In a double-blind, placebo-controlled crossover study in 16 healthy volunteers, LSD showed dose-proportional pharmacokinetics and produced dose-dependent subjective and autonomic effects from 25 µg, with a ceiling for positive ("good") effects at 100 µg while 200 µg increased ego dissolution, anxiety and duration of effects. Pretreatment with the 5‑HT2A antagonist ketanserin blocked the effects of 200 µg, indicating that LSD's full psychedelic effects are primarily mediated by 5‑HT2A receptor activation and informing dose selection for future research.
Growing interest has been seen in using lysergic acid diethylamide (LSD) in psychiatric research and therapy. However, no modern studies have evaluated subjective and autonomic effects of different and pharmaceutically well-defined doses of LSD. We used a double-blind, randomized, placebo-controlled, crossover design in 16 healthy subjects (eight women, eight men) who underwent six 25 h sessions and received placebo, LSD (25, 50, 100, and 200 µg), and 200 µg LSD 1 h after administration of the serotonin 5-hydroxytryptamine-2A (5-HT 2A ) receptor antagonist ketanserin (40 mg). Test days were separated by at least 10 days. Outcome measures included self-rating scales that evaluated subjective effects, autonomic effects, adverse effects, plasma brain-derived neurotrophic factor levels, and pharmacokinetics up to 24 h. The pharmacokinetic-subjective response relationship was evaluated. LSD showed dose-proportional pharmacokinetics and first-order elimination and dose-dependently induced subjective responses starting at the 25 µg dose. A ceiling effect was observed for good drug effects at 100 µg. The 200 µg dose of LSD induced greater ego dissolution than the 100 µg dose and induced significant anxiety. The average duration of subjective effects increased from 6.7 to 11 h with increasing doses of 25–200 µg. LSD moderately increased blood pressure and heart rate. Ketanserin effectively prevented the response to 200 µg LSD. The LSD dose–response curve showed a ceiling effect for subjective good effects, and ego dissolution and anxiety increased further at a dose above 100 µg. These results may assist with dose finding for future LSD research. The full psychedelic effects of LSD are primarily mediated by serotonin 5-HT 2A receptor activation.
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Passie, T., Halpern, J. H., Stichtenoth, D. O. et al. · CNS Neuroscience and Therapeutics (2008)
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Holze and colleagues situate LSD as a classical serotonergic psychedelic that produces complex alterations of consciousness primarily via serotonin 5-HT2A receptor stimulation. Renewed clinical and research interest in LSD has not been matched by modern within-subject data comparing multiple, pharmaceutically well-characterised acute doses in the same participants. The authors note gaps in dose–response knowledge, the need to document plasma exposure (pharmacokinetics, PK) alongside subjective effects, and interest in potential biomarkers of neuroplasticity such as brain-derived neurotrophic factor (BDNF). The study therefore set out to characterise acute subjective, autonomic and biomarker (plasma BDNF) responses to a range of LSD base doses (25, 50, 100 and 200 µg) in healthy volunteers, to define PK-PD relationships, and to test the role of 5-HT2A receptors by administering ketanserin (40 mg) prior to a 200 µg LSD dose. The investigators hypothesised dose-dependent effects that would be blocked by ketanserin and aimed to provide dose-finding data relevant to future research and therapeutic applications.
This was a double-blind, randomised, placebo-controlled, crossover study in 16 healthy adults (eight men, eight women; mean age 29 ± 6.4 years, range 25–52). Each participant completed six 25 h test sessions separated by at least 10 days, receiving in counterbalanced order: placebo, 25 µg LSD, 50 µg LSD, 100 µg LSD, 200 µg LSD, and 200 µg LSD given 1 h after 40 mg ketanserin. Block randomisation and a double-dummy procedure (two capsules and two solutions per session) were used to preserve blinding. The study adhered to Good Clinical Practice and was registered at ClinicalTrials.gov. Eligible participants were screened for medical and psychiatric illness, medication use, substance-use history and pregnancy; exclusion criteria included major psychiatric disorder, interfering medications, significant physical illness, heavy tobacco use and recent illicit drug use. Six participants had prior LSD exposure (1–3 occasions) and most had some lifetime experience with other recreational drugs; drug screens during the study were negative. The LSD solution formulations were manufactured under good manufacturing practice and analytically confirmed (25 µg formulation 25.7 ± 0.57 µg; 100 µg formulation 98.7 ± 1.6 µg). Ketanserin and placebo capsules were encapsulated to match appearance. Procedures began with baseline measures and drug-administration at 09:00 (ketanserin or its placebo at 08:00). Sessions took place in a calm hospital room with continuous staff presence for the first 16 h. Subjective effects were measured repeatedly with visual analogue scales (VAS) at numerous timepoints up to 24 h and with the Adjective Mood Rating Scale (AMRS). The 5D-ASC and mystical experience questionnaires (MEQ43/MEQ30) were administered 24 h after dosing to retrospectively rate peak effects. Autonomic measures (blood pressure, heart rate, tympanic temperature) and adverse effects (list of complaints) were recorded; plasma BDNF was measured at baseline, 6, 12 and 24 h. Plasma LSD and the main metabolite O-H-LSD were quantified by ultra-high-performance liquid chromatography tandem mass spectrometry with a lower limit of quantification of 5 pg/ml. PK parameters were estimated using a one-compartment model with first-order input and elimination; predicted concentrations were linked to pharmacodynamics via a sigmoid Emax model. Time-to-onset, time-to-peak, time-to-offset and effect duration were derived from modelled VAS "any drug effect" curves using a 10% of maximum individual response threshold. Repeated-measures ANOVA with drug as within-subject factor and Tukey post hoc testing was used for statistical analysis, with p < 0.05 considered significant; no correction for multiple testing was applied.
Sixteen participants completed all sessions. Plasma concentrations of LSD and O-H-LSD were measurable in all subjects at all doses and timepoints. PKs were dose-proportional across the 25–200 µg range and followed first-order elimination; noncompartmental and model parameters were reported, and no sex differences in PKs or effects were observed. Ketanserin had no significant effect on LSD pharmacokinetics. Subjective effects. LSD produced dose-dependent subjective effects beginning at 25 µg, where "any drug effect" on VAS differed significantly from placebo (p < 0.05). Positive subjective effects ("good drug effect" and drug liking) exhibited a ceiling at 100 µg, with typically no significant increase at 200 µg. In contrast, the 200 µg dose produced significantly greater ego dissolution on VAS, greater anxious ego dissolution on the 5D-ASC, and higher negative "nadir" effects than 100 µg (all p < 0.05). Only the 200 µg dose induced significant anxiety on the 5D-ASC and AMRS (both p < 0.01); 100 µg did not. Peak subjective-effect durations lengthened with dose: time-to-onset shortened and time-to-offset increased, giving longer overall effect durations as dose increased. Ketanserin markedly attenuated subjective responses to 200 µg LSD (most comparisons p < 0.001), reducing effects approximately to the levels seen after 25 µg LSD; a small delayed residual VAS "good drug effect" remained after ketanserin. Participants did not show significant differences in subjective responses according to prior LSD experience. Retrospective blinding data showed that 100 and 200 µg were generally recognised as high doses but could not be reliably distinguished from each other; 25 µg was mostly distinguished from placebo. Autonomic and adverse effects. LSD moderately increased blood pressure at doses ≥50 µg and increased heart rate at 100 and 200 µg; body temperature was unaffected. Total acute adverse-effect scores (0–12 h) were higher after 100 and 200 µg versus placebo and other conditions. Ketanserin prevented the LSD-induced heart rate increase and transiently reduced the blood pressure response up to about 6 h. No severe adverse events occurred. BDNF and PK-PD modelling. Plasma BDNF rose significantly after 200 µg compared with placebo, peaking at about 6 h; increases after lower doses or after ketanserin plus LSD were nonsignificant. PK-PD modelling reproduced the dose-proportional PKs and the ceiling in predicted VAS any-drug and good-drug effects at 100 µg, while predicted bad-drug effects and ego dissolution increased further at 200 µg.
Holze and colleagues interpret the findings as demonstrating dose-dependent subjective effects of LSD that begin at 25 µg and reach a plateau for positive subjective effects at about 100 µg, while ego dissolution and anxiety continue to increase at 200 µg. The authors emphasise that plasma-confirmed, pharmaceutically characterised dosing and full PK characterisation strengthen the internal validity of the dose–response data. They report no sex differences in PKs or effects and note that PKs were consistent with prior single-dose studies. The ceiling effect for positive subjective effects at 100 µg is contrasted with earlier reports that suggested greater effects at 200 µg; the investigators attribute those discrepancies to unstable formulations and between-study comparisons in prior work rather than within-subject dosing. They propose that 100 µg may be an appropriate starting dose for therapeutic applications where high positive acute effects (e.g. Oceanic Boundlessness) but lower acute anxiety are desirable, whereas doses above 100 µg could be chosen if ego dissolution is the specific aim but with increased risk of anxiety. The 50 µg dose produced substantial positive mood effects with minimal anxious ego dissolution and is suggested as a possible initial dose for psychedelic-naïve or more sensitive patients. Ketanserin substantially blocked the acute subjective and some autonomic effects of high-dose LSD, supporting the conclusion that 5-HT2A receptor activation mediates the primary psychedelic effects in humans. The authors also report a significant increase in plasma BDNF after 200 µg with a 6 h peak but note that the timing and relationship of BDNF changes to clinical outcomes remain uncertain and warrant further study. Strengths highlighted include within-subject comparison of multiple analytically confirmed doses, randomised double-blind crossover design, equal sex representation, validated psychometric instruments, inclusion of a receptor-blocking condition and comprehensive PK sampling. Limitations acknowledged are the controlled laboratory setting, inclusion only of healthy volunteers (many with some prior drug experience), potential positive expectations among volunteers and the consequent limited generalisability to other environments or patient populations. The authors also propose a practical dosing terminology—"microdose" (1–20 µg), "minidose" (21–30 µg) and "psychedelic dose" (>30 µg)—and suggest subcategories within psychedelic doses (30–100 µg favouring positive effects; >100 µg more associated with ego dissolution and anxiety).
The study characterised acute, dose-dependent subjective, autonomic and biomarker effects of LSD across 25–200 µg in healthy volunteers and linked these effects to plasma-confirmed exposures. LSD showed dose-proportional pharmacokinetics with first-order elimination and produced measurable subjective effects from 25 µg. Positive subjective effects reached a ceiling at about 100 µg, whereas ego dissolution and anxiety increased further at 200 µg. Ketanserin nearly abolished the high-dose subjective response, confirming a primary role for 5-HT2A receptor activation in LSD's acute psychedelic effects. These results are presented as dose-finding data to inform future research and LSD-assisted therapy.
Peak (E max and/or E min ) or peak change from baseline (ΔE max ) values were determined for repeated measures. The values were then analyzed using repeated-measures analysis of variance, with drug as the within-subjects factor, followed by the Tukey post hoc test. The data were analyzed using Statistica 12 software (StatSoft, Tulsa, OK, USA). The criterion for significance was p < 0.05. No correction for multiple testing was applied.
The present study investigated acute effects of LSD using a range of well-defined doses in healthy subjects. Previous recent studies mostly used LSD products that were not developed according to pharmaceutical standards, as discussed elsewhere. Additionally, we determined plasma LSD concentrations as measures of exposure to the substance in the body that are a prerequisite for a valid dose-finding study. We used LSD doses in the psychedelic effect dose range (25-200 µg of LSD base) that were expected to induce full subjective effects of LSD as previously reported by comparable studies that used single-dose levels. Plasma LSD concentrations increased proportionally with increasing doses and decreased according to first-order elimination. The PK parameters were consistent with single-dose studies. A preliminary report of a longer terminal elimination half-life of LSDwas not confirmed in the present study. We found no sex differences in LSD concentrations or effects consistent with previous studies using no body weight adjustment of LSD doses. LSD dose-dependently increased subjective effects that were largely similar to previous studies that used single-dose levels. Importantly, a ceiling effect was reached at higher doses of LSD (>100 µg) with regard to its positive subjective effects, with no difference in good drug effects between the 100 and 200 µg doses. However, the 200 µg dose of LSD produced significantly greater ego dissolution and anxious ego dissolution than the 100 µg dose. Additionally, only the 200 µg dose and not the 100 µg dose of LSD-induced significant anxiety. However, doses above 100 µg may be used if the goal is to induce the experience of ego dissolution or disembodiment. These experiences, however, were produced at doses that also produced more anxiety compared with lower doses. LSD doses of 100 and 200 µg were both subjectively identified as high doses but could not be subjectively distinguished with certainty from each other. Both of these doses can clearly be considered full psychedelic doses and have previously been investigated in healthy subjects. No previous studies directly compared LSD doses of 100 and 200 µg. In contrast to the present findings, we previously reported moderately greater effects of a 200 µg dose of LSD in one studycompared with 100 µg in another study. Specifically, 200 µg LSD produced significantly greater total scores on the 5D-ASC scale, including higher ratings of blissful state, insightfulness, and changed meaning of percepts compared with 100 µg.. In a previous study, the 200 µg dose of LSD also produced higher ratings of good drug effects, bad drug effects, fear, open, and trust on the VAS compared with 100 µg. There are two explanations for the absence of an LSD dose response for good drug effects in the present study compared with our previous studies. First, the true doses that were used in the previous studies were 60-70 and 150 µg rather than the reported 100 and 200 µg doses because of the use of an unstable formulation with a lower LSD content, as discussed elsewhere. Second, the past comparison was between different subjects and studies, whereas the present study used valid within-subject and within-study comparisons. In the present study, we observed a ceiling effect on the dose-response curve. Considering that the previously reported 200 µg dose likely contained only 150 µg of active LSD, additional positive effects may be reached with 150 µg compared with 100 µg. This possibility remains to be tested. One of our recent studies also used an analytically confirmed LSD dose of 100 µg, which produced scores on the VAS and 5D-ASC scale that were nominally higher than those that were reported after 100 µg administration in the present studyand more similar to the scores that were reported herein after 200 µg administration. Altogether, the available data support the view that mainly high acute positive effects of LSD can be induced at a 100 µg dose of LSD base. Therefore, we speculate that a dose of 100 µg of LSD may be selected for the treatment of depression or anxiety where higher Oceanic Boundlessness and lower anxiety ratings acutely induced by psychedelics predicted better treatment efficacy. The 50 µg dose that was used in the present study also produced substantial positive mood effects and notably only very small and nonsignificant anxious ego dissolution, with no anxiety. Ketanserin (K) transiently decreased blood pressure, heart rate, and body temperature, with a delayed increase to the levels that were reached after the administration of LSD alone. LSDor placebo was administered at t = 0 h. Ketanserin (K) or placebo was administered at t = -1 h. The data are expressed as the mean ± SEM in 16 subjects. Maximal effects and statistics are shown in Supplementary Table. AUC ∞ area under the plasma concentration-time curve from time zero to infinity, CL/F apparent total clearance, C max estimated maximum plasma concentration, t 1/2 estimated plasma elimination half-life, t max estimated time to reach C max , k 01 first-order absorption koefficient, λ z first-order elimination coefficient, V z /F volume of distribution. Thus, the 50 µg dose may be useful for inducing a moderately intense and predominantly positive psychedelic experience. This low psychedelic dose would likely be a good starting dose to be used in patients with no previous experience with psychedelics or in subjects who are considered to be more sensitive to the effects of psychedelics. In the present study, LSD produced moderate elevations of arterial blood pressure and heart rate starting at the 50 µg dose that were largely similar to the effects of 100 and 200 µg. Similarly, previous studies that used pharmaceutically not wellcharacterized doses of 100 and 200 µg LSD found no difference in the acute cardiostimulant effects of these doses. A previous study in patients did not observe any increases in blood pressure using a non-confirmed dose of 200 µg of LSD. Methylenedioxymethamphetamine clearly has more pronounced cardiostimulant effects and a less favorable overall physical safety profile than LSD. In contrast, the psychotropic effects of LSD are significantly greater compared with MDMA. In the present study, administration of the 5-HT 2A receptor antagonist ketanserin 1 h before LSD administration markedly reduced the subjective response to the 200 µg LSD dose to levels that were similar to the 25 µg dose. Retrospective reports showed that ketanserin and LSD together were identified correctly by the participants or mistaken as a low dose of LSD but never mistaken for a high dose of LSD. The present findings are consistent with a previous study in which ketanserin administration prior to the administration of 100 µg LSD almost completely prevented the acute effects of LSD. These findings support the view that LSD primarily produces its acute psychedelic effects in humans via 5-HT 2A receptor activation, which was also shown for a high and fully psychedelic dose of LSD. Ketanserin also prevented acute adverse effects of LSD and the LSD-induced heart rate response. However, the weak blood pressure-elevating effects of LSD were only transiently prevented by ketanserin and reappeared later during the LSD response. This observation is consistent with the relatively short half-life of ketanserin (i.e., 2 h) during the first 1-9 h following administration. In the present study, 200 µg LSD significantly increased BDNF plasma concentration compared with placebo with a peak at 6 h. Additionally, there were nonsignificant increases in plasma BDNF after lower doses of LSD or after ketanserin with LSD. In previous studies, 100 µg LSD had no effect on BDNF plasma levelsup to 5 h while the psychedelic ayahuasca increased BDNF at 2 days. Further, higher BDNF levels were associated with lower depression ratings after administration of ayahuasca. More research is needed to define the time course of the BDNF response and whether there is a link between psychedelics, BDNF, and the antidepressant response. In addition to providing dose-response data on full psychedelic doses of LSD, the present study further characterized the effects of small doses of LSD. The lowest dose that was used in the present study contained 25 µg of LSD base. This dose produced subjective "any drug effects" that were significantly different from placebo and retrospectively identified as LSD by the majority (>85%) of the participants. Very low doses of LSD have typically been referred to as "microdoses." Psychedelic microdoses have been postulated to have beneficial prolonged effects on mood while producing no or only minimal acute adverse subjective effects. Positive long-term effects of psychedelic microdoses remain to be documented, and remaining unclear are the LSD doses that actually have no acute subjective effects and thus could be considered microdoses. Very low to low doses of LSD were recently studied in two placebo-controlled trials. One study also provided preliminary PK data. In older healthy volunteers, 5-20 µg of LSD tartrate produced small but significant linear dose-dependent increases in ratings of all of the following: subjective drug effects, vigilance reduction, dizziness, and changes in body feeling. The frequency of Fig.Pharmacokinetics and subjective effects of lysergic acid diethylamide (LSD). a Plasma LSD concentration-time curves for 25, 50, 100, and 200 µg doses of LSD. b-e LSD effect-time curves for Visual Analog Scale ratings (0-100%) of (b) "any drug effect," (c) "good drug effect," (d) "bad drug effect," and (e) "ego dissolution." LSD administration resulted in dose-proportional increases in plasma concentrations of LSD, but subjective good drug effects reached a ceiling at the 100 μg dose and did not further increase at the 200 µg dose. In contrast, bad drug effects and ego dissolution increased further at the 200 µg dose compared with 100 µg. Therefore, LSD doses higher than 100 µg produced no further increases in good drug effects but more ego dissolution and anxiety. The data are expressed as the mean ± SEM in 16 subjects. LSD was administered at t = 0 h. The lines represent the means of the individual pharmacokinetic-pharmacodynamic (subjective effect) model predictions. adverse effects of LSD at doses up to 20 µg was not different from placebo. The mean plasma C max values of LSD (non-compartmental analyses) were 0.44 ng/ml (n = 8) after the administration of 20 µg of LSD tartrateand 0.51 ng/ml after the administration of 25 µg of LSD base in the present study, indicating comparable dose-proportional peak concentrations. The previous study included younger healthy subjects and found dosedependent increases in subjective ratings of "feel drug" and "like drug" on VASs and on the 5D-ASC scale after the administration of 6.5, 13, and 26 µg of LSD tartrate. Notably, a 26 µg dose of LSD tartrate would be lower than the 25 µg dose of LSD base (i.e., 31 µg of LSD tartrate equivalent) that was used in the present study. Nevertheless, the 26 µg dose of LSD tartrate produced significant effects on the 5D-ASC scale compared with placebo and nominally greater ratings on the 5D-ASC subscales than the 25 µg dose that was used in the present study. Unfortunately, no plasma LSD concentration data have been published for the 26 µg dose of LSD tartrate. Therefore, a comparison of drug exposures between this previous study and the present study to further validate the dose comparison is not possible. Altogether, the available data from these controlled studies, including the present study that used very small and small doses of LSD, indicate that the 25 µg dose of LSD is clearly acutely psychoactive in the majority of subjects. Doses in the range of 21-30 µg of LSD base may thus be considered "minidoses" rather than "microdoses." Doses of LSD base in the 1-20 µg range may be considered "microdoses" but need further study. However, these doses may already elicit small dose-dependent subjective effects, although they are unlikely to relevantly impair cognition or produce adverse effects. Overall, the present dose-response study characterized a range of LSD doses. Based on the available data, the following dosing terminology may be useful for future LSD research: "microdose" (1-20 µg), "minidose" (21-30 µg), and "psychedelic dose" (>30 µg). Within the psychedelic LSD dose range, good effects likely predominate at doses of 30-100 µg (good-effect dose), whereas ego dissolution and anxiety increase at doses above 100 µg (egodissolution dose). The present study has numerous strengths. Four different doses of LSD were used within subjects and compared with placebo under double-blind conditions in a controlled laboratory setting. A ketanserin-LSD condition was also included to elucidate the mechanism of action of LSD and enhance blinding between the different conditions. We also included equal numbers of male and female participants and used internationally established standardized and validated psychometric outcome measures. The doses of LSD were pharmaceutically well-characterized, and plasma LSD concentrations and PK parameters were determined up to 24 h for all doses. Notwithstanding these strengths, the present study also has limitations. The study used a highly controlled setting and included only healthy subjects. Additionally, participants willing to participate in LSD research are likely to have positive expectations and some participants had past substance experiences. Thus, subjects in different environments and patients with psychiatric disorders may respond differently to LSD.
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