Alcohol and Drug Abuse and Dependence

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20 Alcohol and Drug Abuse and Dependence

Most physicians are intimately familiar with the protean manifestations of alcohol abuse and dependence (Fig. 20-1) and its characteristic clinical signs (Fig. 20-2). Incidence rates vary widely between cultural groups (alcoholism is almost unheard of in traditional Muslim communities), but lifetime rates of 5–10% are the rule in North America and Europe. Therefore, physicians who state that they never see alcoholism may not be recognizing the diagnosis. Patient denial significantly contributes to overlooking this potential diagnosis. This denial has several sources. Admitting to a problem with alcohol or other drugs may be humiliating for patients. Furthermore, alcohol use, even at dangerous levels, is a culturally embedded and approved, often pleasurable part of social life.

The rubric of drug and alcohol abuse subsumes dozens of syndromes, but a few useful generalizations can be offered. Most drugs have safe and unsafe uses. Physicians routinely employ opiates, sedative-hypnotics, psycho stimulants, and dissociative anesthetics, all of which have abuse and addiction potential. Even over-the-counter drugs, including anticholinergics, pseudoephedrine, and dextromethorphan, can be abused. Conversely, illegal or widely abused substances such as cannabinoids and nicotine have or are likely to have future medical uses.

Potentially abusable drugs cause dopamine release directly or indirectly in several forebrain structures. Beyond this, what makes a drug dangerous are the dosage, route of administration, and social context. High doses, routes of administration that rapidly deliver drug to the brain, and their ingestion beyond a stable social or religious context all predispose to initial abuse and eventual addiction. These factors rather than, for example, the pharmacology of cocaine per se, explain why the Peruvian practice of chewing coca leaves is safe; however, in contrast, smoking freebase cocaine is extremely harmful as is sometimes evidenced in many Western societies.

Etiology

Liability to alcohol abuse and dependence, especially early-onset abuse, runs in families, but the mechanism of inheritance is not understood. Findings of a link between alcoholism and a particular dopamine DR-2 receptor allele remain controversial. Some Asian populations are relatively protected from alcoholism because they possess a variant form of the enzyme alcohol dehydrogenase and metabolize alcohol poorly. This causes them to become flushed and nauseated with minimal doses. Conversely, young adults with a high alcohol tolerance, evaluated on measures of incoordination or subjectively, are at increased risk for later alcoholism. Young adults often assume they are not getting into difficulties with drinking because of their tolerance. Physicians must convince them that this is wrong.

Alcohol is a central nervous system (CNS) depressant with cross-tolerance to benzodiazepines, barbiturates, and some other sedatives. It is distinguished within this group by its ease of manufacture, legal status, wide availability, rapid absorption, and exceptionally low therapeutic index. The lethal dose of alcohol is only a few times the intoxicating dose; one bottle of whiskey can be lethal to an individual who has not acquired tolerance. The dose at which tissue damage occurs is lower in this setting and falls within the range of commonly ingested doses. In most adults, chemical signs of hepatic injury are detectable after consumption of three or more drinks within 24 hours. Alcohol is a potent fetal teratogen with no threshold dose; it is absolutely contraindicated in pregnancy.

Clinical Presentation

Acute alcohol intoxication at moderate doses causes disinhibition and incoordination. Even at socially acceptable doses, it impairs driving and is implicated in approximately half of all highway accidents and deaths. Alcohol is linked to a similar proportion of sexual assaults.

Patients with most major psychiatric illnesses have increased rates of alcohol abuse. Alcohol interacts with psychiatric illnesses and treatments. Many patients use alcohol to treat mood disorders, anxiety, or insomnia, but it is not a safe or effective treatment for any medical disorder. The toxicity and short duration of action of alcohol make it useless as an anxiolytic, and it disrupts sleep architecture and decreases sleep efficiency. The combination of alcohol abuse and depression is especially lethal. Alcohol use makes patients who are depressed more depressed and interferes with antidepressant response. Drinkers who are depressed experience an approximately 10-fold increase in suicide rate compared with nondrinkers who are depressed.

Alcohol has direct toxic effects on multiple tissues, including the central nervous system, liver, the pancreas, and the heart. Patients may present with acute or chronic hepatitis, cirrhosis, esophageal varices, cardiomyopathy, and dementia. Acute withdrawal syndromes occur occasionally, leading to delirium tremens, Wernicke encephalopathy, and Korsakoff psychosis, as illustrated in Chapter 17.

Wernicke syndrome