LSD Analogues for Health & Longevity - Quick Reference Sheet

LSD Analogues for Health & Longevity

Created on 09/22/2026 – Quick Reference based on Evidence Review created using AI4L / Opus 5 – Audit

LSD analogues are laboratory-made relatives of LSD sold online, used mostly as repeated tiny oral doses for mood and mental sharpness. Most are shells the body strips away to release ordinary LSD, inheriting its effects, risks and doses. A smaller engineered group keeps the brain-remodelling effects without the visions, but remains almost entirely in animals. Evidence is early, thin, and commercially entangled; unregulated manufacture means labels are often wrong. (Full Review)

Protocol

Dose
100–200 µg parent-compound equivalent
Supervised full-dose model. Per 100 µg parent: ≈113 µg ALD-52, 117 1P-LSD, 121 1cP-LSD, 126 1V-LSD. Low-dose model a tenth or less.
Timing
Morning, full doses before 10:00
The 8–12 hour active period must end well before sleep onset; delayed-onset analogues start earlier. Single dosing only; in-session redosing is counterproductive.
Interval
14 days minimum between full doses
Cycling is a pharmacological requirement, not a precaution. Low-dose: one on, two off (Fadiman) or four on, three off (Stamets); 8–12 weeks, then ≥4 weeks off.
Time to effect
Full-dose onset
30–90 minutes
Shorter-chain prodrugs; later for delayed-onset. Peak 2–4 hours, resolving over 8–12 hours.
Mood benefit
Days after a session
In the trial literature it appears after a session, not during it.
Low-dose energy effect
1–2 hours
Cumulative effects over 2–4 weeks are described, not confirmed by controlled evidence.

Benefits

Contraindications
  • Current lithium therapy
  • Personal or first-degree history of psychotic or bipolar I disorder
  • Active suicidal ideation or suicide attempt within 12 months
  • Uncontrolled hypertension above 140/90 mmHg
  • Myocardial infarction within 6 months, unstable angina, NYHA III–IV heart failure
  • Moderate or severe valvular regurgitation
  • Seizure disorder
  • Child-Pugh B or C liver impairment
  • Pregnancy or breastfeeding
  • Existing hallucinogen persisting perception disorder
  • Driving or safety-critical work within 24 hours
Key Interactions
  • Selective serotonin and serotonin-noradrenaline reuptake inhibitors (fluoxetine, sertraline, venlafaxine)
  • Monoamine oxidase inhibitors (phenelzine, tranylcypromine)
  • Tricyclics and non-lithium mood stabilisers (amitriptyline, valproate, lamotrigine)
  • Antipsychotics (risperidone, olanzapine)
  • Other 5-HT2B agonists and ergot derivatives (cabergoline, pergolide)
  • Triptans and vasoconstrictive migraine drugs (sumatriptan)
  • Stimulants and decongestants (amphetamine, methylphenidate, pseudoephedrine)
  • Dextromethorphan and diphenhydramine
  • Serotonergic supplements (5-HTP, L-Tryptophan, St. John's wort)
  • Supplements raising blood pressure (synephrine, yohimbine, high-dose caffeine)
  • Supplements that may blunt response (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 (conflicted); 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 Valve status before cumulative 5-HT2B exposure
Electrocardiogram, QTc interval < 440 ms men, < 450 ms women Rhythm vulnerability flagged by computational models
ALT and AST ALT 10–26 U/L women, 10–30 U/L men; AST 10–26 U/L 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 Predicted blood-cell toxicity for 1P-LSD and 1B-LSD
eGFR with creatinine and cystatin C > 90 mL/min/1.73 m² 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 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 heart rate before and 2 hours after each dose; blood panel at 3 months into a repeated regimen, then every 6–12 months; echocardiogram at 24 months when dosing more often than monthly.

Qualitative Assessment

  • Sleep quality and continuity: tracked on off-days; not normalised by the second off-day indicates too dense a schedule
  • Daytime energy and subjective vigour: the most useful single subjective marker
  • Cognitive clarity and working memory in real tasks: recorded against work output, not impression
  • Anxiety and mood, scored rather than described: a brief validated self-report scale weekly
  • Emotional reactivity and interpersonal friction: reported by someone else where possible
  • Absence of between-dose perceptual disturbance: the earliest signal warranting discontinuation