Alcohol MOC

Hub

• Alcohol

Mechanisms

• GABA-A receptor — primary intoxication target; α1/δ subunit potentiation → neuronal inhibition
• NMDA receptor — secondary; glutamate antagonism → excitotoxicity during withdrawal
• CYP2E1 and ROS — metabolic ROS source; drives NF-κB → IL-6/TNF-α inflammatory cascade
• Acetaldehyde myth — acetaldehyde does NOT cross BBB; hangover is inflammatory, not acetaldehyde toxicity
• Acetate and CNS — acetate crosses BBB freely; brain shifts to acetate as fuel during alcohol metabolism
• NADH NAD+ disruption — gluconeogenesis inhibition → hypoglycaemia; fatty acid synthesis → hepatic steatosis
• ADH ALDH genetics — ALDH22 (East Asian flush): acetaldehyde IS a direct toxin; oesophageal SCC risk 17.3× homozygotes, 14.5× heterozygotes vs 2.2× normal ALDH2. ADH1B2 (protective fast-metaboliser); BChE polymorphisms affect cocaine toxicity risk

Biometrics

• HRV signatures (alcohol) — RMSSD ↓ 30–50% acute; dose-dependent; sympathetic shift
• Sleep architecture (alcohol) — REM ↓, SWS ↑ early then ↓, WASO ↑; recovery severely impaired

Risks & Recovery

• Hangover mechanism — IL-6/TNF-α inflammatory cascade via CYP2E1/ROS/NF-κB; prostaglandin E2 headache
• Hangover countermeasures — two systematic reviews: no effective commercial intervention; NSAID + glucose + time only evidence-based

Detection

• Alcohol detection model — HRV suppression + elevated RHR + sleep efficiency drop + motion context

Interactions

• Alcohol peptide interactions — Retatrutide: flattened/delayed BAC (triple agonist > semaglutide), reward modulation (GLP-1 VTA/NAc), glucagon may compound hypoglycaemia, continuous interaction; BPC-157 (gastroprotection); TB-500 (hepatoprotective, preclinical); GHK-Cu (antioxidant, NOT Fenton risk)