2012.736842. eISSN 2159-9777. ISSN 0279-1072. 
  9. Grof, Stanislav (1993). Realms of the Human Unconscious: Observations from LSD Research. London: Souvenir Press. pp. 13–14. ISBN 0-285-64882-9. Archived from the original on January 28, 2011. Retrieved January 3, 2020. 
  10. Lüscher, Christian; Ungless, Mark A. (2006). "The Mechanistic Classification of Addictive Drugs". PLOS Medicine. 3 (11). doi:10.1371/journal.pmed.0030437. eISSN 1549-1676. ISSN 1549-1277. PMID 17105338. 
  11. Strassmann, Rick (1984). "Adverse reactions to psychedelic drugs. A review of the literature". Journal of Nervous and Mental Disease. 172 (10): 577–595. doi:10.1097/00005053-198410000-00001. ISSN 0022-3018. OCLC 1754691. PMID 6384428. 
  12. Nichols, David (May 24, 2003). "Hypothesis on Albert Hofmann's Famous 1943 "Bicycle Day"". at Mindstates IV: Berkeley, CA: Transcription & Editing by Erowid. Retrieved January 3, 2020. 
  13. 13.0 13.1 13.2 Hofmann, Albert (1980). LSD - My Problem Child. Translated by Ott, Jonathan. New York: McGraw-Hill. ISBN 978-0-07029-325-0. OCLC 6251390. 
  14. Zentner, Joseph L. (1976). "The Recreational Use of LSD-25 and Drug Prohibition". Journal of Psychedelic Drugs. 8 (4): 299–305. doi:10.1080/02791072.1976.10471853. eISSN 2159-9777. ISSN 0279-1072. 
  15. Veysey, Laurence R. (1978). The Communal Experience: Anarchist and Mystical Communities in Twentieth-Century America. Chicago IL: University of Chicago Press. p. 437. ISBN 0-226-85458-2. 
  16. "Public Law 90-639" (PDF). Erowid. Retrieved January 3, 2020. 
  17. Gasser, Peter (1995). "Psycholytic Therapy with MDMA and LSD in Switzerland". Newsletter of the Multidisciplinary Association for Psychedelic Studies. MAPS. 5 (3): 3–7. Retrieved January 3, 2020. 
  18. 18.0 18.1 Shulgin, Alexander; Shulgin, Ann (1997). "#26. LSD-25". TiHKAL: The Continuation. United States: Transform Press. ISBN 0-9630096-9-9. OCLC 38503252. 
  19. "Chemical Datasheet: D-Lysergic Acid Diethylamide". CAMEO Chemicals. Retrieved November 15, 2020. 
  20. Carhart-Harris, R. L.; Muthukumaraswamy, S.; Roseman, L.; Kaelen, M.; Droog, W.; Murphy, K.; Tagliazucchi, E.; Schenberg, E. E.; Nest, T.; Orban, C.; Leech, R.; Williams, L. T.; Williams, T. M.; Bolstridge, M.; Sessa, B.; McGonigle, J.; Sereno, M. I.; Nichols, D.; Hellyer, P. J.; Hobden, P.; Evans, J.; Singh, K. D.; Wise, R. G.; Curran, H. V.; Feilding, A.; Nutt, D. J. (2016). "Neural correlates of the LSD experience revealed by multimodal neuroimaging". Proceedings of the National Academy of Sciences. 113 (17): 4853–4858. doi:10.1073/pnas.1518377113. eISSN 1091-6490. ISSN 0027-8424. OCLC 43473694. 
  21. Aghajanian, G. K.; Bing, O. H. (1964). "Persistence Of Lysergic Acid Siethylamide In The Plasma Of Human Subjects". Clinical Pharmacology & Therapeutics. 5 (5): 611–614. doi:10.1002/cpt196455611. ISSN 1532-6535. PMID 14209776. 
  22. Nelson, D. L. (2004). "5-HT5 receptors". Current Drug Targets-CNS & Neurological Disorders. 3 (1): 53–58. doi:10.2174/1568007043482606. ISSN 1568-007X. PMID 14965244. 
  23. 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. doi:10.1016/j.neulet.2011.01.046. ISSN 0304-3940. OCLC 1874501. PMID 21276828. 
  24. Marona-Lewicka, Danuta; Thisted, Ronald A.; Nichols, David 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. doi:10.1007/s00213-005-2183-9. eISSN 1432-2072. ISSN 0033-3158. PMID 15723230. 
  25. Hanna, Jon; Manning, Tania (2012). "The End of a Chemistry Era...: Dave Nichols Closes Shop". Erowid Extracts. Erowid. 23: 2–7. Retrieved January 3, 2020. 
  26. Friedman, Steven A.; Hirsch, Stuart E. (1971). "Extreme Hyperthermia After LSD Ingestion". JAMA: The Journal of the American Medical Association. 217 (11): 1549–1550. doi:10.1001/jama.1971.03190110067020. eISSN 1538-3598. ISSN 0098-7484. OCLC 1124917. 
  27. 27.0 27.1 Fisher, D. D.; Ungerleider, J. T. (1967). "Grand mal seizures following ingestion of LSD". California Medicine. 106 (3): 210–211. ISSN 0008-1264. PMC 1502729 . PMID 4962683. 
  28. 28.0 28.1 28.2 28.3 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. doi:10.1177/0269881112439253. eISSN 1461-7285. ISSN 0269-8811. OCLC 19962867. PMID 22406913. 
  29. 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. doi:10.1002/nrc.20023. eISSN 1520-6769. 
  30. Gudelsky, Gary A.; Yamamoto, Bryan; Nash, J. Frank (1994). "Potentiation of 3,4-methylenedioxymethamphetamine-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists". European Journal of Pharmacology. 264 (3): 325–330. doi:10.1016/0014-2999(94)90669-6. eISSN 1879-0712. ISSN 0014-2999. OCLC 01568459. 
  31. Capela, J. P.; Fernandes, E.; Remião, F.; Bastos, M. L.; Meisel, A.; Carvalho, F. (2007). "Ecstasy induces apoptosis via 5-HT2A-receptor stimulation in cortical neurons". NeuroToxicology. 28 (4): 868–875. doi:10.1016/j.neuro.2007.04.005. ISSN 0161-813X. PMID 17572501. 
  32. Anttila, S. A. K.; Leinonen, E. V. J. (2001). "A Review of the Pharmacological and Clinical Profile of Mirtazapine". CNS Drug Reviews. 7 (3): 249–264. doi:10.1111/j.1527-3458.2001.tb00198.x. eISSN 1755-5949. ISSN 1755-5930. OCLC 221972947. PMC 6494141 . PMID 11607047. 
  33. Greiner, Theodore; Burch, Neil R.; Edelberg, Robert (1958). "Psychopathology and Psychophysiology of Minimal LSD-25 Dosage: A Preliminary Dosage-Response Spectrum". A.M.A. Archives of Neurology and Psychiatry. 79 (2): 208–210. doi:10.1001/archneurpsyc.1958.02340020088016. ISSN 0096-6886. OCLC 994501808. PMID 13497365. 
  34. Jim Newton (July 27, 1992). "Long LSD Prison Terms--It's All in the Packaging : Drugs: Law can mean decades in prison for minuscule amounts. DEA official says no change is needed". Los Angeles Times. Retrieved January 3, 2020. 
  35. Maclean, J. R.; Macdonald, D. C.; Odgen, F.; Wilby, E. (1967). "LSD-25 and Mescaline as Therapeutic Adjuvants: Experience from a Seven Year Study". In Abramson, H. A. The Use of LSD in Psychotherapy and Alcoholism (PDF). New York: Bobbs-Merrill. pp. 74–80. OCLC 302168. 
  36. Hoffer, A. (1967). "A Program for the Treatment of Alcoholism: LSD, Malvaria and Nicotinic Acid". In Abramson, H. A. The Use of LSD in Psychotherapy and Alcoholism (PDF). New York: Bobbs-Merrill. pp. 353–402. OCLC 302168. 
  37. Mangini, Mariavittoria (1998). "Treatment of Alcoholism Using Psychedelic Drugs: A Review of the Program of Research". Journal of Psychoactive Drugs. 30 (4): 381–418. doi:10.1080/02791072.1998.10399714. eISSN 2159-9777. ISSN 0279-1072. 
  38. Kast, Eric (1967). "Attenuation of anticipation: A therapeutic use of lysergic acid diethylamide". Psychiatric Quarterly. 41 (4): 646–657. doi:10.1007/BF01575629. eISSN 1573-6709. ISSN 0033-2720. OCLC 01715671. 
  39. 39.0 39.1 Sewell, R. A.; Halpern, J. H.; Pope, H. G. (2006). "Response of cluster headache to psilocybin and LSD". Neurology. 66 (12): 1920–1922. doi:10.1212/01.wnl.0000219761.05466.43. eISSN 1526-632X. ISSN 0028-3878. OCLC 960771045. 
  40. "LSD and Psilocybin Research: Research into psilocybin and LSD as potential treatments for people with cluster headaches". Multidisciplinary Association for Psychedelic Studies. Archived from the original on January 29, 2007. Retrieved January 6, 2020. 
  41. dvp (July 28, 2009). "Psychiater Gasser bricht sein Schweigen" (in German). Basler Zeitung. Archived from the original on September 2, 2014. Retrieved January 6, 2020. 
  42. David Jay Brown (May 26, 2011). "Landmark Clinical LSD Study Nears Completion". Patch. Retrieved January 6, 2020. 
  43. Ly, Calvin; Greb, Alexandra C.; Cameron, Lindsay P.; Wong, Jonathan M.; Barragan, Eden V.; Wilson, Paige C.; Burbach, Kyle F.; Soltanzadeh Zarandi, Sina; Sood, Alexander; Paddy, Michael R.; Duim, Whitney C.; Dennis, Megan Y.; McAllister, A. Kimberley; Ori-McKenney, Kassandra M.; Gray, John A.; Olson, David E. (2018). "Psychedelics Promote Structural and Functional Neural Plasticity". Cell Reports. 23 (11): 3170–3182. doi:10.1016/j.celrep.2018.05.022. ISSN 2211-1247. 
  44. Nutt, D.; King, L. A.; Saulsbury, W.; Blakemore, C. (2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Health Policy. 369 (9566): 1047–1053. doi:10.1016/S0140-6736(07)60464-4. eISSN 1872-6054. ISSN 0168-8510. OCLC 10960514. PMID 17382831. 
  45. 45.0 45.1 45.2 45.3 Nichols, David E. (2004). "Hallucinogens". Pharmacology & Therapeutics. 101 (2): 131–181. doi:10.1016/j.pharmthera.2003.11.002. eISSN 1879-016X. ISSN 0163-7258. OCLC 04981366. 
  46. "Does LSD have any medical uses?". LSD. Drug Science. Retrieved January 7, 2020. 
  47. Halpern, J. H.; Pope Jr, H. G. (2003). "Hallucinogen persisting perception disorder: what do we know after 50 years?" (PDF). Drug and Alcohol Dependence. 69 (2): 109–119. doi:10.1016/S0376-8716(02)00306-X. ISSN 0376-8716. PMID 12609692. 
  48. 48.0 48.1 48.2 "LSD: Interactions". Erowid. November 18, 2003. Retrieved January 7, 2020. 
  49. Nayak, S., Gukasyan, N., Barrett, F. S., Erowid, E., Erowid, F., & Griffiths, R. R. (2021, February 24). Classic psychedelic coadministration with lithium, but not lamotrigine, is associated with seizures: an analysis of online psychedelic experience reports.
  50. "wanderlei" (October 3, 2010). "A Nice Little Trip to the Hospital: Lithium & LSD". Erowid Experience Vaults. Erowid. ExpID: 83935. Retrieved January 7, 2020. 
  51. "MissDja1a" (December 16, 2008). "Having a Seizure and Passing Out: Lithium & LSD". Erowid Experience Vaults. Erowid. ExpID: 75153. Retrieved January 7, 2020. 
  52. "throwaway_naut" (2014). "Please Read: a cautionary tale concerning LSD". r/Psychonaut. Reddit. Retrieved January 7, 2020. 
  53. Bonson, Katherine R.; Murphy, Dennis L. (1995). "Alterations in responses to LSD in humans associated with chronic administration of monoamine oxidase inhibitors or lithium". Behavioural Brain Research. 73 (1-2): 229–233. doi:10.1016/0166-4328(96)00102-7. eISSN 1872-7549. ISSN 0166-4328. OCLC 06183451. PMID 8788508. 
  54. 54.0 54.1 54.2 "Tripsit Factsheets - LSD". Tripsit. Retrieved January 7, 2020. 
  55. 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. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. PMC 3550327 . PMID 19415589. 
  56. 56.0 56.1 "Poisons Standard October 2015". Federal Register of Legislation. 
  57. "Bundesrecht konsolidiert: Gesamte Rechtsvorschrift für Suchtmittelgesetz" (in German). Rechtsinformationssystem der Republik Österreich (RIS). Retrieved November 17, 2020. 
  58. "RESOLUÇÃO DA DIRETORIA COLEGIADA - RDC N° 130, DE 2 DE DEZEMBRO DE 2016" (in Portuguese). Agência Nacional de Vigilância Sanitária (Anvisa) [National Sanitary Surveillance Agency]. December 5, 2016. Archived from the original on September 24, 2020. 
  59. "Schedule III". Controlled Drugs and Substances Act (S.C. 1996, c. 19). Government of Canada. Retrieved January 1, 2020. 
  60. "Droga, Psihotropnih Tvari I Biljaka Iz Kojih Se Može Dobiti Droga Te Tvari Koje Se Mogu Uporabiti Za Izradu Droga" (in Croatian). Ministarstvo Zdravlja [Ministry of Health] (published January 29, 2016). January 20, 2016. 
  61. Benjamin Cunningham (December 23, 2009). "New drug guidelines are Europe's most liberal". The Prague Post. Retrieved November 16, 2020. 
  62. "Samlet liste over euforiserende stoffer opført på bilag 1 til bekendtgørelsen om euforiserende stoffer nr. 557 af 31. maj 2011 og stoffer reguleret herefter via ændringsbekendtgørelser" (in Danish). Lægemiddelstyrelsen [Danish Medicines Agency]. June 13, 2018. Retrieved January 1, 2020. 
  63. "Gesetz über den Verkehr mit Betäubungsmitteln: Anlage I" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  64. "Vierte Verordnung über die den Betäubungsmitteln gleichgestellten Stoffe" (PDF). Bundesgesetzblatt Teil I: 1967 Nr. 10 (in German). Bundesanzeiger Verlag. February 24, 1967. p. 197. ISSN 0341-1095. 
  65. "Gesetz über den Verkehr mit Betäubungsmitteln: § 29" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  66. "Tabella I" (PDF) (in Italian). Ministero della Salute [Ministry of Health]. p. 11. Archived from the original (PDF) on July 13, 2019. 
  67. "麻薬及び向精神薬取締法" [Narcotic and Psychotropic Drugs Control Act] (in Japanese). 厚生労働省 [Ministry of Health, Labour and Welfare]. Retrieved August 14, 2020. 
  68. "Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem" (in Latvian). VSIA Latvijas Vēstnesis. November 10, 2005. Retrieved January 1, 2020. 
  69. Règlement grand-ducal du 26 mars 1974 établissant la liste des stupéfiants |
  70. "Opiumwet" [Opium Act] (in Dutch). Ministerie van Binnenlandse Zaken en Koninkrijksrelaties [Ministry of the Interior and Kingdom Relations]. January 1, 2020. Retrieved January 8, 2020. 
  71. "Forskrift om narkotika (narkotikaforskriften)" (in Norwegian). Lovdata. September 1, 2020. Retrieved November 17, 2020. 
  72. Glenn Greenwald (April 2, 2009). "Drug Decriminalization in Portugal: Lessons for Creating Fair and Successful Drug Policies". White Paper Series. Cato Institute. Retrieved January 7, 2020. 
  73. "Постановление Правительства РФ от 30.06.1998 N 681 "Об утверждении перечня наркотических средств, психотропных веществ и их прекурсоров, подлежащих контролю в Российской Федерации" (с изменениями и дополнениями)" (in Russian). ГАРАНТ [GARANT]. Retrieved January 8, 2020. 
  74. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  75. "Läkemedelsverkets författningssamling" (PDF) (in Swedish). Christina Rångemark Åkerman (Läkemedelsverket [Swedish Medical Products Agency]). September 21, 2011. p. 24. ISSN 1101-5225. Archived from the original (PDF) on July 22, 2019. 
  76. "Part I: Class A Drugs". "Misuse of Drugs Act 1971". UK Government. Retrieved January 7, 2020. 
  77. "Controlled Substances: by CSA Schedule" (PDF). U.S. Department of Justice. August 21, 2019. p. 5. Retrieved January 7, 2020.