Introduction: how a prohibited compound reached the NEJM
Twenty years ago a clinical trial of psilocybin was nearly impossible to run — not for scientific reasons but regulatory ones. Today psilocybin-assisted therapy appears in The New England Journal of Medicine, JAMA and Nature. Johns Hopkins, Imperial College London, NYU Langone and the international COMPASS Pathways consortium have run dozens of trials in depression, addiction and existential distress.
This is one of those topics where enthusiasm runs ahead of the data. Popular reviews tend to list positive results one after another, and the picture comes out close to triumphant. But three papers published in 2025–2026 change that picture substantially, and none of them appear in the popular round-ups.
The key point: the evidence base for psilocybin is neither "strong" nor "weak" — it is inconsistent. The more rigorous the methodology, the more modest the effect. Below, indication by indication with levels of evidence, plus what an endocrinologist is obliged to exclude in "treatment-resistant" depression before a patient goes looking for experimental answers.
| Trial | Design | Result |
|---|---|---|
| Carhart-Harris 2016 (n=12) | open-label, TRD | symptom reduction up to 3 months |
| Davis 2021 (n=27) | RCT, waiting-list control | >50% remission by week 4 |
| NEJM 2021 (n=59) | double-blind vs escitalopram | primary endpoint NOT significant |
| COMPASS 2022 (n=233) | double-blind, phase IIb | 25 mg > 1 mg at week 3 |
| JAMA 2023 (n=104) | double-blind, active placebo | significant reduction by week 6 |
| *EPISODE 2026 (n=144)* | *triple-blind, active placebo* | *17.0% vs 10.6%, p=0.19 — NOT significant* |
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Depression: where the evidence is strongest and where it cracked
The modern era begins with an open-label pilot in treatment-resistant depression (Carhart-Harris RL, et al. Lancet Psychiatry 2016;3:619–627. DOI 10.1016/S2215-0366(16)30065-7, level 2b — uncontrolled open-label, n=12). All participants received two supported sessions; most improved, and in some the effect held for three months. The study established feasibility and safety — not efficacy: without a control arm there is no way to separate the drug from the effect of intensive attention.
A randomised trial in major depressive disorder followed (Davis AK, et al. JAMA Psychiatry 2021;78:481–489. DOI 10.1001/jamapsychiatry.2020.3285, level 1b, n=27). More than half the participants reached remission by week four. The important caveat: the control was a waiting list — a group receiving nothing at all. That design systematically inflates the apparent effect of any active intervention.
The first attempt at a fair comparison was the escitalopram trial (Carhart-Harris R, et al. N Engl J Med 2021;384:1402–1411. DOI 10.1056/NEJMoa2032994, level 1b, n=59). Here is what popular summaries mention only in passing: on the primary endpoint there was no difference between psilocybin and a standard antidepressant. Most secondary measures — remission rate, social functioning — favoured psilocybin, but secondary endpoints do not substitute for the primary one; they generate hypotheses rather than prove effects.
The largest trial of its time came from COMPASS Pathways (Goodwin GM, et al. N Engl J Med 2022;387:1637–1648. DOI 10.1056/NEJMoa2206443, level 1b, n=233). A 25 mg dose significantly outperformed the 1 mg comparator by week three, while 10 mg showed no advantage. A single 25 mg dose was then confirmed against active placebo in major depressive disorder (Raison CL, et al. JAMA 2023;330:843–853. DOI 10.1001/jama.2023.14530, level 1b, n=104).
Durability looked convincing: twelve months after two sessions, 75% of participants maintained a clinical response and 58% were in remission (Gukasyan N, et al. J Psychopharmacol 2022;36:151–158. DOI 10.1177/02698811211073759, level 2b — open prospective follow-up, n=27). In the larger COMPASS cohort, however, effect size declined over time and some patients required repeat courses (J Clin Psychiatry 2025. DOI 10.4088/JCP.24m15449, level 2b — observational follow-up).
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What 2026 changed
In May 2026 the EPISODE trial was published: two centres, triple blinding (investigator, participant, rater), active placebo, in patients with treatment-resistant depression withdrawn from antidepressants (Mertens LJ, et al. JAMA Psychiatry 2026;83:448–460. DOI 10.1001/jamapsychiatry.2026.0132, PMID 41848690, level 1b, n=144).
On the primary endpoint (≥50% reduction on HAMD-17 at week 6) response rates were 17.0% on 25 mg, 12.5% on 5 mg and 10.6% on nicotinamide. The adjusted odds ratio for 25 mg versus placebo was 1.73 (95% CI 0.53–6.23), p=0.19. The difference did not reach significance and, under the hierarchical testing plan, no further formal testing was performed. The authors note a clinically meaningful symptom reduction on secondary measures but describe the trial itself as inconclusive.
Note the absolute numbers: 17% versus 10.6%. That is a long way from "more than half of patients in remission" reported against a waiting list. The gap between those figures is not a difference between compounds — it is a difference between study designs.
Six- and twelve-month follow-up of the same cohort was published separately (Psychother Psychosom 2026. DOI 10.1159/000552272, PMID 42201843, level 2b — naturalistic follow-up).
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Why one negative trial outweighs five positive ones
This is not special pleading against an inconvenient result. It is a basic principle of evidence-based medicine: a study weighs according to its protection from bias, not the direction of its conclusion.
The central problem across this field is blinding. A systematic review of 112 randomised psychedelic trials (JAMA Psychiatry 2026. DOI 10.1001/jamapsychiatry.2026.0255, PMID 41984443) found that only 29.5% assessed blinding integrity, although 57.1% cited blinding as a limitation. In psilocybin, LSD and ayahuasca studies, unblinding among participants and raters frequently exceeded 90%. No control strategy reliably preserved blinding.
Why this matters so much here: someone who has received 25 mg of psilocybin knows it almost without error — the experience cannot be mistaken for placebo. They understand they are in the "real" arm, and the expectation of improvement becomes part of the treatment. With subjective endpoints such as depression rating scales, that expectation is recorded as effect.
A second methodological thread concerns how control groups behave. A meta-analysis compared outcomes in control arms across trials of psilocybin, SSRIs and esketamine (JAMA Netw Open 2025;8:e2524119. DOI 10.1001/jamanetworkopen.2025.24119, PMID 40736734). When control arms behave differently across fields, directly comparing "response percentages" between trials loses meaning — which is exactly how popular summaries are usually assembled.
The practical conclusion as of July 2026 is "an effect probably exists, it is moderate, and its size is not yet established" — not "psilocybin outperforms antidepressants".
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Addiction: the most unexpected result
The paradox is that the most convincing numbers come not from depression but from tobacco dependence. The first pilot produced a figure that looked implausible: 80% of participants were not smoking at six months (Johnson MW, et al. J Psychopharmacol 2014;28:983–992. DOI 10.1177/0269881114548296, level 2b — open pilot, n=15). At roughly 2.5 years, 60% remained abstinent (DOI 10.3109/00952990.2016.1170135, level 2b, n=15).
The key confirmation arrived in 2026 as a head-to-head against standard care. All participants completed the same 13-week cognitive behavioural programme, then received either a single psilocybin dose or a course of nicotine patches (JAMA Netw Open 2026. DOI 10.1001/jamanetworkopen.2026.0972, level 1b — pilot RCT, n=82). At six months, complete abstinence was 40.5% versus 10% — more than a sixfold higher probability of quitting. No serious treatment-related adverse events were recorded.
In alcohol use disorder, the first large RCT reported fewer heavy drinking days and complete abstinence in about 48% versus 24% on active placebo over eight months of follow-up (Bogenschutz MP, et al. JAMA Psychiatry 2022;79:953–962. DOI 10.1001/jamapsychiatry.2022.2096, level 1b, n=93). A Swiss phase 2 trial conducted after detoxification, however, found no significant difference in either abstinence duration or consumption — only a greater reduction in craving (eClinicalMedicine 2025. DOI 10.1016/j.eclinm.2025.103149, level 1b, n=37).
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Cancer and existential distress
Palliative psychiatry is where the modern research programme began. Two 2016 trials — NYU (Ross S, et al. J Psychopharmacol 2016;30:1165–1180. DOI 10.1177/0269881116675512, level 1b, n=29) and Johns Hopkins (Griffiths RR, et al. J Psychopharmacol 2016;30:1181–1197. DOI 10.1177/0269881116675513, level 1b, n=51) — showed marked reductions in anxiety, depression and fear of death, sustained for at least six months.
Re-assessment of the NYU participants at an average of 4.5 years found persistently lower distress, and most described the experience as among the most significant events of their lives (Agin-Liebes GI, et al. J Psychopharmacol 2020;34:155–166. DOI 10.1177/0269881119897615, level 2b — observational follow-up, n=16). A group-therapy format in cancer patients with depression has been studied separately (Cancer 2024;130:1101–1112. DOI 10.1002/cncr.35010, PMID 38105655, level 2b — open-label, n=30).
The honest appraisal of this whole body of work comes from Cochrane: certainty of evidence for psychedelic-assisted therapy in anxiety, depression and existential distress in people with life-threatening illness was graded low (Cochrane Database Syst Rev 2024. DOI 10.1002/14651858.CD015383.pub2, PMID 39260823). Small samples, unachievable blinding, short follow-up.
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Mechanism: what neuroimaging shows
Psilocybin is an agonist at serotonin 5-HT2A receptors, densely expressed in the cortex. The first fMRI study produced an unexpected result: instead of the anticipated activation, it found reduced activity in the medial prefrontal and posterior cingulate cortex — key hubs of the Default Mode Network (Carhart-Harris RL, et al. PNAS 2012;109:2138–2143. DOI 10.1073/pnas.1119598109).
This underpinned the "entropic brain" model: psychedelics temporarily loosen the rigidity of established neural networks, increasing flexibility of information processing (Front Hum Neurosci 2014;8:20. DOI 10.3389/fnhum.2014.00020). Direct confirmation came from high-resolution functional MRI: psilocybin desynchronises large-scale networks, most strongly the Default Mode Network, with synchrony subsequently restored (Siegel JS, et al. Nature 2024;632:131–138. DOI 10.1038/s41586-024-07624-5).
A separate line links the depth of subjective experience to outcome. A systematic review of 12 clinical studies found that in 10 of them the intensity of mystical-type experience statistically predicted symptom reduction (Front Psychiatry 2022;13:917199. DOI 10.3389/fpsyt.2022.917199). Interpret with care: this is a correlation, and it may partly express the same unblinding problem — the stronger the experience, the more obvious to the participant that they received the active compound.
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What I check as an endocrinologist before any conversation about psychedelics
This section appears in no popular review, and for clinical practice it matters more than the rest. Treatment-resistant depression is a diagnosis of exclusion. Before calling depression resistant, one has to be sure it is not being sustained by an unrecognised organic cause. In my practice that regularly turns out to be endocrine or nutritional.
The minimum panel before experimental therapy is even discussed:
▸TSH, free T4, TPO antibodies — not TSH alone. Depression and anxiety are statistically associated with Hashimoto thyroiditis even with normal TSH and T4: in euthyroid Hashimoto, lifetime odds of depression run about 6.6 times higher and of anxiety disorder about 4.9 times higher. ▸Vitamin D, vitamin B12, ferritin — iron deficiency without anaemia and low-normal B12 produce fatigue and low mood indistinguishable from depressive symptoms. ▸Fasting glucose and HbA1c — insulin resistance is associated with depressive symptoms and fatigue. ▸Morning cortisol where clinically suspected — both hyper- and hypocortisolism masquerade as affective disorders.
The point is not to declare all depression hormonal — that would be as much of an overreach as promising miracles from psilocybin. The point is sequence: first exclude the causes that have cheap, safe and well-proven treatment, and only then discuss a therapy whose odds ratio is 1.73 with a confidence interval crossing unity.
The endocrine side is covered in detail in a separate article: hypothyroidism, Hashimoto and the link with depression and anxiety.
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The leading axis: how I work through a case before prescribing anything
The panel above is only the first layer. What actually determines the decision in my practice comes next: assessment by axes. Instead of listing complaints linearly, I grade several systems by severity of dysfunction and identify the leading axis — the one dragging the others behind it.
The axes assessed are: immune-inflammatory (including age-related low-grade inflammation and the aftermath of past viral infection), hormonal-regulatory (thyroid, adrenals, sex hormones), metabolic (glycaemia, insulin resistance, body composition), gastrointestinal and microbiotic, the stress–sleep–neuroendocrine axis, and nutritional — the deficiencies that constrain every other system.
The purpose is not to find "all the abnormalities" but to establish a hierarchy. The axes interact: gastrointestinal dysfunction may be feeding the immune-inflammatory axis rather than being a standalone problem. Treating a secondary axis in isolation from the leading one means acting on the consequence while the cause keeps running.
Why this matters so much in a conversation about depression and anxiety. A configuration I encounter regularly is one where low mood, anxiety and disrupted sleep are secondary to the immune-inflammatory or hormonal axis. Some of these states develop through what the literature calls sickness behaviour: an inflammatory signal alters behaviour and affect, and subjectively it is indistinguishable from "real" depression.
The practical implication is uncompromising: if an affective symptom is secondary, acting on it in isolation is a dead end. That holds equally for anxiolytics, for adaptogens and — all the more — for experimental psychedelic therapy with an odds ratio of 1.73 and a confidence interval crossing unity. Each of those scenarios reproduces the same error: treating a downstream symptom while the leading axis remains untouched. Only the cost of the error differs.
Hence my answer to "should I consider psilocybin for long-standing depression": first establish which axis is leading. If the affective picture turns out to be the summit of an immune-inflammatory or thyroid cascade, discussing psychedelic therapy is premature — regardless of what the trials showed.
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The same standard, applied to my own data
An article that grades other people's research by level of evidence is obliged to hold the same ruler up to itself. Data from my own practice is kept to a formalised scheme, and here is what it consists of.
▸Prospective structured records. Each case is recorded against a single set of fields — baseline measures, change at defined checkpoints, therapy adjustments — rather than reconstructed from memory after the fact. Identification is anonymised: working records use a coded identifier, never a name. ▸Accounting by participant-flow (CONSORT-style): how many enquired, how many met criteria, how many received the protocol, how many reached analysis. Withdrawals and those lost to follow-up are counted separately rather than vanishing from the denominator — which is precisely what separates an honest percentage from a marketing one. ▸An adverse-event log with date, grade and resolution (resolved / resolved with sequelae / ongoing). ▸STROBE reporting — the standard for describing observational research: inclusion criteria, data sources, measures against bias, limitations. ▸An append-only corrections log. If a previously published figure turns out to be wrong, it is not silently overwritten — the correction is recorded as its own entry. ▸A single source of truth for numbers. Figures live in one place and flow to the pages from there, instead of being duplicated across dozens of files and quietly drifting apart. The rule inside that scheme is simple: an unknown value stays marked unknown rather than being filled in with a plausible-sounding number.
And now the honest conclusion from all of the above. However carefully such work is conducted, it is observational data: no randomisation, no control group, no blinding. By the very hierarchy I use throughout this article, a case series from practice is level 2b–4. It describes practice and generates hypotheses. It does not prove efficacy and cannot serve as a counterargument to a randomised trial.
That is exactly why I do not set my own percentages against the EPISODE data, and do not present them here as evidence. Clinical experience is valuable for something else: it indicates where to look for the cause and in what order to exclude possibilities. Proof that an intervention works comes from a different type of study — and in the case of psilocybin, that type of study is so far returning an inconclusive result.
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Safety: what is known about the risks
Under controlled conditions the safety profile is broadly favourable but not flawless. A meta-analysis and systematic review of psychedelic psychotherapy safety summarises the adverse-event data (Psychiatry Res 2024;335:115880. DOI 10.1016/j.psychres.2024.115880, PMID 38579460).
Specific signals from the most rigorous trial (EPISODE, 2026):
▸Two serious adverse reactions after 25 mg, including one case of hallucinogen persisting perception disorder (HPPD) — a condition in which visual disturbances persist after the drug has worn off. ▸Reports of suicidal ideation on dosing days: 4% versus 1–2% in comparator groups. This is precisely the patient population in which such a signal demands maximum caution. ▸Most adverse events were acute, occurring during the session itself.
Trial screening is strict, and that is fundamental to interpreting the results. Exclusions typically include a personal history of psychotic disorders, psychosis or bipolar I disorder in first-degree relatives, uncontrolled hypertension and significant cardiac disease, and pregnancy. People who enter these trials are not the average patient with depression.
Drug interactions deserve separate attention: SSRIs and other serotonergic agents alter the subjective response (EPISODE deliberately withdrew participants from antidepressants), and combination with lithium has been described as increasing the risk of adverse neurological events. Stopping an antidepressant on one's own for a "cleaner experience" is a distinct and entirely real hazard.
A particular concern is microdosing. A 2024 review notes that psilocybin and LSD are structurally similar to drugs that caused cardiac fibrosis and valvulopathy with regular use (methysergide, pergolide, fenfluramine) through 5-HT2B receptor stimulation (J Psychopharmacol 2024;38:217–224. DOI 10.1177/02698811231225609, PMID 38214279). The long-term cardiac safety of a "two to four times a week for months" regimen has not been studied.
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What is NOT proven
▸Microdosing as treatment. A review of controlled studies (Maastricht University, 2025) concludes that small doses produce subtle changes in mood and neural activity but no convincing clinical advantage over placebo. ▸Alzheimer disease and neurodegeneration. Only preclinical data on dendritic growth and reduced neuroinflammation. There is no clinical evidence of efficacy in patients. ▸Anorexia nervosa. A single phase 1 open-label study in females, n=10 (Nat Med 2023;29:1947–1953. DOI 10.1038/s41591-023-02455-9). That is a tolerability assessment, not efficacy. ▸OCD. A 2006 pilot (n=9, DOI 10.4088/JCP.v67n1110) and a 2025 study using 10 mg (Compr Psychiatry 2025. DOI 10.1016/j.comppsych.2025.152619) where symptom reduction lasted about a week. Early stage. ▸Durability for most patients. COMPASS data show gradual decay; some patients need repeat courses. ▸Transfer of results to retreats and ceremonies. This is arguably the most important item. Trials involve screening for contraindications, a known dose of synthetic compound, preparation, medical supervision during the session and psychotherapeutic integration afterwards. Remove any of those components and you are studying something else. There are no safety or efficacy data outside that structure.
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Legal status
Psilocybin is a controlled substance in most countries and legal access is limited to clinical research. Specific regulatory exceptions exist: since July 2023 authorised psychiatrists in Australia may prescribe psilocybin for treatment-resistant depression, and Oregon and Colorado operate supervised-session programmes. In the European Union and Ukraine, therapy is available only within research protocols.
This article is a review of scientific data, not a guide to action or a recommendation for use. I do not provide psilocybin-assisted therapy and do not advise on access to controlled substances.
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Conclusion
Over twenty years psilocybin research moved from impossible to publishable in the leading journals, which is a scientific event in itself. The most convincing data concern tobacco dependence (40.5% versus 10%) and existential distress in cancer patients, though Cochrane grades the certainty of the latter as low.
For depression the picture is more complicated than it is usually presented. The two most rigorous trials — the escitalopram comparison (2021) and EPISODE (2026) — missed their primary endpoints. The systematic review of blinding showed the field suffers unblinding rates above 90%. That does not mean there is no effect; it means the true effect is smaller than advertised and not yet precisely established.
The practical implication for a patient with long-standing, unresponsive depression: before pursuing experimental options, it is worth excluding the causes that have cheap and proven treatment — the thyroid first of all, then B12, iron and vitamin D deficiency and disorders of carbohydrate metabolism. Less exciting than the neurobiology of mystical experience, but far ahead on the ratio of benefit, risk and evidence.
This article is informational and does not replace a medical consultation. Psilocybin is a controlled substance; all results cited were obtained under medical supervision and do not apply to unsupervised use. If you are experiencing depression, consult a physician: treatments exist with proven efficacy and a known safety profile.
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References
▸Mertens LJ, et al. Efficacy and Safety of Psilocybin in Treatment-Resistant Major Depression: The EPISODE Randomized Clinical Trial. JAMA Psychiatry 2026;83(5):448–460. DOI 10.1001/jamapsychiatry.2026.0132, PMID 41848690 — level 1b (triple-blind RCT, active placebo, n=144); primary endpoint not met. ▸Blinding Integrity in Psychedelic Randomized Clinical Trials: A Systematic Review. JAMA Psychiatry 2026. DOI 10.1001/jamapsychiatry.2026.0255, PMID 41984443 — systematic review of 112 RCTs. ▸Control Group Outcomes in Trials of Psilocybin, SSRIs, or Esketamine for Depression: A Meta-Analysis. JAMA Netw Open 2025;8:e2524119. DOI 10.1001/jamanetworkopen.2025.24119, PMID 40736734. ▸Carhart-Harris RL, et al. Psilocybin with psychological support for treatment-resistant depression. Lancet Psychiatry 2016;3:619–627. DOI 10.1016/S2215-0366(16)30065-7 — level 2b (open-label, n=12). ▸Davis AK, et al. Effects of Psilocybin-Assisted Therapy on Major Depressive Disorder. JAMA Psychiatry 2021;78:481–489. DOI 10.1001/jamapsychiatry.2020.3285 — level 1b (n=27, waiting-list control). ▸Carhart-Harris R, et al. Trial of Psilocybin versus Escitalopram for Depression. N Engl J Med 2021;384:1402–1411. DOI 10.1056/NEJMoa2032994 — level 1b (n=59); primary endpoint not significant. ▸Goodwin GM, et al. Single-Dose Psilocybin for a Treatment-Resistant Episode of Major Depression. N Engl J Med 2022;387:1637–1648. DOI 10.1056/NEJMoa2206443 — level 1b (n=233). ▸Raison CL, et al. Single-Dose Psilocybin Treatment for Major Depressive Disorder. JAMA 2023;330:843–853. DOI 10.1001/jama.2023.14530 — level 1b (n=104). ▸Gukasyan N, et al. Efficacy and safety of psilocybin-assisted treatment for major depressive disorder: prospective 12-month follow-up. J Psychopharmacol 2022;36:151–158. DOI 10.1177/02698811211073759 — level 2b (n=27). ▸Long-term observational follow-up after a single dose of psilocybin for treatment-resistant depression. J Clin Psychiatry 2025. DOI 10.4088/JCP.24m15449 — level 2b. ▸Psilocybin-assisted psychotherapy for treatment-resistant depression: randomized trial of repeated doses. Med 2024. DOI 10.1016/j.medj.2024.01.005, PMID 38359838 — level 1b (n=56). ▸Johnson MW, et al. Pilot study of the 5-HT2AR agonist psilocybin in the treatment of tobacco addiction. J Psychopharmacol 2014;28:983–992. DOI 10.1177/0269881114548296 — level 2b (n=15). ▸Johnson MW, et al. Long-term follow-up of psilocybin-facilitated smoking cessation. Am J Drug Alcohol Abuse 2017;43:55–60. DOI 10.3109/00952990.2016.1170135 — level 2b (n=15). ▸Psilocybin or Nicotine Patch for Smoking Cessation: A Pilot Randomized Clinical Trial. JAMA Netw Open 2026. DOI 10.1001/jamanetworkopen.2026.0972 — level 1b (n=82); 40.5% versus 10%. ▸Bogenschutz MP, et al. Percentage of Heavy Drinking Days Following Psilocybin-Assisted Psychotherapy vs Placebo in Alcohol Use Disorder. JAMA Psychiatry 2022;79:953–962. DOI 10.1001/jamapsychiatry.2022.2096 — level 1b (n=93). ▸Psilocybin-assisted therapy for relapse prevention in alcohol use disorder: a phase 2 randomized clinical trial. eClinicalMedicine 2025. DOI 10.1016/j.eclinm.2025.103149 — level 1b (n=37); no significant difference. ▸Ross S, et al. Rapid and sustained symptom reduction following psilocybin treatment for anxiety and depression in patients with life-threatening cancer. J Psychopharmacol 2016;30:1165–1180. DOI 10.1177/0269881116675512 — level 1b (n=29). ▸Griffiths RR, et al. Psilocybin produces substantial and sustained decreases in depression and anxiety in patients with life-threatening cancer. J Psychopharmacol 2016;30:1181–1197. DOI 10.1177/0269881116675513 — level 1b (n=51). ▸Agin-Liebes GI, et al. Long-term follow-up of psilocybin-assisted psychotherapy for psychiatric and existential distress in patients with life-threatening cancer. J Psychopharmacol 2020;34:155–166. DOI 10.1177/0269881119897615 — level 2b (n=16). ▸Psilocybin-assisted group therapy in patients with cancer diagnosed with a major depressive disorder. Cancer 2024;130:1101–1112. DOI 10.1002/cncr.35010, PMID 38105655 — level 2b (n=30). ▸Psychedelic-assisted therapy for treating anxiety, depression, and existential distress in people with life-threatening diseases. Cochrane Database Syst Rev 2024. DOI 10.1002/14651858.CD015383.pub2, PMID 39260823 — certainty of evidence low. ▸Carhart-Harris RL, et al. Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin. PNAS 2012;109:2138–2143. DOI 10.1073/pnas.1119598109. ▸Carhart-Harris RL, et al. The entropic brain. Front Hum Neurosci 2014;8:20. DOI 10.3389/fnhum.2014.00020. ▸Siegel JS, et al. Psilocybin desynchronizes the human brain. Nature 2024;632:131–138. DOI 10.1038/s41586-024-07624-5. ▸Psychedelics, Mystical Experience, and Therapeutic Efficacy: A Systematic Review. Front Psychiatry 2022;13:917199. DOI 10.3389/fpsyt.2022.917199. ▸Safety and risk assessment of psychedelic psychotherapy: a meta-analysis and systematic review. Psychiatry Res 2024;335:115880. DOI 10.1016/j.psychres.2024.115880, PMID 38579460. ▸Rouaud A, et al. Microdosing psychedelics and the risk of cardiac fibrosis and valvulopathy. J Psychopharmacol 2024;38:217–224. DOI 10.1177/02698811231225609, PMID 38214279. ▸Peck SK, et al. Psilocybin therapy for females with anorexia nervosa: a phase 1, open-label feasibility study. Nat Med 2023;29:1947–1953. DOI 10.1038/s41591-023-02455-9 — level 2b (n=10). ▸Moreno FA, et al. Safety, tolerability, and efficacy of psilocybin in 9 patients with obsessive-compulsive disorder. J Clin Psychiatry 2006;67:1735–1740. DOI 10.4088/JCP.v67n1110 — level 4 (n=9).
Related article: hypothyroidism, Hashimoto and the link with depression and anxiety — what to check first when low mood persists.
