LSD Analogues for Health & Longevity - Quick Reference Sheet

LSD Analogues for Health & Longevity

Created on 08/05/2026 – Quick Reference based on Evidence Review created using AI4L / Opus 5 Audit

Most LSD analogues are shells the body strips away to release ordinary LSD; their strongest documented benefit is delivery, not health outcomes. A smaller engineered group removes the visions but remains largely in animals. Harms include raised blood pressure and heart rate, nausea, headache, fear, impaired judgement, and mania in susceptible people. Unregulated manufacture means labels are often wrong. (Full Review)

Protocol

Supervised full-dose model
100–200 µg
Parent-compound dose. Per 100 µg, analogue equivalents are approximately 113 µg ALD-52, 117 µg 1P-LSD, 121 µg 1cP-LSD, 126 µg 1V-LSD.
Low-dose repeated model
One dose, two days off
Fadiman schedule, repeated for several weeks; a Paul Stamets variant runs four days on, three off. Doses typically a tenth or less of a full dose.
Best time of day
Morning, before 10:00
Single dosing, not split. The 8–12 hour active period must end well before sleep onset; delayed-onset analogues start earlier.
Time to effect
Onset
30–90 min
Full doses of the shorter-chain prodrugs; later for delayed-onset compounds. Peak at 2–4 hours, resolving over 8–12 hours.
Mood benefit
Days after a session
Any therapeutic mood benefit in the trial literature appears in the days following a session rather than during it.
Low-dose energy
1–2 hours
Acute effects on energy. Proponents describe cumulative effects over 2–4 weeks that controlled evidence has not confirmed.

Benefits

Contraindications
  • Personal history of any psychotic disorder or bipolar I disorder, or a first-degree relative with either
  • Active suicidal ideation, or a suicide attempt within the past 12 months
  • Current lithium therapy
  • Uncontrolled hypertension above 140/90 mmHg
  • Myocardial infarction within 6 months, unstable angina, or NYHA Class III to IV heart failure
  • Known moderate or severe valvular regurgitation
  • A seizure disorder
  • Child-Pugh Class B or C liver impairment
  • Pregnancy or breastfeeding
  • Existing hallucinogen persisting perception disorder
  • Any situation requiring driving or safety-critical work within 24 hours of dosing
Key Interactions
  • Selective serotonin reuptake inhibitors and serotonin-noradrenaline reuptake inhibitors (fluoxetine, sertraline, venlafaxine)
  • Monoamine oxidase inhibitors (phenelzine, tranylcypromine, selegiline)
  • Tricyclic antidepressants and non-lithium mood stabilisers (amitriptyline, nortriptyline; valproate, lamotrigine)
  • Antipsychotics (risperidone, olanzapine, quetiapine)
  • Other 5-HT2B agonists and ergot derivatives (cabergoline, pergolide, ergotamine)
  • Triptans and vasoconstrictive migraine drugs (sumatriptan, rizatriptan)
  • Stimulants, prescription and over-the-counter (amphetamine, methylphenidate, pseudoephedrine, high-dose caffeine)
  • Over-the-counter dextromethorphan and diphenhydramine
  • Serotonergic supplements (5-HTP, L-Tryptophan, St. John's wort)
  • Supplements with additive blood-pressure or vasoconstrictive effects (synephrine, yohimbine, liquorice root, ephedra)
  • Supplements that plausibly blunt or modify the response (high-dose magnesium, cannabidiol, ashwagandha)
  • Transcranial magnetic stimulation or ketamine therapy
  • Alcohol

Risk & Side Effects

  • High: Acute anxiety, panic, and confusion; acute rise in blood pressure and heart rate; nausea, headache, dizziness, and fatigue; impaired judgement, coordination, and accident risk; dose uncertainty from unregulated manufacture
  • Medium: Precipitation of mania, hypomania, or psychosis; worsening depression and emergent suicidality; rapid tolerance with repeated dosing; next-day impairment and sleep disruption
  • Low: Hallucinogen persisting perception disorder; cardiac valve fibrosis with chronic exposure; predicted organ toxicity signals from computational modelling
  • Speculative: Impurity and by-product exposure from grey-market synthesis; long-term receptor regulation from sustained low-dose use

Monitoring

Marker Target Why
Seated blood pressure 105–120 / 65–80 mmHg Determines tolerable dose ceiling
Resting heart rate 50–70 bpm Baseline for the reliable acute rise
Echocardiogram, valve morphology No regurgitation beyond trace at any valve Documents valve status before cumulative 5-HT2B exposure
Electrocardiogram, QTc interval < 440 ms men, < 450 ms women Screens for the rhythm vulnerability that computational models flag
ALT and AST ALT 10–26 U/L women, 10–30 U/L men; AST 10–26 U/L Confirms hepatic capacity to clear the released compound
Complete blood count Haemoglobin 13.5–15.0 g/dL men, 12.5–14.5 women; platelets 200–300 ×109/L Addresses the hematotoxicity signal predicted for 1P-LSD and 1B-LSD
eGFR with creatinine and cystatin C > 90 mL/min/1.73 m2 Confirms clearance of downstream metabolites
hs-CRP < 0.5 mg/L Baseline for the speculative anti-inflammatory claim
Prolactin Men < 15 ng/mL; women < 20 ng/mL Detects sustained endocrine effect of ergoline exposure
CYP2D6 genotype Normal metaboliser (two functional copies) Predicts exposure and duration at a given dose

Cadence: Blood pressure and resting heart rate before and 2 hours after each dose; a repeat blood panel at 3 months after starting any repeated regimen, then every 6–12 months while use continues; a repeat echocardiogram at 24 months for anyone dosing more often than monthly.

Qualitative Assessment

  • Sleep quality and continuity
  • Daytime energy and subjective vigour
  • Cognitive clarity and working memory in real tasks
  • Anxiety and mood, scored rather than described
  • Emotional reactivity and interpersonal friction
  • Absence of between-dose perceptual disturbance