Lysergic acid diethylamide
(LSD),[a] also known colloquially as acid, is a
potent psychedelic drug.[12] Effects typically include intensified thoughts, emotions, and
sensory perception.[13] At sufficiently high dosages LSD manifests primarily mental,
visual, as well as auditory, hallucinations.[14][15] Dilated pupils, increased blood pressure,
and increased body temperature are typical.[16] Effects typically begin within half an hour
and can last for up to 20 hours.[16][17] LSD is also capable of causing mystical
experiences and ego dissolution.[18][15] It is used mainly as a recreational drug or
for spiritual reasons.[16][19] LSD is both the prototypical psychedelic and one of the
"classical" psychedelics, being the psychedelics with the greatest scientific and cultural
significance.[12] LSD is typically either swallowed or held under the tongue.[13] It is most
often sold on blotter paper and less commonly as tablets, in a watery solution or
in gelatin squares called panes.[16]
LSD is considered to be non-addictive with low potential for abuse.[20][21] Frequent use
rapidly builds tolerance, requiring exponentially larger doses to feel an effect. Adverse
psychological reactions are possible, such as anxiety, paranoia, and delusions.[7] LSD is
active in small amounts relative to other psychoactive compounds with doses measured
in micrograms.[22] It is possible for LSD to induce either intermittent or chronic visual
hallucinations, in spite of no further use. Common effects include visual
snow and palinopsia. In cases where this causes distress or impairment it is diagnosed
as hallucinogen persisting perception disorder (HPPD).[23][24] While overdose from LSD is
unknown, LSD can cause injury and death as a result of accidents stemming from
psychological impairment.[16][12] The effects of LSD are thought to stem primarily from it
being an agonist at the 5-HT2A (serotonin) receptor, and while exactly how LSD exerts
its effects by agonism at this receptor is still not fully known, corresponding
increased glutamatergic neurotransmission and reduced default mode network activity
are thought to be key mechanisms of action.[21][7][12][25][26] In addition to serotonin, LSD
also binds to dopamine D1 and D2 receptors, which is why LSD tends to be more
stimulating than compounds such as psilocybin.[27][28] In pure form, LSD is clear or white
in color, has no smell, and is crystalline.[13] It breaks down with exposure to ultraviolet
light.[16]
LSD was first synthesized by Swiss chemist Albert Hofmann in 1938 from lysergic acid,
a chemical derived from the hydrolysis of ergotamine, an alkaloid found in ergot, a
fungus that infects grain.[16][23] LSD was the 25th of various lysergamides Hofmann
synthesized from lysergic acid while trying to develop a new analeptic, hence the
alternate name LSD-25. Hofmann discovered its effects in humans in 1943, after
unintentionally ingesting an unknown amount, possibly absorbing it through his skin.[29]
[30][31]
LSD was subject to exceptional interest within the field of psychiatry in the 1950s
and early 1960s, with Sandoz distributing LSD to researchers under the trademark
name Delysid in an attempt to find a marketable use for it.[30]
LSD-assisted psychotherapy was used in the 1950s and early 1960s by psychiatrists
such as Humphry Osmond, who pioneered the application of LSD to the treatment
of alcoholism, with promising results.[32][30][33][34] Osmond coined the term "psychedelic"
(lit. mind manifesting) as a term for LSD and related hallucinogens, superseding the
previously held "psychotomimetic" model in which LSD was believed to
mimic schizophrenia. In contrast to schizophrenia, LSD induces transcendental
experiences with lasting psychological benefit.[12][30] During this time, the Central
Intelligence Agency (CIA) began using LSD in the research project Project MKUltra,
which used psychoactive substances to aid interrogation. The CIA administered LSD to
unwitting test subjects in order to observe how they would react, and the most well-
known example of this is Operation Midnight Climax.[30] LSD was one of several
psychoactive substances evaluated by the U.S. Army Chemical Corps as possible non-
lethal incapacitants in the Edgewood Arsenal human experiments.[30]
In the 1960s, LSD and other psychedelics were adopted by, and became synonymous
with, the counterculture movement due to their perceived ability to expand
consciousness. This resulted in LSD being viewed as a cultural threat to American
values and the Vietnam war effort, and it was designated as a Schedule I (illegal for
medical as well as recreational use) substance in 1968.[35] It was listed as a Schedule 1
controlled substance by the United Nations in 1971 and currently has no approved
medical uses.[16] As of 2017, about 10% of people in the United States have used LSD
at some point in their lives, while 0.7% have used it in the last year.[36] It was most
popular in the 1960s to 1980s.[16] The use of LSD among US adults increased 56.4%
from 2015 to 2018.[37]
Uses[edit]
Recreational[edit]
LSD is commonly used as a recreational drug in the company of friends, in large crowds, or by
oneself.[38]
Spiritual[edit]
LSD can catalyze intense spiritual experiences and is thus considered an entheogen. Some users
have reported out of body experiences. In 1966, Timothy Leary established the League for Spiritual
Discovery with LSD as its sacrament.[39][40] Stanislav Grof has written that religious and mystical
experiences observed during LSD sessions appear to be phenomenologically indistinguishable from
similar descriptions in the sacred scriptures of the great religions of the world and the texts of
ancient civilizations.[41]
Medical[edit]
See also: Lysergic acid diethylamide § Research
LSD currently has no approved uses in medicine.[42][43] A meta analysis concluded that a single dose
was effective at reducing alcohol consumption in alcoholism.[34] LSD has also been studied in
depression, anxiety,[44][45] and drug dependence, with positive preliminary results.[46][47]
Effects[edit]
Some symptoms reported for LSD[48][49]
LSD is exceptionally potent, with as little as 20 μg capable of producing a noticeable effect.[16]
Physical[edit]
LSD can cause pupil dilation, reduced appetite, profuse sweating, and wakefulness. Other physical
reactions to LSD are highly variable and nonspecific, some of which may be secondary to the
psychological effects of LSD. Among the reported symptoms are elevated body temperature, blood
sugar, and heart rate, alongside goose bumps, jaw clenching, mouth dryness, and hyperreflexia. In
negative experiences, numbness, weakness, nausea, and tremors have also been exhibited.[16]
Psychological[edit]
The most common immediate psychological effects of LSD are visual
hallucinations and illusions (colloquially known as "trips"), which vary depending on how much is
used and how the dosage interacts with the brain. Trips usually start within 20–30 minutes of taking
LSD orally (less if snorted or taken intravenously), peak three to four hours after ingestion, and can
last up to 20 hours in high doses. Users may also experience an "afterglow" of improved mood or
perceived mental state for days or even weeks after ingestion in some experiences.[50] Good trips are
reportedly deeply stimulating and pleasurable, and typically involve intense joy or euphoria, a greater
appreciation for life, reduced anxiety, a sense of spiritual enlightenment, and a sense of belonging or
interconnectedness with the universe.[51][52] Negative experiences, colloquially known as "bad trips,"
evoke an array of dark emotions, such as irrational fear, anxiety, panic, paranoia, dread,
distrustfulness, hopelessness, and even suicidal ideation.[53] While it is impossible to predict when a
bad trip will occur, one's mood, surroundings, sleep, hydration, social setting, and other factors can
be controlled (colloquially referred to as "set and setting") to minimize the risk of a bad trip.[54][55]
Sensory[edit]
LSD causes an animated sensory experience of senses, emotions, memories, time,
and awareness for 6 to 20 hours, depending on dosage and tolerance.[17] Generally beginning within
30 to 90 minutes after ingestion, the user may experience anything from subtle changes in
perception to overwhelming cognitive shifts. Changes in auditory and visual perception are also
typical.[56][57]
Some sensory effects may include an experience of radiant or more vibrant colors, objects and
surfaces appearing to ripple, "breathe," or otherwise move, spinning fractals superimposed on one's
vision, colored patterns behind closed eyelids, an altered sense of time, geometric patterns
emerging on walls and other textured objects, and morphing objects.[56] Some users also report a
strong metallic taste for the duration of the effects.[58] Food's texture or taste may be different, and
users may also have an aversion to foods that they would normally enjoy. Similar effects have also
been found in rats.[59]
Some report that the inanimate world appears to animate in an inexplicable way; for instance,
objects that are static in three dimensions can seem to be moving relative to one or more additional
spatial dimensions.[60] Many of the basic visual effects resemble the phosphenes seen after applying
pressure to the eye and have also been studied as form constants. Sometimes these effects and
patterns can be changed when concentrated on, or can change based on thoughts, emotions or
music.[61] The auditory effects of LSD may include echo-like distortions of sounds, changes in ability
to discern concurrent auditory and visual stimuli, and a general intensification of the experience of
music. Higher doses often cause intense and fundamental distortions of sensory perception such
as synesthesia, the experience of additional spatial or temporal dimensions, and
temporary dissociation.
Adverse effects[edit]
Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and
legal services engaged in delphic analysis regarding 20 popular recreational drugs. LSD was ranked 14th in
dependence, 15th in physical harm, and 13th in social harm.[62]
Out of the 20 drugs ranked in order of individual and societal harm by David Nutt, LSD was third to
last, or approximately 1/10th as harmful as alcohol. The most significant adverse effect of LSD was
impairment of mental functioning while intoxicated.[63]
Mental disorders[edit]
LSD may trigger panic attacks or feelings of extreme anxiety, known colloquially as a "bad trip". LSD
is capable of exacerbating mental illnesses and precipitating the early onset of schizophrenia in
vulnerable individuals.[12] Although population studies have not found an increased incidence of
mental illness in psychedelic drug users overall, with psychedelic users actually having lower rates
of depression and substance abuse than the control group,[64][65] there is evidence that people with
severe mental illnesses like schizophrenia have a higher likelihood of experiencing adverse effects
from taking LSD.[66]
Flashbacks[edit]
"Flashbacks" are a reported psychological phenomenon in which an individual experiences an
episode of some of LSD's subjective effects after the drug has worn off, persisting for days or
months after hallucinogen use.[71][72] Individuals with hallucinogen persisting perception
disorder experience intermittent or chronic flashbacks that cause distress or impairment in life and
work.[24]
The etiology of the "flashback" phenomenon appears to be varied. Some researchers such as Krebs
and Johansen (2015[73]) attribute at least some of the cases to be related to somatic symptom
disorder, when people fixate on normal somatic experiences and perceptions that they weren't
aware of before consuming the drug. Other researchers relate it to an associative reaction to a
contextual cue akin to what people that have faced trauma or strongly emotional experiences face
when receiving a triggering stimulus (Holland and Passie 2011[74]). There is no consensus on what
are the risk factors but some researchers theorize that pre-existing psychopathologies may be a
significant contributor (Abraham and Duffy 1996[75])
The prevalence of HPPD is difficult to estimate but appears to be very rare (Halpern et al 2016[76]),
with estimates ranging from 1 in 20 users for the transitory and less serious type 1 HPPD, to 1 in
50,000 users for the more concerning type 2 HPPD.[77]
Contrary to rumors circulating the internet that LSD is stored in the spinal cord or other parts of your
body long-term,[78] the pharmacological evidence (Passie et all 2008[79]) shows LSD has a short half-
life of 175 minutes, undergoing enzymatic metabolism into more polar and therefore water-soluble
compounds such as 2-oxo-3-hydroxy-LSD that are eliminated through the urine. No evidence of long
term storage of LSD in the body exists.
Addiction and tolerance[edit]
Tolerance to LSD builds up with consistent use[81] and cross-tolerance has been demonstrated
between LSD, mescaline,[82] and psilocybin.[83] Researchers believe that tolerance returns to baseline
after two weeks of not using psychedelics.[84]
The NIH states that LSD is addictive,[23] while most other sources state it is not.[20][85] A 2009 textbook
states that it "rarely produce[s] compulsive use."[5] A 2006 review states it is readily abused, but does
not result in addiction.[20] There are no recorded successful attempts to train animals to self-
administer LSD in laboratory settings.[21]
Overdose[edit]
A report in 2008 stated that, though there was no "comprehensive review since the 1950s" and
"almost no legal clinical research" since the 1970s, there had been "no documented human deaths
from an LSD overdose". Eight individuals who accidentally consumed very high amounts by
mistaking LSD for cocaine developed comatose states, hyperthermia, vomiting, gastric bleeding, and
respiratory problems—all survived, however, with hospital treatment and without residual effects.
[7]
According to more recent reports, several behavioral-related fatalities and suicides have occurred
due to LSD.[86][87] Reassurance in a calm, safe environment is beneficial. Agitation can be safely
addressed with benzodiazepines such as lorazepam or diazepam. Neuroleptics such
as haloperidol are not recommended because they may have adverse effects. LSD is rapidly
absorbed, so activated charcoal and emptying of the stomach is of little benefit, unless done within
30–60 minutes of ingesting an overdose of LSD. Sedation or physical restraint is rarely required, and
excessive restraint may cause complications such as hyperthermia (over-heating)
or rhabdomyolysis.[88]
Massive doses "should be treated with supportive care, including respiratory support
and endotracheal intubation if needed. Hypertension [high blood pressure], tachycardia [rapid heart-
beat], and hyperthermia should be treated symptomatically. Hypotension [low blood pressure] should
be treated initially with fluids and subsequently with pressors if required." "Intravenous administration
of anticoagulants, vasodilators, and sympatholytics may be useful" when treating ergotism.[88]
Pharmacology[edit]
Pharmacodynamics[edit]
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
Dissociation constant of various serotonin
receptors show
Most serotonergic psychedelics are not significantly dopaminergic, and LSD is therefore atypical in
this regard. The agonism of the D2 receptor by LSD may contribute to its psychoactive effects in
humans.[28][89]
LSD binds to most serotonin receptor subtypes except for the 5-HT3 and 5-HT4 receptors. However,
most of these receptors are affected at too low affinity to be sufficiently activated by the brain
concentration of approximately 10–20 nM.[85] In humans, recreational doses of LSD can affect 5-
HT1A (Ki=1.1nM), 5-HT2A (Ki=2.9nM), 5-HT2B (Ki=4.9nM), 5-HT2C (Ki=23nM), 5-HT5A (Ki=9nM [in cloned
rat tissues]), and 5-HT6 receptors (Ki=2.3nM).[90][91] Although not present in humans, 5-
HT5B receptors found in rodents also have a high affinity for LSD.[92] The psychedelic effects of LSD
are attributed to cross-activation of 5-HT2A receptor heteromers.[93] Many but not all 5-
HT2A agonists are psychedelics and 5-HT2A antagonists block the psychedelic activity of LSD. LSD
exhibits functional selectivity at the 5-HT2A and 5HT2C receptors in that it activates the signal
transduction enzyme phospholipase A2 instead of activating the enzyme phospholipase C as the
endogenous ligand serotonin does.[94]
Exactly how LSD produces its effects is unknown, but it is thought that it works by
increasing glutamate release in the cerebral cortex[85] and therefore excitation in this area, specifically
in layers IV and V.[95] LSD, like many other drugs of recreational use, has been shown to
activate DARPP-32-related pathways.[96] The drug enhances dopamine
D2 receptor protomer recognition and signaling of D2–5-HT2A receptor complexes,[27] which may
contribute to its psychotropic effects.[27] LSD has been shown to have low affinity for H1 receptors,
displaying antihistamine effects.[97][98][99]
LSD is a biased agonist that induces a conformation in serotonin receptors that preferentially
recruits β-arrestin over activating G proteins.[100][101] LSD also has an exceptionally long residence
time when bound to serotonin receptors lasting hours, consistent with the long lasting effects of LSD
despite its relatively rapid clearance.[100][101] A crystal structure of 5-HT2B bound to LSD reveals an
extracellular loop that forms a lid over the diethylamide end of the binding cavity which explains the
slow rate of LSD unbinding from serotonin receptors.[102][103][104] The related lysergamide lysergic acid
amide (LSA) that lacks the diethylamide moiety is far less hallucinogenic in comparison.[104]
Pharmacokinetics[edit]
The effects of LSD normally last between 6 and 12 hours depending on dosage, tolerance, and age.
[105]
The Sandoz prospectus for "Delysid" warned: "intermittent disturbances of affect may
occasionally persist for several days."[106] Aghajanian and Bing (1964) found LSD had an elimination
half-life of only 175 minutes (about 3 hours).[90] However, using more accurate techniques, Papac
and Foltz (1990) reported that 1 µg/kg oral LSD given to a single male volunteer had an apparent
plasma half-life of 5.1 hours, with a peak plasma concentration of 5 ng/mL at 3 hours post-dose.[107]
The pharmacokinetics of LSD were not properly determined until 2015, which is not surprising for a
drug with the kind of low-μg potency that LSD possesses.[9][6] In a sample of 16 healthy subjects, a
single mid-range 200 μg oral dose of LSD was found to produce mean maximal concentrations of
4.5 ng/mL at a median of 1.5 hours (range 0.5–4 hours) post-administration.[9][6] Concentrations of
LSD decreased following first-order kinetics with a half-life of 3.6±0.9 hours and a terminal half-life of
8.9±5.9 hours.[9][6]
The effects of the dose of LSD given lasted for up to 12 hours and were closely correlated with the
concentrations of LSD present in circulation over time, with no acute tolerance observed.[9][6] Only 1%
of the drug was eliminated in urine unchanged, whereas 13% was eliminated as the
major metabolite 2-oxo-3-hydroxy-LSD (O-H-LSD) within 24 hours.[9][6] O-H-LSD is formed
by cytochrome P450 enzymes, although the specific enzymes involved are unknown, and it does not
appear to be known whether O-H-LSD is pharmacologically active or not.[9][6] The
oral bioavailability of LSD was crudely estimated as approximately 71% using previous data
on intravenous administration of LSD.[9][6] The sample was equally divided between male and female
subjects and there were no significant sex differences observed in the pharmacokinetics of LSD.[9][6]
Chemistry[edit]
The four possible stereoisomers of LSD. Only (+)-LSD is psychoactive.
LSD is a chiral compound with two stereocenters at the carbon atoms C-5 and C-8, so that
theoretically four different optical isomers of LSD could exist. LSD, also called (+)-D-LSD,[citation
needed]
has the absolute configuration (5R,8R). The C-5 isomers of lysergamides do not exist in nature
and are not formed during the synthesis from d-lysergic acid. Retrosynthetically, the C-5
stereocenter could be analysed as having the same configuration of the alpha carbon of the naturally
occurring amino acid L-tryptophan, the precursor to all biosynthetic ergoline compounds.
However, LSD and iso-LSD, the two C-8 isomers, rapidly interconvert in the presence of bases, as
the alpha proton is acidic and can be deprotonated and reprotonated. Non-psychoactive iso-LSD
which has formed during the synthesis can be separated by chromatography and can be isomerized
to LSD.
Pure salts of LSD are triboluminescent, emitting small flashes of white light when shaken in the dark.
[105]
LSD is strongly fluorescent and will glow bluish-white under UV light.
Synthesis[edit]
LSD is an ergoline derivative. It is commonly synthesized by reacting diethylamine with an activated
form of lysergic acid. Activating reagents include phosphoryl chloride[108] and peptide coupling
reagents.[99] Lysergic acid is made by alkaline hydrolysis of lysergamides like ergotamine, a
substance usually derived from the ergot fungus on agar plate; or, theoretically possible, but
impractical and uncommon, from ergine (lysergic acid amide, LSA) extracted from morning
glory seeds.[109] Lysergic acid can also be produced synthetically, although these processes are not
used in clandestine manufacture due to their low yields and high complexity.[110][111]
Dosage[edit]
White on White blotters (WoW) for sublingual administration
A single dose of LSD may be between 40 and 500 micrograms—an amount roughly equal to one-
tenth the mass of a grain of sand. Threshold effects can be felt with as little as 25 micrograms of
LSD.[113][114] The practice of using sub-threshold doses is called microdosing.[115] Dosages of LSD are
measured in micrograms (µg), or millionths of a gram. By comparison, dosages of most drugs, both
recreational and medicinal, are measured in milligrams (mg), or thousandths of a gram. For
example, an active dose of mescaline, roughly 0.2 to 0.5 g, has effects comparable to 100 µg
(0.0001 g) or less of LSD.[106]
In the mid-1960s, the most important black market LSD manufacturer (Owsley Stanley) distributed
LSD at a standard concentration of 270 µg,[116] while street samples of the 1970s contained 30 to
300 µg. By the 1980s, the amount had reduced to between 100 and 125 µg, dropping more in the
1990s to the 20–80 µg range,[117] and even more in the 2000s (decade).[116][118]
Reactivity and degradation[edit]
"LSD," writes the chemist Alexander Shulgin, "is an unusually fragile molecule ... As a salt, in water,
cold, and free from air and light exposure, it is stable indefinitely."[105]
LSD has two labile protons at the tertiary stereogenic C5 and C8 positions, rendering these centers
prone to epimerisation. The C8 proton is more labile due to the electron-
withdrawing carboxamide attachment, but removal of the chiral proton at the C5 position (which was
once also an alpha proton of the parent molecule tryptophan) is assisted by the inductively
withdrawing nitrogen and pi electron delocalisation with the indole ring.[citation needed]
LSD also has enamine-type reactivity because of the electron-donating effects of the indole ring.
Because of this, chlorine destroys LSD molecules on contact; even though chlorinated tap water
contains only a slight amount of chlorine, the small quantity of compound typical to an LSD solution
will likely be eliminated when dissolved in tap water.[105] The double bond between the 8-position and
the aromatic ring, being conjugated with the indole ring, is susceptible to nucleophilic attacks by
water or alcohol, especially in the presence of UV or other kinds of light. LSD often converts to "lumi-
LSD," which is inactive in human beings.[105]
A controlled study was undertaken to determine the stability of LSD in pooled urine samples.[119] The
concentrations of LSD in urine samples were followed over time at various temperatures, in different
types of storage containers, at various exposures to different wavelengths of light, and at varying pH
values. These studies demonstrated no significant loss in LSD concentration at 25 °C for up to four
weeks. After four weeks of incubation, a 30% loss in LSD concentration at 37 °C and up to a 40% at
45 °C were observed. Urine fortified with LSD and stored in amber glass or nontransparent
polyethylene containers showed no change in concentration under any light conditions. Stability of
LSD in transparent containers under light was dependent on the distance between the light source
and the samples, the wavelength of light, exposure time, and the intensity of light. After prolonged
exposure to heat in alkaline pH conditions, 10 to 15% of the parent LSD epimerized to iso-LSD.
Under acidic conditions, less than 5% of the LSD was converted to iso-LSD. It was also
demonstrated that trace amounts of metal ions in buffer or urine could catalyze the decomposition of
LSD and that this process can be avoided by the addition of EDTA.
Detection[edit]
LSD may be quantified in urine as part of a drug abuse testing program, in plasma or serum to
confirm a diagnosis of poisoning in hospitalized victims or in whole blood to assist in a forensic
investigation of a traffic or other criminal violation or a case of sudden death. Both the parent drug
and its major metabolite are unstable in biofluids when exposed to light, heat or alkaline conditions
and therefore specimens are protected from light, stored at the lowest possible temperature and
analyzed quickly to minimize losses.[120]
Maximum plasma concentrations were found to be 1.4 and 1.5 hours after oral administration of
100µg and 200µg respectively with a plasma half-life of 2.6 hours (ranging from 2.2–3.4 hours
among 40 human test subjects).[121]
LSD can be detected using an Ehrlich's reagent and a Hofmann's reagent.
History[edit]
... affected by a remarkable restlessness, combined with a slight dizziness. At home I lay down and sank into a not unpleasant
intoxicated-like condition, characterized by an extremely stimulated imagination. In a dreamlike state, with eyes closed (I found
the daylight to be unpleasantly glaring), I perceived an uninterrupted stream of fantastic pictures, extraordinary shapes with
intense, kaleidoscopic play of colors. After some two hours this condition faded away.
—Albert Hofmann, on his first experience with LSD[122]
Main article: History of lysergic acid diethylamide
LSD was first synthesized on November 16, 1938[123] by Swiss chemist Albert Hofmann at the Sandoz
Laboratories in Basel, Switzerland as part of a large research program searching for medically
useful ergot alkaloid derivatives. The abbreviation "LSD" is from the German
"Lysergsäurediethylamid".[124]
LSD's psychedelic properties were discovered 5 years later when Hofmann himself accidentally
ingested an unknown quantity of the chemical.[125] The first intentional ingestion of LSD occurred on
April 19, 1943,[126] when Hofmann ingested 250 µg of LSD. He said this would be a threshold dose
based on the dosages of other ergot alkaloids. Hofmann found the effects to be much stronger than
he anticipated.[127] Sandoz Laboratories introduced LSD as a psychiatric drug in 1947 and marketed
LSD as a psychiatric panacea, hailing it "as a cure for everything from schizophrenia to criminal
behavior, 'sexual perversions', and alcoholism."[128] Sandoz would send the drug for free to
researchers investigating its effects.[29]
Albert Hofmann in 2006
5:29
'Effects of Lysergic Acid Diethylamide (LSD) on Troops Marching' – 16mm film produced by the United States
military circa 1958
Beginning in the 1950s, the US Central Intelligence Agency (CIA) began a research program code
named Project MKUltra. The CIA introduced LSD to the United States, purchasing the entire world's
supply for $240,000 and propagating the LSD through CIA front organizations to American hospitals,
clinics, prisons and research centers.[129] 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. The
project was revealed in the US congressional Rockefeller Commission report in 1975.
In 1963, the Sandoz patents on LSD expired[117] and the Czech company Spofa began to produce the
substance.[29] Sandoz stopped the production and distribution in 1965.[29]
Several figures, including Aldous Huxley, Timothy Leary, and Al Hubbard, had begun to advocate
the consumption of LSD. LSD became central to the counterculture of the 1960s.[130] In the early
1960s the use of LSD and other hallucinogens was advocated by new proponents of consciousness
expansion such as Leary, Huxley, Alan Watts and Arthur Koestler,[131][132] and according to L. R.
Veysey they profoundly influenced the thinking of the new generation of youth.[133]
On October 24, 1968, possession of LSD was made illegal in the United States.[134] 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.[135]
In November 2020, Oregon became the first US state to decriminalize possession of small amounts
of LSD after voters approved Ballot Measure 110.
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