Aetiology

Alcohol-use disorder is a chronic illness with a multifactorial aetiology, with genetic as well as social, psychological, and environmental antecedents.[12][13] The heritability of alcohol-use disorder has been estimated to be between 40% and 70%, but concordance between twins is less than 50%.[14]​ Thus, though genetics may play a role, other environmental factors are important. Chronic brain exposure to alcohol can result in long-term adaptive changes that initially produce increased reinforcement for alcohol use, and over time progress to withdrawal and negative affective states, so that regular alcohol use is required to feel normal.[15]​ These changes can persist for months after an individual ceases to use alcohol, putting the individual at risk for return to use, and representing an important and effective target for treatment.

Heavy drinking seems to be particularly harmful, with heavy drinking episodes linked to increased mortality, even when overall alcohol intake is low.[16]

Pathophysiology

Several neurobehavioural effects of alcohol have been related to the development of alcohol-use disorder. The pleasurable effects of alcohol are mediated by a dopaminergic pathway projecting from the ventral tegmental area to the nucleus accumbens.[12] Repeated alcohol ingestion sensitises this pathway and leads to dependence. Long-term exposure to alcohol causes adaptive changes in several neurotransmitter systems, including down-regulation of inhibitory neuronal gamma-aminobutyric acid receptors, up-regulation of excitatory glutamate receptors, and increased central norepinephrine (noradrenaline) activity.[17]

Discontinuation of alcohol ingestion leaves this excitatory state unopposed, resulting in the nervous system hyperactivity and dysfunction that characterise alcohol withdrawal. It has also been suggested that withdrawal symptoms intensify as withdrawal episodes grow in number, a phenomenon called 'kindling'.[17][18]​ Patients with alcohol-use disorder often experience craving, defined as the conscious desire or urge to drink alcohol. Cravings are linked to dopaminergic, serotonergic, and opioid systems that mediate positive reinforcement, and to the gamma-aminobutyric acid, glutamatergic, and noradrenergic systems that mediate withdrawal.[13] Long-term use of alcohol is also proposed to enhance corticotrophin-releasing factor, neuropeptide Y, and other stress-producing neurotransmitters and hormones, so that continued alcohol use becomes necessary to reduce stress and dysphoria. 

Classification

Unhealthy alcohol use is defined by the US National Institute on Alcohol Abuse and Alcoholism (NIAAA) as more than 3 drinks per day or 7 per week for women and more than 4 drinks per day or 14 per week for men.[1]

Diagnostic and statistical manual of mental disorders, 5th edition, text revision (DSM-5-TR)[3]

Classification of alcohol-use disorder:

  • A problematic pattern of alcohol use over a 12-month period that results in clinically significant impairment or distress.

  • At least 2 of 11 diagnostic criteria must be met. See Criteria.

International classification of diseases, 11th edition (ICD-11)​[4]

Alcohol dependence is a pattern of recurrent episodic or continuous use of alcohol with evidence of impaired regulation of alcohol use. The features of dependence are usually evident over a period of at least 12 months but, the diagnosis may be made if use is continuous for at least 3 months.

Harmful alcohol use is a pattern of use that has caused clinically significant damage to a person’s physical or mental health, or has resulted in behaviour leading to harm to the health of others.

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