Cannabis
TL;DR — Acute HR spike (+16–17 bpm) → same-night REM suppression → next-day recovery distortion. Edibles hit harder because oral THC converts to 11-OH-THC (2–5× more psychoactive). Tolerance hides signal from wearables but not risk.
Key Facts
| Intoxicating compound | Δ9-THC |
| Key active metabolite | 11-OH-THC — explains edible potency |
| Primary receptor | CB1 receptor |
| Strongest biometric signature | Acute HR rise + REM suppression |
| Acute HR effect | +16–17 bpm typical; 20–60% above baseline in some studies |
| REM effect | ~34 min reduction same night |
| FDA-approved CUD treatment | None |
| Main stack conflict | Cannabis peptide interactions — blunts Retatrutide appetite suppression |
Pharmacokinetics
| Route | Onset | Tmax | Key trait |
|---|---|---|---|
| Inhaled | ~minutes | ~9 min | Rapid, titratable; acute HR spike visible within 2–3 min |
| Oral/edible | 30–120 min | 1–6 h | First-pass → 11-OH-THC; delayed overconsumption risk |
| Sublingual | 15–45 min | — | Intermediate kinetics |
Fat solubility: THC accumulates in adipose tissue. Terminal half-life 3–4 days initially, 4–12+ days in chronic heavy users. Functional detection window is weeks in heavy users.
Mechanisms
- Acute: CB1 activation → broad GABAergic/glutamatergic modulation → altered salience, appetite, HR, memory
- Tolerance: Chronic use → 15–20% CB1 downregulation (PET evidence); cortical regions most affected
- Recovery: CB1 normalization starts ~2 days abstinence; near-complete by ~4 weeks
- Withdrawal: Combined CB1 downregulation + reduced endocannabinoid tone + CRF-driven amygdala reactivity → Cannabis withdrawal
Biometric Phases
Acute (0–3 h)
- HR rises +16–17 bpm; sinus tachycardia (>100 bpm) in ~19% of acute users
- HF-HRV shifts sympathetic; BP biphasic (rise then orthostatic drop)
- Appetite stimulations via hypothalamic CB1 receptor
Overnight
- REM ↓ ~34 min; REM latency ↑ ~66 min
- Sleep may feel easier; architecture is objectively worse
- Sleep architecture and REM suppression both relevant
Next-day
- RHR elevated, HRV suppressed, recovery/readiness lower
- Executive function impaired 6–8+ h, longer in heavy users
- Occasional users: loud signal. Heavy users: muted acute spike but persistent sleep/cognitive effects.
Risks
- Psychosis: OR 1.4 (any use), 2.3–3.0 (daily), up to 5.7 (high-potency) — Psychosis risk
- Cardiovascular: ACS RR 1.29, stroke RR 1.20, CV death RR 2.10; strongest with smoked use — Cardiovascular risk
- CHS: Paradoxical vomiting from TRPV1 desensitization; hot showers/capsaicin help — CHS
Detection
Cannabis detection model — Best wearable candidate after alcohol. Expected AUC ~0.75–0.85 in occasional users; worse in heavy users unless tolerance-adjusted. Primary features: HR delta from baseline, REM suppression, motion context, sleep efficiency drop.
Interactions
Cannabis peptide interactions — The only meaningful Ben-stack conflict: cannabis blunts Retatrutide appetite suppression via opposing hypothalamic signaling. No dangerous PK interactions with BPC-157, TB-500, or GHK-Cu.