COMPOUNDS / GABAERGIC / ALCOHOL
GABAERGIC

ALCOHOL

HIGH RISK
BEST FOR:Social●●○○○○○○○○2/10
ALCOHOL · ETHANOL · ETHYL ALCOHOL · ETOH · BOOZE · LIQUOR · SPIRITS
DepressantGABAergicSocialHepatotoxicDependence

A widely used CNS depressant that enhances GABA and inhibits glutamate, producing disinhibition, sedation, and significant dependence risk.

ROUTE / DOSAGE
LOW10-20g
STANDARD20-30g
HIGH40g+
Note: Doses refer to grams of pure ethanol; absorption faster on empty stomach
CYCLE
No daily use recommended max 2-3 standard drinks per occasion several alcohol-free days per week
BIOAVAILABILITY
~80% oral
ACTIVE DURATION
4-8h (subjective)
STORAGE
Room temperature sealed container away from heat and open flame
HALF-LIFE
4-5h (plasma)
DURATION BREAKDOWN
Total4-8 hours
Onset5-30min
Come up15-45min
Peak1-3h
Offset2-4h
After effects4-12h
Duration varies by route, dose, and individual. Source: community reports.
§ 01 — EFFECTS
8 documented
Euphoria and disinhibition
Sedation and drowsiness
Impaired coordination and motor control
Slurred speech
Reduced social inhibitions
Memory impairment and blackouts
Analgesia
Nausea and vomiting at high doses
§ 02 — RISKS
Respiratory depression and death at high doses, especially combined with other CNS depressants
Physical dependence and severe withdrawal syndrome including seizures and delirium tremens
Liver disease including fatty liver, alcoholic hepatitis, and cirrhosis
Increased risk of multiple cancers including oral, esophageal, liver, and breast cancer
Immune suppression leading to increased susceptibility to infections
Neurocognitive impairment and brain atrophy with chronic use
§ 03 — INTERACTIONS
No interaction with your stack
VIEW STACK
CAUTION
Stimulants
Cannabis
Amphetamines
AMT
MDMA
Nitrous
SSRIs
AVOID · DANGEROUS
Depressants
Dissociatives
Benzodiazepines
DXM
GHB
GBL
Ketamine
MXE
Opioids
Tramadol
Cocaine
MAOIs
PCP
ALDH2 inhibitors
Hepatotoxic drugs
§ 04 — SCIENCE

Alcohol disrupts the balance between inhibitory and excitatory neurotransmission; acute exposure favors inhibition while chronic exposure induces compensatory changes leading to tolerance and withdrawal syndrome upon cessation (Valenzuela, 1997). Alcohol significantly impairs both innate and adaptive immune function, increasing susceptibility to bacterial and viral infections, with chronic use promoting proinflammatory responses central to alcoholic liver disease and pancreatitis (Szabo & Saha, 2015). Hangover pathology involves alcohol metabolites, neurotransmitter alterations, inflammatory factors, and mitochondrial dysfunction, though human hangover studies suffer from poor methodological control (Palmer et al., 2019). Chronic heavy consumption reduces testosterone levels and impairs male reproductive function at the hypothalamic, pituitary, and testicular levels (Emanuele & Emanuele, 1998). Research on alcohol's neurobiobehavioral effects in women remains underrepresented despite evidence of significant neuropsychological compromise (Nixon et al., 2023).

§ 06 — SOURCES
[1]
Alcohol Hangover: Underlying Biochemical, Inflammatory and Neurochemical Mechanisms
pubmed.ncbi.nlm.nih.gov ↗
[2]
Alcohol's effect on lactation
pubmed.ncbi.nlm.nih.gov ↗
[3]
Alcohol and neurotransmitter interactions
pubmed.ncbi.nlm.nih.gov ↗
[4]
Alcohol's Effect on Host Defense
pubmed.ncbi.nlm.nih.gov ↗
[5]
Women's use of alcohol: Neurobiobehavioral concomitants and consequences
pubmed.ncbi.nlm.nih.gov ↗
[6]
Toxic alcohol diagnosis and management: an emergency medicine review
pubmed.ncbi.nlm.nih.gov ↗
[7]
Alcohol's contribution to compromised immunity
pubmed.ncbi.nlm.nih.gov ↗
[8]
Alcohol's effects on male reproduction
pubmed.ncbi.nlm.nih.gov ↗
[9]
PsychonautWiki - Alcohol
psychonautwiki.org ↗
Disclaimer. Protokol.wiki is an informational reference. Nothing on this site is medical advice. Compounds listed may be unapproved, unregulated, or illegal in your jurisdiction. Consult a licensed physician before use. Data compiled from peer-reviewed literature.
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