In a double‑blind, placebo‑controlled crossover study in 16 healthy volunteers, a single 200 μg dose of LSD produced significant acute increases in circulating glucocorticoids (cortisol, cortisone, corticosterone and 11‑dehydrocorticosterone) and dehydroepiandrosterone. These steroid rises were temporally correlated with plasma LSD concentrations and peak psychedelic effects, with no evidence of acute pharmacological tolerance.
Lysergic acid diethylamide (LSD) is a serotonin 5‐hydroxytryptamine‐2A (5‐HT2A) receptor agonist that is used recreationally worldwide. Interest in LSD research in humans waned after the 1970s, although the use of LSD in psychiatric research and practice has recently gained increasing attention. LSD produces pronounced acute psychedelic effects, although its influence on plasma steroid levels over time has not yet been characterised in humans. The effects of LSD (200 μg) or placebo on plasma steroid levels were investigated in 16 healthy subjects using a randomised, double‐blind, placebo‐controlled, cross‐over study design. Plasma concentration–time profiles were determined for 15 steroids using liquid‐chromatography tandem mass‐spectrometry. LSD increased plasma concentrations of the glucocorticoids cortisol, cortisone, corticosterone and 11‐dehydrocorticosterone compared to placebo. The mean maximum concentration of LSD was reached at 1.7 h. Mean peak psychedelic effects were reached at 2.4 h, with significant alterations in mental state from 0.5 h to > 10 h. Mean maximal concentrations of cortisol and corticosterone were reached at 2.5 h and 1.9 h, and significant elevations were observed 1.5–6 h and 1–3 h after drug administration, respectively. LSD also significantly increased plasma concentrations of the androgen dehydroepiandrosterone but not other androgens, progestogens or mineralocorticoids compared to placebo. A close relationship was found between plasma LSD concentrations and changes in plasma cortisol and corticosterone and the psychotropic response to LSD, and no clockwise hysteresis was observed. In conclusion, LSD produces significant acute effects on circulating steroids, especially glucocorticoids. LSD‐induced changes in circulating glucocorticoids were associated with plasma LSD concentrations over time and showed no acute pharmacological tolerance.
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Lysergic acid diethylamide (LSD) is a prototypic serotonergic hallucinogen that acts primarily at serotonin 5-HT1 and 5-HT2 receptors and has a pharmacology that also includes dopaminergic and adrenergic receptor interactions. Earlier research showed that many psychoactive drugs activate the hypothalamic–pituitary–adrenal (HPA) axis and raise glucocorticoid levels, but data on LSD's effects on circulating steroid hormones in humans have been limited and fragmentary. Animal studies and early human urine studies suggested HPA activation after LSD, and a prior human report by the group found an increase in plasma cortisol at 180 min, but comprehensive time courses and a broader steroid panel had not been examined over the full duration of LSD's effects. Strajhar and colleagues set out to characterise the acute effects of a single oral dose of LSD on a wide panel of plasma steroids over 24 h in healthy volunteers and to compare steroid time-courses with LSD plasma concentrations and psychotropic effects. The study aimed to determine which steroid classes (glucocorticoids, mineralocorticoids, androgens, progestogens) are altered by LSD, the timing of those changes relative to subjective effects and LSD exposure, and whether any concentration–effect hysteresis or acute tolerance is evident.
The study used a double-blind, placebo-controlled, cross-over design with two experimental sessions per subject in balanced order and washouts of at least 7 days. Sixteen healthy adults (eight men, eight women; mean age 28.6 ± 6.2 years) participated. Exclusion criteria included pregnancy, personal or first-degree family history of psychotic or major affective disorder, regular medication use, significant medical illness, recent or frequent illicit drug use, and positive urine drug screens. Subjects refrained from caffeine and limited alcohol before sessions; light smokers were allowed to maintain usual habits but were not to smoke during sessions. Each session began at 08:00 with baseline measures; a single oral dose of LSD 200 μg or placebo was administered at 09:00. Subjects remained resting in a calm laboratory environment; standardised lunch and dinner were provided. Blood for steroid assays was sampled 1 h before and at 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10 and 24 h after dosing via an indwelling catheter. Plasma was stored at −20 °C. Plasma LSD concentrations were measured by LC-MS/MS; 15 steroids (including cortisol, cortisone, corticosterone, 11-dehydrocorticosterone, aldosterone, 11-deoxycorticosterone, 11-deoxycortisol, DHEA, DHEAS, androstenedione, testosterone, 5α-dihydrotestosterone, androsterone, progesterone, 17α-hydroxyprogesterone) were quantified by UPLC-MS/MS after solid-phase extraction. Method performance reported coefficients of variation <15%, accuracy 85–115% and recoveries 80–120%. Statistical comparisons between LSD and placebo used repeated-measures ANOVA on Cmax and AUC values; time courses were analysed with two-way ANOVAs (drug × time) and Tukey's post-hoc tests. AUCs were calculated from 0.5 h to 10 h (AUC10) by the trapezoidal method. Sex was included as a between-subject factor to test sex differences. The relationship between LSD exposure and steroid or subjective responses was explored with hysteresis plots and Spearman rank correlations between mean LSD concentrations and mean responses across the 12 time points; 17 correlations were tested and a Bonferroni-corrected significance threshold of P < 0.003 was applied. Analyses were performed in STATISTICA v12.
LSD (200 μg) produced significant increases in circulating glucocorticoids compared with placebo. Specifically, plasma cortisol, cortisone, corticosterone and 11-dehydrocorticosterone were elevated after LSD; sums (cortisol + cortisone and corticosterone + 11-dehydrocorticosterone) and the ratios cortisol/cortisone and corticosterone/11-dehydrocorticosterone were also increased, consistent with increased glucocorticoid production. No LSD effect was found on the cortisol precursor 11-deoxycortisol or on the mineralocorticoids aldosterone and 11-deoxycorticosterone. Among androgens, LSD significantly increased dehydroepiandrosterone (DHEA; both Cmax and AUC10) and increased the AUC10 but not Cmax of androstenedione. No changes were observed in DHEAS, testosterone, 5α-dihydrotestosterone or androsterone. Progestogens (progesterone and 17α-hydroxyprogesterone) were unaffected. There were no significant drug × sex interaction effects for the steroid responses; as expected, baseline testosterone was higher in men than women but the response to LSD did not differ by sex. Pharmacokinetic and temporal relationships were reported: mean LSD Cmax occurred at 1.7 ± 1.0 h and mean peak psychotropic effects (measured by VAS) at 2.4 ± 0.8 h. Corticosterone peaked earlier (1.9 ± 0.5 h) and returned to baseline earlier than cortisol, which peaked at 2.5 ± 0.8 h. Significant elevations were observed for corticosterone from 1–3 h and for cortisol from 1.5–6 h post-dose. Counterclockwise hysteresis was observed for the overall subjective 'any drug effect' and cortisol, consistent with an initial delay due to absorption/distribution; beyond ~2.5 h the psychotropic and cortisol changes paralleled plasma LSD decline, indicating a close concentration–effect relationship up to 24 h. Average plasma LSD levels correlated strongly with average subjective 'any drug effects' (Rs = 0.94, P < 0.001) and with average cortisol over time (Rs = 0.97, P < 0.001). Average subjective 'any drug effect' was also closely related to cortisol (Rs = 0.97, P < 0.001) and corticosterone (Rs = 0.90, P < 0.001). 'Good drug effects' and 'stimulation' correlated with LSD and with cortisol and corticosterone, whereas 'bad drug effects' and 'fear' did not correlate with glucocorticoid changes. By contrast, the authors note that in their prior MDMA dataset the concentration–effect plots showed clockwise hysteresis and evidence of acute tolerance, a pattern not seen with LSD in the present study.
Strajhar and colleagues interpret the findings as evidence that a single 200 μg oral dose of LSD acutely stimulates the HPA axis in healthy humans, producing increases in both inactive (cortisone, 11-dehydrocorticosterone) and active (cortisol, corticosterone) glucocorticoids. The temporal covariation between plasma LSD levels, glucocorticoid concentrations and psychotropic effects suggests a close exposure–response relationship for LSD. Importantly, no clockwise hysteresis was observed for LSD's subjective or glucocorticoid effects, indicating a lack of acute pharmacological tolerance within the 24 h observation window; this contrasts with the authors' earlier data on MDMA, which showed acute tolerance. The authors discuss mechanistic implications in the context of serotonergic stimulation: both LSD and other serotonergic hallucinogens (for example psilocybin) increase cortisol and prolactin, supporting a role for serotonin receptors in HPA axis activation. Comparisons with other stimulants suggest that serotonin and norepinephrine systems are more strongly linked to cortisol responses than dopamine alone; methylphenidate (predominantly dopaminergic) produced little cortisol change in prior work. The relatively larger relative increase in corticosterone versus cortisol is highlighted because corticosterone has greater brain penetration owing to differential transport at the blood–brain barrier, implying the possibility of more pronounced central effects mediated by corticosterone. The increase in DHEA is noted and the authors briefly consider its relevance given DHEA's neuroactive and putative anxiolytic/antidepressant properties. They acknowledge limitations, including evaluation of a single high dose, the healthy and drug-naive sample (which may limit generalisability to chronic or polydrug users), and the absence of measurements of upstream mediators such as corticotrophin-releasing factor or ACTH. The authors conclude that LSD induces acute glucocorticoid release via serotonergic mechanisms, that corticosterone in particular tracked subjective effects closely, and that LSD's glucocorticoid response showed no acute tolerance compared to MDMA.
To determine differences between LSD and placebo, maximum concentration (C max ) values and areas under the concentration-time curve (AUCs) were compared for each steroid using repeated-measures ANOVA, with drug (LSD versus placebo) as the within-subject factor. Sex differences were determined by including sex (male versus female) as a between-subject factor in the ANOVA. To test how long the subjective and endocrine responses last over time, data were also analysed using two-way ANOVAs with drug and time as factors and Tukey's test was used for post-hoc comparisons between corresponding time points. C max was determined directly from the concentrationtime curves. AUC values were determined from time 0.5 h to 10 h (AUC 10 ) using the trapezoidal method. The LSD exposure-steroid concentration response relationships were explored by plotting the LSD response as a function of steroid concentration after LSD administration minus the individual time-matched concentration after placebo as a function of LSD plasma concentrations at each time point (hysteresis curves). Correlations between mean LSD concentrations and mean LSD-induced subjective (five scales) or endocrine responses (cortisol and corticosterone) over time and correlations between subjective and endocrine responses over time (n = 12 time points) within the 16 subjects were then analysed using Spearman's rank correlations. P < 0.05 was considered statistcally significant. Seventeen correlations were tested, giving a Bonferroni-corrected statistical threshold of P < 0.003. The statistical analyses were performed using STATISTICA, version 12 (StatSoft, Tulsa, OK, USA).
The present study provides insights into the acute effects of LSD on the plasma levels of a series of steroids in healthy humans. LSD increased circulating glucocorticoid levels, with the levels of both inactive 11-dehydrocorticosterone and cortisone and active corticosterone and cortisol being elevated compared to placebo, indicating HPA axis stimulation. The LSD-induced changes in circulating cortisol and corticosterone had, in contrast to the glucocorticoid response to MDMA, a close relationship with both the plasma concentrations of LSD and the psychotropic response to LSD. No clockwise hysteresis in the LSD concentration-effect plots was observed, thus indicating no acute tolerance to the effects of LSD on glucocorticoid concentrations or subjective drug effects, in contrast to the pronounced acute tolerance observed with MDMA. LSD also significantly increased plasma concentrations of the androgens DHEA (AUC 10 , C max ) and androstenedione (AUC 10 ), although the concentration of testosterone was unaltered, and the ratio of active to inactive androgens (testosterone/androstenedione) decreased. Other androgens, as well as progestogens and mineralocorticoids, were unaffected by LSD. The LSD-induced relative increase in corticosterone was greater than the increase in cortisol. The brain penetration of corticosterone is greater compared to cortisol because of differential transport by P-glycoprotein at the blood-brain barrier. Thus, the effect of LSD on brain corticosterone concentrations may be more prominent. Additionally, the LSD-induced changes in circulating corticosterone in the present study also more closely reflected psychotropic alterations over time, in which plasma cortisol levels increased later in time than the subjective effects of LSD after drug administration. Stimulation of the HPA axis by LSD has previously been demonstrated in animals, as well as in a preliminary study in humans. The present study in humans provided a more comprehensive analysis of plasma concentration-over-time profiles up to 24 h after drug administration and of a series of different steroids. LSD is a prototypic serotonergic hallucinogen that mainly acts as a potent serotonin 5-HT 1 and 5-HT 2 receptor agonist. It also less potently binds to dopamine D 1-3 and adrenergic a 1 receptors but does not inhibit monoamine transporters. In the present study, LSD also increased plasma levels of prolactin (3), which is a marker of increased serotonergic activity. Similar to LSD in the present study, the hallucinogen psilocybin increased plasma levels of cortisol in healthy humans, along with increases in prolactin and ACTH. Importantly, psilocybin (psilocin) activates 5-HT receptors similar to LSD but does not exhibit relevant binding to D 1-3 and a 1 receptors, unlike LSD, indicating that HPA axis activation by serotonergic hallucinogens including LSD involves Fig.. Plasma concentration-time profiles of glucocorticoids and mineralocorticoids following lysergic acid diethylamide (LSD) or placebo administration. The values, obtained from 16 subjects, are expressed as the mean AE SEM. LSD or placebo was administered at t = 0 h. LSD significantly increased the plasma concentrations of the glucocorticoids cortisol (B), cortisone (C), corticosterone (D) and 11-dehydrocorticosterone (E) compared to placebo. LSD did not alter plasma concentrations of the cortisol precursor 11-deoxycortisol (A) or the mineralocorticoids 11-deoxycorticosterone (F) and aldosterone (G). 11b-HSD, 11b-hydroxysteroid dehydrogenase; CYP, cytochrome P450. *P < 0.05, **P < 0.01 and ***P < 0.001 compared to the time-matched placebo concentration (Tukey's test based on significant drug 9 time interactions in the two-way analysis of variance). C receptors stimulate ACTH and corticosterone release and activate corticotrophin-releasing factor-expressing cells in the hypothalamic periventricular nucleus. Many psychotropic drugs activate the HPA axis. Acute administration of serotonin transporter inhibitors, but not dopamine transporter inhibitors, increases plasma cortisol levels, indicating that serotonin rather than dopamine mediates HPA axis stimulation. Cocaine inhibits presynaptic serotonin, dopamine and norepinephrine reuptake transporters, and increases ACTH and cortisol in humans. Amphetamine activates the norepinephrine and dopamine but not serotonin systems and increases cortisol, although to a lesser extent than the serotonergic drugs LSD and MDMA. One speculation is that the stimulantinduced increase in cortisol may depend on dopamine-mediated HPA axis stimulation. However, the stimulatory effects of amphetamines on ACTH secretion are mediated by adrenergic receptorsand not by dopamine. Additionally, methylphenidate activates the dopamine system and produces effects of stimulation and euphoria that are similar to those produced by amphetamines, although methylphenidate did not increase plasma cortisol levelsor only to a small extent. Furthermore, the MDMA-induced increase in circulating cortisol was reduced by pharmacologically blocking the MDMA-induced release Fig.. Plasma concentration-time profiles of androgens and progestogens following lysergic acid diethylamide (LSD) or placebo administration. The values, obtained from 16 subjects (eight per sex for testosterone), are expressed as the mean AE SEM. LSD or placebo was administered at t = 0 h. LSD significantly increased plasma concentrations of dehydroepiandrosterone (DHEA) compared to placebo (A). LSD also increased the area under the concentration-time curve but not the maximal concentration of androstenedione compared to placebo (C). By contrast, LSD did not alter plasma concentrations of dehydroepiandrosterone sulphate (DHEAS) (B) or testosterone (D, F). Similarly, LSD did not change plasma levels of the progestogens progesterone (G) and 17a-hydroxyprogesterone (E). 17b-HSD, 17b-hydroxysteroid dehydrogenase; CYP, cytochrome P450. *P < 0.05 and ***P < 0.001 compared to the time-matched placebo concentration (Tukey's test based on significant drug 9 time interactions in the two-way analysis of variance). LSD (ng/ml) of serotonin and norepinephrinebut not when dopamine release was blocked. The greater effects of amphetamine on cortisol release compared to methylphenidate are thus likely attributable to its greater noradrenergic versus dopaminergic properties compared to methylphenidate. Nonetheless, the present study shows that stimulation of the serotonin system by LSD increased cortisol levels similarly to MDMA, which has more amphetamine-type properties and stimulates both the serotonin and norepinephrine systems. Stimulation of the HPA axis involves serotonin and norepinephrine systems. Similar to LSD, the serotonin and norepinephrine releaser MDMA increased the plasma concentrations of the glucocorticoids cortisol, corticosterone and 11-dehydrocorticosterone. Unlike LSD and MDMA, methylphenidate, which activates dopamine and norepinephrine systems but not the serotonin system, did not significantly alter plasma steroid levels in humans, further supporting a role for serotonin receptors in druginduced HPA axis stimulation. Unexpectedly, the glucocorticoid response was more pronounced after LSD administration than after MDMA administration. This is consistent with the greater psychotropic response to LSD compared to MDMA(see Supporting information, Fig.). By contrast, MDMA produced more stimulant-type effects, including greater increases in blood pressure and heart rate. The greater glucocorticoid response after LSD compared to MDMA indicates that the direct serotonergic stimulation of postsynaptic 5-HT 1 and 5-HT 2 receptors by LSD similarly or even more effectively stimulated the HPA axis compared to the release of both serotonin and norepinephrine by MDMA. The relatively similar time courses of the glucocorticoid response and the psychotropic effects of LSD, together with the greater glucocorticoid and psychotropic responses to LSD compared to MDMA, raise the issue of whether the subjective effects of LSD contribute to or further enhance HPA axis stimulation by LSD. We observed a close relationship between LSD-induced subjective drug effects and changes in plasma corticosterone levels. Associations between amphetamine-induced increases in cortisol and subjective arousal and euphoria have been reported previously. The covariance of the psychological and endocrine drug responses indicates that both are mediated by the same transmitter, likely norepinephrine in the case of amphetamineand serotonin in the case of LSD. It is unlikely that glucocorticoids critically mediate the psychotropic drug response because the subjective effects of methamphetamineand cocaineare unaltered when the drug-induced cortisol response is pharmacologically augmented or blocked. On the other hand, the psychotropic effects of LSD might have contributed to the endocrine stress response. Indeed, the subjective effects occurred faster than the cortisol response to LSD. However, only the subjective 'good drug effects' and 'stimulation' induced by LSD and not the 'bad drug effects' or 'fear' correlated with the steroid response over time. Thus, the endocrine changes in response to LSD appear be related to the positive and stimulant subjective LSD effects but not to anxiety. Both cortisol and prolactin levels increase when the serotonin system is pharmacologically activated. Interestingly, the prolactin response was greater after MDMA administrationthan after LSD administration (3), whereas the glucocorticoid response was less, indicating differential effects of LSD and MDMA on markers of serotonergic activity, and further supporting the view that the LSD-induced increase in glucocorticoids may have been enhanced by the more pronounced subjective effects of LSD. A striking difference was found between the plasma concentration-effect curves of LSD in the present study and the plasma concentration-effect curves of MDMA in our previous study. Specifically, the plasma concentration-effect curve of MDMA showed pronounced clockwise hysteresis for the psychotropic effects of MDMAand also for the cortisol and corticosterone responses (see Supporting information, Fig.), suggesting acute tolerance to the effects of MDMA. By contrast, we observed no tolerance to the effects of LSD. This means that the effects of LSD on the HPA axis are longer-lasting than those of MDMA, although MDMA has a longer plasma half-life than LSD. The finding could be explained by the pharmacological mechanisms of MDMA and LSD. MDMA releases endogenous serotonin and norepinephrine from presynaptic terminals, whereas LSD directly interacts with postsynaptic 5-HT receptors. Indeed, the MDMA-induced cortisol response was blocked after duloxetine pre-Fig.. Lysergic acid diethylamide (LSD) exposure-response relationships. LSD responses are shown as LSD effect (item 'any subjective drug effect' reflecting the overall subjective response to LSD, cortisol or corticosterone concentration) minus the individual time-matched effect of placebo. Any subjective responses to LSD (A) and LSD-induced changes in cortisol (C) and corticosterone (E) over time are presented with the corresponding LSD concentrations over time (mean AE SEM) in 16 subjects. LSD or placebo was administered at t = 0 h. Subjective responses to LSD (B) and LSD-induced changes in cortisol (D) and corticosterone (F) concentrations (mean AE SEM) are plotted as a function of mean LSD plasma concentrations (hysteresis curves). The time of sampling is noted next to each point (in hours after LSD administration). The maximum concentration of LSD was reached 1.7 AE 1 h after LSD administration (A, B). The peak psychotropic effect was reached at 2.4 AE 0.8 h, with significant alterations in mental state from 0.5 h to > 10 h after LSD administration (A, B) [drug 9 time interaction in the two-way analysis of variance (ANOVA): F 11,165 = 41.39; P < 0.001]. Maximum concentrations of cortisol (C, D) and corticosterone (E, F) were reached at 2.5 AE 0.8 h and 1.9 AE 0.5 h (mean AE SD), with significant elevations from 1.5 to 6 h and from 1 to 3 h after LSD administration, respectively (F 11,165 = 17.71; P < 0.01 and F 11,165 = 13.35, P < 0.001, respectively). Counterclockwise hysteresis was observed for any drug effects (B) and cortisol (D), which is consistent with an initial delay between plasma concentration and an effect that was attributable to drug absorption. Beyond 2 h after LSD administration, the psychotropic effects (A) and changes in plasma cortisol levels (C) decreased slowly, in parallel with the plasma levels of LSD, exhibiting a close concentration-effect relationship up to 24 h (B, D). LSD significantly increased plasma levels of cortisol 1.5-6 h after LSD administration (C). By contrast, plasma levels of corticosterone increased more rapidly but fell more quickly back to baseline levels, resulting in significant differences in plasma levels 1-3 h after LSD administration and compared to placebo (E). There was no evidence of acute pharmacological tolerance (clockwise hysteresis) for any of the effects of LSD. After drug administration, subjective drug effects increased together with plasma levels of corticosterone but more rapidly than plasma levels of cortisol (G, H). *P < 0.05 and ***P < 0.001 compared to the time-matched placebo concentration (Tukey's test based on significant drug 9 time interactions in the twoway ANOVAs). treatment, which prevents MDMA from interacting with the serotonin and norepinephrine transporters. In the case of cocaine, cocaine-induced euphoria is also short-lasting and exhibits acute tolerance, which is similar to MDMA, whereas the cortisol concentration-time curve is concordant with the cocaine-plasma concentration time curve, similar to LSD. Unlike LSD, MDMA also increased the mineralocorticoids 11-deoxycorticosterone and aldosterone. Mineralocorticoids promote sodium retention and increase extracellular fluid volume, thereby increasing blood pressure. The MDMA-induced increase in mineralocorticoids may thus contribute to the greater increase in blood pressure after MDMA administration (33) compared to LSD. The mechanisms that underlie the differential effects of MDMA and LSD on mineralocorticoid production remain unclear. LSD increased DHEA. DHEA is a precursor of many other steroids and may itself modulate c-aminobutyric acid-ergic and glutamatergic neurotransmission. DHEA has well-documented anxiolytic and antidepressant effects. An interesting line of investigation would be to evaluate further the role of DHEA in the potential anxiolytic effects of LSD that are reported in terminally ill patients. The present study has limitations. First, only a single dose and single administration of LSD were used. However, a relatively high dose of LSD was administered, which produced pronounced psychotropic effects and was within the range of doses used clinically (4) and recreationally. Additionally, we present LSD exposureeffect relationships that can partially substitute for a multiple dose-level study. Second, only psychiatrically and somatically healthy subjects with limited previous experience with hallucinogenic drugs were included. LSD may differentially affect steroid profiles in chronic LSD or polydrug users. Third, we did not assess concentrations of corticotrophin-releasing factor or ACTH to describe the effects of the drug on other mediators within the HPA axis. In conclusion, LSD induced significant effects on plasma glucocorticoids, which is consistent with HPA axis stimulation via serotonergic receptors. Plasma levels of cortisol and particularly corticosterone covaried in close relationship to the plasma levels of LSD over time. The corticosterone response was also closely related to the subjective effects of LSD. The glucocorticoid response to LSD showed no acute pharmacological tolerance, in contrast to the response to MDMA.
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