Alcohol Use Disorder

Alcohol use disorder is a pattern of drinking causing clinically significant impairment, ranging from mild to severe, and it produces nutritional consequences that are unusually specific and unusually dangerous. Thiamine deficiency is the headline. Alcohol impairs thiamine absorption, storage and activation, and depleted body stores can be exhausted within weeks. The result is Wernicke encephalopathy — confusion, eye movement abnormalities and ataxia, though the full triad appears in a minority — which, if untreated or treated with glucose before thiamine, progresses to Korsakoff syndrome with permanent anterograde amnesia. This is why parenteral thiamine before any glucose administration is a fixed rule in emergency care, and why oral thiamine is standard in anyone drinking heavily. Withdrawal is the other acute hazard. In dependent drinkers, abrupt cessation can produce seizures within 48 hours and delirium tremens with mortality that remains meaningful even with treatment. Detoxification should be medically supervised, not attempted alone. Beyond thiamine, deficiencies of folate, magnesium, zinc, vitamin B6 and vitamin D are common, and magnesium depletion both provokes arrhythmia and prevents correction of potassium. Effective treatment for the disorder itself exists and is underused: naltrexone and acamprosate have solid randomised support, as do behavioural therapies.

• •Craving and loss of control over drinking
• •Tolerance requiring more for the same effect
• •Morning shakes relieved by drinking
• •Sweating and anxiety between drinks
• •Poor appetite and weight loss
• •Memory gaps
• •Peripheral tingling or numbness

• •GABA and glutamate neuroadaptation
• •Genetic susceptibility
• •Trauma and psychiatric comorbidity
• •Chronic stress
• •Social availability and drinking culture

Neuroadaptation of GABA and glutamate systems producing tolerance and withdrawal, reward pathway reinforcement, genetic susceptibility including alcohol dehydrogenase variants, trauma and psychiatric comorbidity, and social and environmental availability. Nutritional deficiency arises from impaired absorption, displaced dietary intake and hepatic dysfunction.