In a double-session, within-subjects study of 20 healthy volunteers, intravenous LSD (75 µg) produced acute psychosis‑like symptoms alongside heightened mood but led to increased optimism and trait openness two weeks later without raising delusional thinking. The authors propose that 5‑HT2A‑mediated increases in cognitive flexibility produce transient emotional lability during intoxication and leave a mid‑term “loosened cognition” that supports improved psychological wellbeing.
Background
Lysergic acid diethylamide (LSD) is a potent serotonergic hallucinogen or psychedelic that modulates consciousness in a marked and novel way. This study sought to examine the acute and mid-term psychological effects of LSD in a controlled study.
Method
A total of 20 healthy volunteers participated in this within-subjects study. Participants received LSD (75µg, intravenously) on one occasion and placebo (saline, intravenously) on another, in a balanced order, with at least 2 weeks separating sessions. Acute subjective effects were measured using the Altered States of Consciousness questionnaire and the Psychotomimetic States Inventory (PSI). A measure of optimism (the Revised Life Orientation Test), the Revised NEO Personality Inventory, and the Peter's Delusions Inventory were issued at baseline and 2 weeks after each session.
Results
LSD produced robust psychological effects; including heightened mood but also high scores on the PSI, an index of psychosis-like symptoms. Increased optimism and trait openness were observed 2 weeks after LSD (and not placebo) and there were no changes in delusional thinking.
Conclusions
The present findings reinforce the view that psychedelics elicit psychosis-like symptoms acutely yet improve psychological wellbeing in the mid to long term. It is proposed that acute alterations in mood are secondary to a more fundamental modulation in the quality of cognition, and that increased cognitive flexibility subsequent to serotonin 2A receptor (5-HT2AR) stimulation promotes emotional lability during intoxication and leaves a residue of ‘loosened cognition’ in the mid to long term that is conducive to improved psychological wellbeing.
Papers cited by this study that are also in Blossom
Bogenschutz, M. P., Forcehimes, A. A., Pommy, J. A. et al. · Journal of Psychopharmacology (2015)
Bouso, J. C., González, D., Fondevila, S. et al. · PLOS ONE (2012)
Rodríguez-Fornells, A., Ribeiro, S., Sanches, R. F. et al. · European Neuropsychopharmacology (2015)
Carhart-Harris, R. L., Brugger, S., Nutt, D. J. et al. · Journal of Psychopharmacology (2013)
Psychedelic lysergic acid diethylamide (LSD) produces profound, unusual alterations in consciousness and historically has been described both as a model of psychosis and as a therapeutic adjunct. Early clinical use in the 1950s and 1960s explored LSD for 'analytical' psychotherapy and for experimentally modelling psychoses, but research largely ceased in the late 1960s. More recent controlled studies with other classic psychedelics have revived interest by reporting a paradox: acute experiences often contain distressing or psychosis-like elements yet can be followed by durable improvements in wellbeing and personality (for example, increased openness and optimism in healthy volunteers and clinical benefits in addiction and anxiety contexts). Population studies and meta-analyses have not found strong evidence that psychedelic exposure increases long-term mental-health problems when screening and set/setting are adequate. Carhart-Harris and colleagues designed the present study to examine this apparent paradox directly for LSD in healthy volunteers. The stated aim was to measure both acute subjective effects and mid-term (2-week) psychological outcomes after a single controlled administration, using validated instruments to quantify altered states, psychotomimetic symptoms, optimism, personality traits and delusional thinking. The authors hypothesised that LSD would produce emotional lability and psychosis-like symptoms acutely, but would increase psychological wellbeing and trait openness at the 2-week follow-up.
The study used a placebo-controlled, within-subjects crossover design with balanced dosing order. Twenty healthy volunteers were recruited and each attended a screening visit and two dosing sessions separated by at least 2 weeks. Participants were blind to session order; the research team was not, and dosing order was assigned sequentially so that odd-numbered recruits received LSD in session 1 and even-numbered recruits in session 2. The study was conducted under institutional and regulatory approvals and followed Good Clinical Practice. Eligibility screening excluded people younger than 21, those with diagnosed psychiatric illness or a first-degree family history of psychosis, individuals without prior experience of classic psychedelics, pregnancy, problematic alcohol use, or other medically significant conditions. Screening procedures included routine blood tests, ECG, vital signs and a brief neurological exam. All enrolled participants were judged physically and mentally healthy and had no histories of dependence. On dosing days participants arrived in the morning, provided urine samples and were prepared for administration; a cannula was placed. The dose described in the extracted text was 75 µg of LSD; however, the extraction contains inconsistent statements about route and infusion (some passages state intravenous administration and infusion over 2 minutes, others state oral administration). Because the extraction is unclear on this point, the exact route and infusion procedure cannot be definitively reconstructed from the provided text. After dosing, participants underwent a neuroimaging protocol (mock scanner habituation, MRI at ≈1 h post-dose, then MEG at ≈3.5 h post-dose) followed by behavioural and cognitive testing later in the day. A psychiatrist and a dedicated researcher attended each participant throughout dosing; the same researcher accompanied each volunteer for both sessions. Participants completed acute subjective measures at the end of each dosing day and mid-term measures electronically at baseline and 2 weeks after each session. Primary acute outcomes were the Altered States of Consciousness questionnaire (ASC) and the Psychotomimetic States Inventory (PSI), completed with reference to peak effects or overall experience. Mid-term outcomes at 2 weeks included the Revised Life Orientation Test (LOT-R) for optimism, the Revised NEO Personality Inventory (NEO PI-R) for personality traits, and the Peters' Delusions Inventory (PDI) for delusional thinking. Additional baseline measures included the Beck Depression Inventory, QIDS, STAI, Ruminative Response Scale, Dysfunctional Attitudes Scale and a modified Tellegen Absorption Scale. For analysis, repeated-measures ANOVAs tested between-condition differences on multi-factor instruments (ASC, PSI, PDI). Predicted changes in NEO openness were tested with a paired t test; other NEO domains were examined with paired t tests and Bonferroni correction. The LOT-R was analysed with a paired t test. Order was included as a factor where relevant, effect sizes (Cohen's d) were reported for primary outcomes, and Pearson correlations (two-tailed) were used for predictor analyses, with Bonferroni correction applied for multiple comparisons.
Acute subjective effects: Repeated-measures ANOVA indicated a strong drug effect on altered states (F1,19 = 82.6, p < 0.001) and a significant drug × ASC interaction (F1,19 = 10.3, p < 0.001). Post-hoc tests showed all 11 ASC dimensions were significantly higher after LSD than after placebo (p < 0.01). Visual-perceptual changes (elementary and complex imagery, audio–visual synaesthesia) were prominent, but positive-affect ratings were also elevated: the ASC 'blissful state' factor increased by +0.37 (S.D. = 0.28, Cohen's d = 1.65), while the 'anxiety' factor increased by +0.15 (S.D. = 0.2, Cohen's d = 1.03). PSI scores indicated substantial psychotomimetic effects, with a mean total PSI score of 45.8 (S.D. = 21) under LSD. Mid-term effects (2 weeks): Optimism (LOT-R) increased significantly two weeks after LSD (t = 2.91, df = 18, p = 0.005, Cohen's d = 0.56). Trait openness (NEO PI-R) also increased (t = 1.95, df = 19, p = 0.03, Cohen's d = 0.16). No comparable changes in optimism or personality were observed after placebo. There was an exploratory trend towards increased agreeableness post-LSD (t = 2.2, p = 0.038, Cohen's d = 0.21) that did not survive correction for multiple comparisons (corrected p = 0.15). Peters' Delusions Inventory scores showed no significant change at 2 weeks (p > 0.05); exploratory trends suggested possible reductions in distress and preoccupation related to delusional thoughts (p ≈ 0.07), but these were not significant. Predictors: Several baseline and acute variables correlated with mid-term changes, but none of these correlations survived correction for multiple comparisons. Baseline agreeableness correlated negatively with increases in optimism (r = -0.56, p = 0.014), and baseline depression and anxiety correlated positively with increases in openness (r = 0.53, p = 0.024; r = 0.49, p = 0.04). Acute anxiety correlated negatively with post-LSD increases in optimism (r = -0.47, p = 0.04). Conversely, impaired/disorganized cognition scores on the ASC and PSI correlated positively with later increases in openness (ASC r = 0.44, p = 0.049; PSI r = 0.52, p = 0.019). The authors report that these associations did not meet significance after applying the stricter corrected thresholds.
Carhart-Harris and colleagues interpret the data as supporting the paradoxical profile of LSD: potent acute psychotomimetic and perceptual effects co-occurring with predominantly positive mood in many participants, followed by modest but significant mid-term increases in optimism and openness without increases in delusional thinking. The PSI results are emphasised as indicating stronger psychosis-like effects with LSD than have been observed with ketamine, THC or cannabis in prior comparisons cited by the authors; for context, the paper reports previously published mean PSI totals of 24 (ketamine), 15.9 (THC) and 33.3 (cannabis), versus 45.8 in the present LSD sample. Still, group-level mood effects skewed positive: the ASC 'blissful state' scores exceeded 'anxiety' scores, and previous controlled work with LSD has reported MDMA-like positive mood effects. The authors acknowledge several limitations. Follow-up duration was relatively short (2 weeks) though longer-term follow-up was planned. The study was single-blind: participants were blind to order but the research team was aware, and the authors note that double-blinding is challenging in psychedelic research because the blind is often ineffective. An inert placebo was used to provide a clear baseline for neuroimaging contrasts, but the lack of an active placebo may have reduced the effectiveness of blinding. The neuroimaging procedures (MRI and MEG sessions) required by the protocol could have been demanding and may have influenced acute subjective reports; the authors note that the scanner environment might have contributed to the especially high PSI scores. For mechanism, the discussion centres on serotonin 2A receptor (5-HT2A R) agonism as central to psychedelic pharmacology. The authors outline a hypothesis in which 5-HT2A R stimulation increases cognitive flexibility and induces a transient 'entropic' or disordered mode of brain function. This elevated cognitive entropy could underlie both the positive (e.g. enhanced imagination, euphoric states) and negative (e.g. anxiety, psychosis-like symptoms, impaired concentration) features of the acute state. They propose that an acute 'blast' of 5-HT2A R stimulation leaves a residual loosening of cognition and brain network dynamics that may facilitate improved psychological wellbeing in the mid to long term. The paper notes that 5-HT2A R antagonists (for example ketanserin) attenuate both the positive mood and the psychotomimetic effects of classic psychedelics, consistent with a central role for this receptor. Finally, the authors position their findings relative to previous literature showing enduring personality and wellbeing changes after psychedelics and suggest that deficient 5-HT2A R stimulation may relate to rigid, pessimistic modes of cognition observed in conditions such as depression. They indicate plans to report detailed neuroimaging results in subsequent papers and to pursue longer-term psychological and brain follow-up studies. The discussion closes by reiterating the main empirical outcomes: robust acute psychosis-like but also positive subjective effects after LSD, with increased optimism and openness and no rise in delusional thinking at two weeks, and by proposing the entropic brain/5-HT2A R framework as a mechanistic account.
Lysergic acid diethylamide (LSD) is a potent serotonergic hallucinogen or 'psychedelic' that alters consciousness in a marked and unusual way. The drug was first intentionally consumed by the Swiss chemist Albert Hofmann in 1943 in a self-experiment in which he ingested 250 µg (a high dose) in his laboratory before travelling home. In a detailed report of his experience, written a few days later, Hofmann describes an initially unpleasant experience, characterized by altered perception, fear and paranoia: his next-door neighbour transformed into a 'malevolent, insidious witch with a coloured mask', he sensed a 'disintegration of the outer world', a 'dissolution of [his] ego' and was 'seized by a dreadful fear of going insane'. From this account, it would be reasonable to suspect that Dr Hofmann was negatively affected by this experience but his description of his mental state the next day suggests otherwise: 'I then slept, to awake the next morning with a clear head. . . A sensation of wellbeing and renewed life flowed through me. Breakfast tasted delicious and gave me extraordinary pleasure. When I later walked out into the garden, in which the sun shone now after a spring rain, everything glistened and sparkled in a fresh light. The world was as if newly created.'When LSD was first distributed by Sandoz pharmaceuticals in 1948, product guidelines stipulated two main applications: (1) analytical psychotherapy and (2) experimental studies on psychoses. The rationale for the former was that LSD could 'elicit [the] release of repressed material and provide mental relaxation for anxiety and obsessional neuroses', and, for the latter, that it could model aspects of psychosis and facilitate an understanding of its nature and pathogenesis. These two properties formed the basis of a large number of research projects with LSD in the 1950s and 1960s. However, the apparent paradox by which the same compound can be both a model of, and yet a treatment for, psychopathology has never been properly addressed. In the early years of research with LSD, its remarkable potency (LSD is psychoactive in doses of 25 µg or lower;) led psychiatrists to speculate about the existence of an endogenous LSD-like 'schizotoxin' in the brains of patients with schizophrenia. In subsequent years, however, focus shifted more onto therapeutic applications, such as treating alcohol dependence, mood disorders and anxiety related to dying. Human research with LSD was brought to a halt in the late 1960s due to political pressure, motivated in part by reports of adverse psychological reactions among people using the drug improperly. Ironically, however, at the same time, reports of therapeutic success in the treatment of various psychiatric disorders were beginning to amount). In the last 18 months, five new reports on clinical research with LSD have appeared in the scientific press, one of which focused on the drug's therapeutic effectsand, another, its psychotomimetic effects. Clinical research with psychedelics is currently undergoing a major revival and modern studies are documenting the same paradoxical properties that were historically described with LSD. For example, in a controlled study in healthy volunteers, high-dose psilocybin produced strong or extreme fear in 30% of healthy volunteers and yet 80% reported improvements in wellbeing after the experience, with none reporting any decreases. Remarkably, in follow-up of the same sample, 65% reported improved wellbeing 14 months after their (single) psilocybin experienceand significant increases in the personality trait openness were also evident. These finding in healthy volunteers are supplemented by an increasing number of patient studies. Clinical improvements have been observed with psilocybin-assisted psychotherapy for the treatment of tobacco) and alcohol addiction, obsessive-compulsive disorderand anxiety related to dying. Many of these reports mention some psychological discomfort during the acute experience; yet, the therapeutic benefits have been impressive and enduring. Case reports of persistent psychological problems apparently precipitated by a psychedelic have considerable potential to excite alarm. However, such cases are rare and largely restricted to recreational use. Evidence does not support the view that psychedelics are harmful to mental health. Indeed, to the contrary, two recent population studies found decreased rates of suicidality and psychological distress among persons reporting previous use of psychedelicsand no evidence of any increased rates of mental health problems. Similarly, large meta-analyses of controlled research have found that cases of mental health complications following exposure to a psychedelic are extremely rare (i.e. <0.1%), even in vulnerable populations (i.e. <0.2%), and are rarer still if volunteers are properly screened. The main aim of the present study was to investigate the acute and 'mid-term' (i.e. 2 weeks after the acute experience) psychological effects of LSD in a placebocontrolled study in healthy volunteers. Validated measures of personality, optimism and psychotic symptoms were collected at baseline and 2 weeks post-LSD/placebo and measures of mood, cognition and psychotomimetic states were collected at the end of each dosing day. It was predicted that LSD would induce emotional lability and psychosis-like symptoms acutely but increase psychological wellbeing and openness in the longer term.
This was a placebo-controlled, within-subjects/crossover study, with a balanced-order design. A total of 20 healthy volunteers were recruited to the study via word of mouth. The study received a favourable opinion from NRES Committee London -West London and was conducted in accordance with Good Clinical Practice guidelines, NHS Research Governance Framework and complied with the ethical standards of the declaration of. Imperial College London sponsored the research and a Home Office license was obtained for research with schedule one drugs. All volunteers were sent a study information sheet and asked to read it before their screening visit. Volunteers made three study visits: screening, dosing session 1 and dosing session 2. Dosing sessions were separated by at least 2 weeks in every case and the order of receipt of LSD was balanced, i.e. half of the volunteers received LSD in dosing session 1 and half in dosing session 2. Volunteers were blind to the dosing order but the research team was not. Dosing order was determined sequentially so that all oddnumbered volunteers (i.e. S1 was the first volunteer recruited and S20 was the last) received LSD in dosing session 1, whereas all even-numbered volunteers received it in dosing session 2. Subjective ratings were completed electronically and remotely soon after screening (baseline) and 2 weeks after a dosing session and sent to the researchers via email. Volunteers were instructed to complete the questionnaires in a quiet space without rushing. Two questionnaires pertaining to the acute drug experience were completed electronically within the research centre at the close of dosing days.
Prior to study enrolment, volunteers attended a screening visit at the Imperial Clinical Research Facility (ICRF) at the Hammersmith Hospital in West London. The study design, procedures and psychological effects of LSD were explained and signed informed consent taken. Key exclusion criteria were: <21 years of age, personal history of diagnosed psychiatric illness, immediate family history of a psychotic disorder, an absence of previous experience with a classic psychedelic drug (e.g. LSD, mescaline, psilocybin/magic mushrooms or dimethyltryptamine/ayahuasca), pregnancy, problematic alcohol use (assessed via psychiatric interview and reported weekly units), or a medically significant condition rendering the volunteer unsuitable for the study. The decision to recruit only individuals with prior experience with psychedelics was motivated by safety considerations, i.e. to minimize the risk of an adverse response to the drug. Screening involved routine blood tests, electrocardiogram, heart rate, blood pressure and a brief neurological examination. All enrolled participants were deemed physically and mentally healthy by the study psychiatrist, and none had histories of drug or alcohol dependence or diagnosed psychiatric disorder. Volunteers were asked to remain abstinent from alcohol the evening before a dosing day and to refrain from using other recreational drugs for the duration of the study.
Participants were asked to arrive at the study centre (Cardiff University's Brain Research Imaging Centre, CUBRIC) at a specific time at or before 09.00 hours. A urine test for drugs of abuse and pregnancy (where relevant) was carried out. Participants were re-briefed about the procedures for the day and any recent drug and alcohol use was documented. The study physician inserted a cannula into a vein in the antecubital fossa in preparation for intravenous (i.v.) dosing and the volunteer was encouraged to relax prior to drug/placebo administration. The dose of LSD was 75 µg (by mouth; p.o.) in 10 ml saline. Previous research has found this dose to produce robust psychological effects that are generally well tolerated. Placebo was 10 ml saline (i.v.). Both solutions were infused over 2 min. After dosing, volunteers completed a functional neuroimaging protocol. This aspect of the study will be covered in detail in separate publications. In brief, subjects spent a period habituating to a scanner environment in a mock magnetic resonance imaging (MRI) scanner before entering a real MRI scanner (1 h postdosing). The MRI scanning session lasted for 1 h after which a structured interview was performed and some ratings completed. Participants entered a magnetoencephalography (MEG) scanner approximately 3.5 h post-dosing. MEG scanning lasted for just over 1 h. Participants were then interviewed and completed a battery of cognitive and behavioural tests (these will be detailed in a separate publication). Tasks were completed 6-7 h post-dosing. The subjective effects of LSD were detected approximately 10 min post-infusion, peaked approximately 120 min post-infusion, and subsided to a negligible level approximately 7-8 h post-infusion. Participants were discharged by the study physician when they were considered to be functioning normally. Volunteers were either picked up by a friend or partner, ordered a taxi, or accompanied home by the research team as far as was feasible. Volunteers were asked to contact a researcher via telephone or text message once they had arrived home safely. A study psychiatrist was present for the duration of each dosing session and one researcher was allocated to each participant to assist them throughout the day. For each participant, the same researcher was present for both dosing days.
Participants completed two questionnaires at the end of each study day before being discharged by the study physician. These questionnaires enquired about different aspects of the subjective experience. The first was the Altered States of Consciousness questionnaire (ASC), a well validated and widely used tool for defining different altered states of consciousness that has been usefully revised in recent years) and the second was the Psychotomimetic States Inventory (PSI), a tool developed to probe the psychotomimetic effects of different drugs. Participants were asked to complete the questionnaires with reference to the peak subjective effects of LSD (i.e. when the effects were most intense) or with reference to how they generally felt throughout the daye.g. if they did not notice any effects.
Mid-term outcomes were completed 2 weeks after each dosing session (as well as at baseline) and these included: the Revised Life Orientation Test (LOT-R;, the Revised NEO Personality Inventory (NEO PI-R;and Peters' Delusions Inventory (PDI;). The LOT-R was chosen as it is a well-validated measure of trait or dispositional optimism, the NEO PI-R was chosen as it is well-validated and previous research has shown its sensitivity to the enduring effects of psychedelics (MacLean et al. 2011), and the PDI was chosen as it is a well-validated measure of delusional thinking that has shown to be sensitive to psychotic-like symptoms in the general population.
Additional questionnaires completed at baseline included the Beck Depression Inventory (BDI;, the Quick Inventory of Depressive Symptomatology (QIDS;, the State-Trait Anxiety Inventory (STAI;, the Ruminative Response Scale (RRS;, the Dysfunctional Attitudes Scale (DAS;) and the modified version of the Tellegen Absorption Scale (MODTAS;.
Repeated-measures analyses of variance (ANOVAs) were used to test between-condition differences in the ASC, PSI and PDI, which have multiple factors. However, since a strong prior hypothesis was held that the personality trait 'openness' would be significantly increased post-LSD (MacLean et al. 2011), this was analysed using a paired t test rather than an ANOVA. The remaining four personality dimensions in the NEO PI-R were analysed using paired t tests with Bonferonni correction for multiple comparisons. A paired t test was used to analyse changes in the LOT-R, as this has only one dimension. To test for order confounds in relation to primary outcomes, order was included as a variable in significant tests, and to further test for the influence of placebo/participation, baseline versus 2 weeks post-placebo differences in outcomes were tested for those who received placebo in their first dosing session (potential carryover effects of LSD precludes the inclusion of those who received placebo in their second dosing session). Effect sizes (Cohen's d) were calculated for primary outcomes. For correlational analyses, Pearson productmoment coefficients were calculated and two-tailed hypotheses tested. The problem of multiple comparisons was accounted for by Bonferonni correction.
A repeated-measures ANOVA revealed a significant main effect of drug (F 1,19 = 82.6, p < 0.001) and a significant drug × ASC interaction (F 1,19 = 10.3, p < 0.001). Post-hoc t tests revealed that all 11 dimensions or factors of the ASC were rated significantly higher after LSD than placebo (p < 0.01). Mean scores for each factor are displayed in the radar chart in Fig.. It is notable that although the LSD experience was dominated by changes in visual perception (i.e. elementary imagery, complex imagery and audio-visual synaesthesia), the factor 'blissful state' was markedly elevated under the drug (+0.37, S.D. = 0.28, Cohen's d = 1.65). Although still significantly increased, the factor 'anxiety' was the least elevated under LSD (+0.15, S.D. = 0.2, Cohen's d = 1.03). These results indicate a marked increase in emotional arousal and lability under LSD but with a distinct bias towards positive affect. Reinforcing this, a t test revealed that increases in
Optimism was significantly increased 2 weeks after LSD (t = 2.91, df = 18, p = 0.005, Cohen's d = 0.56), as was trait openness (t = 1.95, df = 19, p = 0.03, Cohen's d = 0.16) (Fig.), and there were no such changes in optimism or personality post-placebo. In exploratory t tests, there was a trend towards an increase in trait agreeableness post-LSD (t = 2.2, df = 19, p = 0.038, Cohen's d = 0.21); however, this did not survive correction for multiple comparisons [corrected p = 0.15]. Repeated-measures ANOVA found no change in delusional thinking (PDI scores) 2 weeks after LSD (p > 0.05). In fact, exploratory t tests suggested a trend towards less distress (t = 1.92, df = 19, p = 0.068) and preoccupation with 'delusional thoughts' (t = 1.92, df = 19, p = 0.07) but these trends were not significant, even before correction for multiple comparisons. There were no changes in PDI scores post-placebo.
Regarding baseline predictors of the mid-term effects of LSD, focus was placed on personality (as measured by the NEO PI-R), depression (measured by the QIDS) and anxiety (measured by the STAI). A negative correlation was found between baseline agreeableness and increases in optimism post-LSD (r = -0.56, r 2 = 0.31, p = 0.014) and positive correlations were found between baseline depression (r = 0.53, r 2 = 0.28, p = 0.024) and anxiety (r = 0.49, r 2 = 0.24, p = 0.04) and the post-LSD increases in openness. However, none of these survived correction for multiple comparisons (revised p = 0.05/7 = 0.007). Regarding acute predictors of the mid-term effects of LSD, there was a negative correlation between acute anxiety (ASC) and post-LSD increases in optimism (r = -0.47, r 2 = 0.22, n = 19, p = 0.04) and positive correlations between impaired/disorganized cognition scores on the ASC and PSI and post-LSD increases in openness (ASC: r = 0.44, r 2 = 0.2, n = 20, p = 0.049; PSI: r = 0.52, r 2 = 0.26, n = 20, p = 0.019) but these correlations also failed to survive correction for multiple comparisons (revised p = 0.5/17 = 0.003).
The primary aim of this study was to investigate the acute and mid-term subjective effects of LSD in a controlled study in order to advance our understanding of its psychological effects. It was hypothesized that LSD would increase emotional lability and psychosis-like symptoms acutely, and increase optimism and openness 2 weeks later, and these hypotheses were supported by the data. Focusing first on LSD's acute effects, scores on the PSI reinforce the view that LSD is a potent psychotomimetic. Previous studies have examined PSI scores after sleep deprivation, dreaming, cannabis, tetrahydrocannabinol (THC)) and ketamine intoxication. Although both dreaming and sleep deprivation elevated subscales of the PSI, only the aforementioned drugs produced appreciable psychosis-like symptomsand still not to the same extent as LSD in the present study. For example, mean total scores on the PSI were 24 (S.D. = 10.9) post-ketamine infusion (150 mg/ml plasma), 15.9 (S.D. = 11) post-THC (10 mg, p.o.) and 33.3 (S.D. = 19.5) post-cannabis use (smoked, quantity unknown), whereas the mean total PSI score in the present study was 45.8 (S.D. = 21). To our knowledge, only cannabis in highly schizotypal individuals) has produced PSI scores of an equivalent magnitude to those seen here with LSD. More generally, relatively strong subjective effects were produced by the present dose of LSD (i.e. 75 µg, i.v.) as indexed by the ASC. In previous studies, psilocybin (115-350 µg/kg, p.o.), MDMA (1.5-1.7 mg/kg, p.o.) and ketamine (6-12 µg/kg per min, i.v.) produced effects of a lower magnitude than those seen herebut in a recent study with 200 µg LSD (p.o.), ASC scores were of a similar magnitude to those observed here. With the PSI results in mind, it is worth briefly discussing the relative merits of different drug models of psychosis. Ketamine is often described as an especially meritorious model of psychosis because it can induce both positive and negative symptoms. However, the premise that negative symptoms can be modelled by an acute drug state is questionable. For example, it has been argued that negative symptoms are non-specific for psychosis (i.e. they are also prevalent in depression;. Positive symptoms are specific for psychosis, but comparison studies have suggested that these are better modelled by classic psychedelics than ketamine. Others have shown that THC is a particularly potent inducer of positive psychotic symptoms. Thus, future studies might compare the psychotomimetic properties of THC, ketamine and a classic psychedelic in a controlled, cross-over design to systematically assess the relative value of these different models. Based on the PSI results, one might infer that participants' acute LSD experiences were dominated by unpleasant psychosis-like phenomena; however, this was not the case. Some volunteers did show frank psychotic phenomena during their LSD experiences (e.g. paranoid and delusional thinking) but at the group level, positive mood was more common. For example, scores on the (positively valenced) 'blissful experience' dimension of the ASC were significantly higher than scores on the (negatively valenced) 'anxiety' dimension. Consistent with the view that LSD is more likely to produce positive than negative mood, a separate study with LSD (200 µg, p.o.) reported marked Values are the mean scores plus the positive standard errors of the mean (S.E.M.) for each of the six factors of the PSI, plus the total score (which is a sum of the scores of the six factors). All factors, except for anhedonia, were scored significantly higher under LSD than placebo. positive mood effects, described as 'MDMA-like'; an important caveat, however, is that both the Schmid et al. study and the present one recruited volunteers with previous experience with psychedelics. Thus, positive prior experiences and positive regard towards LSD may have biased outcomes. The findings that optimism and openness are increased 2 weeks after LSD are consistent with previous findings, suggesting that improved psychological wellbeing and increased openness are relatively reliable mid-to long-term effects of psychedelics. That there were no increases in psychotic symptomatology at the 2 week end point is also consistent with reports of preserved or even improved mental health among populations of people that have used psychedelic drugs. These results are also consistent with previous findings that psychedelics can be useful in treating certain psychiatric disordersas well as the notion that they may have therapeutic potential in the treatment of mood disorders such as depression. High dispositional optimism is associated with a range of positive health and socio-economic outcomes; thus, the increases in optimism observed here may be treated as further evidence of the therapeutic potential of psychedelic drugs. A limitation of the present study was the relatively short duration of the follow-up period (i.e. 2 weeks); however, longer-term follow-up is planned and 2 weeks is still relevant when considering potential therapeutic applications. Another limitation is the single-blind design; however, the classic double-blind model can feel contrived in the context of controlled studies with psychoactive compounds such as LSD, since the blind is almost universally ineffective. A single-blind design allowed us to introduce some uncertainty, however, and so was considered better than an entirely open-label design. The inclusion of an 'active placebo' condition might improve the ineffectiveness of the blind in studies with psychedelics; however, an inert placebo was required in the present study in order to provide a valid baseline for the neuroimaging contrasts. Related to this, a final limitation is that the LSD and placebo sessions involved MRI and MEG scans that each lasted for over 60 min. Brain imaging environments can be demanding for some individuals, particularly under the influence of psychedelics. Individuals are known to be especially sensitive to the environment in which they experience the effects of a psychedelic, and so the drug plus scanner combination may have contributed to the especially high PSI scores observed here with LSD. With these caveats entered, it is important to attempt an explanation of how LSD can be both acutely psychotomimetic and yet psychologically beneficial in the mid to long term, and insights from neurobiology may be helpful in this regard. There is a consensus that serotonin 2A receptor (5-HT 2A R) agonism is central to the psychopharmacology of psychedelics, e.g. affinity for the 5-HT 2A R correlates strongly with their potencies, and pre-treatment with a 5-HT 2A R antagonist effectively abolishes the classic 'psychedelic' effects of psilocybin ). Both optimism and openness were significantly increased after LSD. There was no effect of order of receipt of LSD nor were there any changes in optimism or personality 2 weeks after receipt of placebo. LOT-R, Revised Life Orientation Test; NEO PI-R, Revised NEO Personality Inventory.. The principal psychological purpose or function of the 5-HT 2A R is poorly understood; however, it is known that 5-HT 2A R stimulation promotes certain aspects of learningand cognition. Specifically, 5-HT 2A R stimulation enhances the flexibility of cognition, which may be related to reports of enhanced imagination) and creative thinkingwith psychedelics. Interestingly, an association has been found between positive mood and flexible, creative thinking) and this may explain why both are associated with psychedelics. Indeed, the positive mood effects of psilocybin (a direct 5-HT 2A R agonist) and MDMA (a potent serotonin 'releaser') are significantly attenuated by pretreatment with the 5-HT 2A R antagonist ketanserin. Psychedelics also transiently impair certain aspects of cognition, however, such as the ability to focus and concentrate, which is consistent with the high ratings of impaired cognition in the present study (Figs.and). It is also important to acknowledge that while 5-HT 2A R antagonism attenuates the positive mood effects of psilocybin (and MDMA), it also attenuates the positive psychotic symptoms that can be produced by the drug) and 5-HT 2A R agonism has been linked with anxiety-related behaviours in rodents. Thus, 5-HT 2A R stimulation has been associated with both positive and negative facets of the acute psychedelic state (i.e. positive mood but also anxiety and psychotic symptoms), so how can we reconcile these things with each other? Is there a more fundamental action of psychedelics that can explain both effects? As reported above, 5-HT 2A R stimulation has been associated with enhanced cognitive flexibility, and inspired by recent neuroimaging findings, the psychedelic state has been characterized as an 'entropic' state in which the mind/brain operates outside of its normal, optimal level of order, in a realm of relative disorder). It may be that what underlies both facets of the psychedelic state and can resolve the 'valence paradox' therefore, is this principle of increased cognitive entropy (see Fig.). Accordingly, we predict that disordered or entropic cognition is a more fundamental characteristic of the psychedelic state than either positive or negative mood. This hypothesis could be tested by carrying out a principal components analysis of the ASC data; quality of cognition in the psychedelic state (phase 2). Finally, it is hypothesized that an acute 'onslaught' or 'blast' of 5-HT 2A R stimulation, via the action of a psychedelic, has a residual influence on brain network dynamics and associated cognition (phase 3). 5-HT 2A R stimulation is described as having a 'loosening' or 'lubricating' influence on cognition and this is hypothesized to be conducive to improved psychological wellbeing. * The long-term effects of psychedelics on brain network dynamics have yet to be formally investigated. we would predict that valence non-specific items and particularly those related to 'entropic cognition' (such as loss of self/ego, loss of ego-boundaries, altered meaning and muddled thinking) would load more heavily onto the first principal component than valence-specific items (such as feeling euphoric or sad)e.g. see. Acute entropic processes may also be useful predictors of the mid/longterms effects of psychedelics, and the (trend-level) relationship between impaired/disordered cognition and subsequent increases in trait openness might be suggestive of such an association. Before concluding, it is worth considering one final important matter. The discussion so far has focused mainly on the paradoxical acute psychological effects of psychedelics. However, as the present results have demonstrated, the acute effects of psychedelics can be quite different to their longer-term effects, and it is arguably the latter that are more clinically relevant. Previous studies have shown that trait characteristics, such as personality and outlook, can be significantly altered by psychedelics. Moreover, associations have been found between certain psychological traits and the 5-HT 2A R. Specifically, deficient 5-HT 2A R stimulation has been linked with depression-related behaviours such as suicide, dysfunctional or excessively pessimistic attitudes) and neuroticism. In this context, increased psychological wellbeing, decreased suicidalityand now increased optimism after a 'blast' of 5-HT 2A R stimulation may begin to make functional sense. We predict that deficient 5-HT 2A R stimulation causes cognition to 'stultify', whereas 5-HT 2A R stimulation loosens cognition and associated brain dynamics, serving as a metaphorical 'lubricant' for the mind and brain. We predict that this loosening effect persists beyond the acute intoxication phase and can potentially explain the mid-to long-term psychological effects of psychedelics. Recent reports of enduring brain changes with 5-HT 2A R stimulation and psychedelic drug-use, as well as speculations on the function of serotonin in the brain, may herald the beginnings of an understanding of this important matter. We intend to detail the acute brain effects of LSD in forthcoming neuroimaging papers and to investigate the long-term psychological and brain effects of psychedelics in future studies. In conclusion, this study sought to investigate the paradoxical psychological effects of LSD in a controlled study in healthy volunteers. LSD produced robust acute psychological effects that were characterized by psychosis-like symptoms but also positive mood. Mid-term effects included significant increases in optimism and the personality trait openness and no increases in delusional thinking. A mechanistic explanation for these findings was proposed based on the 'entropic brain' hypothesis).
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