Alcohol and Alcoholism

Alcohol is not only a popular mind-altering drug but is also regarded in many cultures as a food staple. As a source of empty calories, an addictive drug, and a toxin, it can have a broad spectrum of adverse effects on the body.

Absorption and Metabolism

Alcohol is rapidly absorbed from the digestive tract—about 20% of it in the stomach and 80% in the proximal small intestine. Carbonation,

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Physiology: The Unity of Metabolism Companies, 2003 Form and Function, Third Edition

1012 Part Four Regulation and Maintenance as in beer and sparkling wines, increases its rate of absorption, whereas food reduces its absorption by delaying gastric emptying so the alcohol takes longer to reach its place of maximum absorption. Alcohol is soluble in both water and fat, so it is rapidly distributed to all body tissues and easily crosses the blood-brain barrier to exert its intoxicating effects on the brain.

Alcohol is detoxified by the hepatic enzyme alcohol dehydrogenase, which oxidizes it to acetaldehyde. This enters the citric acid cycle and is oxidized to CO2 and H2O. The average adult male can clear the blood of about 10 mL of 100% (200 proof) alcohol per hour—the amount in about 30 mL (1 oz) of whiskey or 355 mL (12 oz) of beer. Women have less alcohol dehydrogenase and clear alcohol from the bloodstream less quickly. They are also more vulnerable to alcohol-related illnesses such as cirrhosis of the liver (discussed shortly).

Tolerance to alcohol, the ability to "hold your liquor," results from two factors: behavioral modification, such as giving in less readily to lowered inhibitions, and increased levels of alcohol dehydrogenase in response to routine alcohol consumption. Alcohol dehydrogenase also deactivates other drugs, and drug dosages must be adjusted to compensate for this when treating alcoholics for other diseases.

Physiological Effects

Nervous System Alcohol is a depressant that inhibits the release of norepinephrine and disrupts the function of GABA receptors. In low doses, it depresses inhibitory synapses and creates sensations of confidence, euphoria, and giddiness. As the dosage rises, however, the breakdown products of ethanol enhance the diffusion of K+ out of neurons, hyperpolarizing them and making them less responsive to neurotransmitters. Thus, the timing and coordination of communication between neurons is impaired, resulting in such symptoms of intoxication as slurred speech, poor coordination, and slower reaction time. These symptoms begin to become significant at a blood alcohol level of 80 to 100 mg/dL—the legal criterion of intoxication in many states. Above 400 mg/dL, alcohol can so disrupt the electrophysiology of neurons as to induce coma and death.

Liver The liver's role in metabolizing alcohol makes it especially susceptible to long-term toxic effects. Heavy drinking stresses the liver with a high load of acetaldehyde and acetate; this depletes its oxidizing agents and reduces its ability to catabolize these intermediates as well as fatty acids. Alcoholism often produces a greatly enlarged and fatty liver for multiple reasons: the calories provided by alcohol make it unnecessary to burn fat as fuel, fatty acids are poorly oxidized, and acetaldehyde is converted to new fatty acids. Acetaldehyde also causes inflammation of the liver and pancreas (hepatitis and pancreatitis), leading to disruption of digestive function. Acetaldehyde and other toxic intermediates destroy hepatocytes faster than they can be regenerated, and the liver exhibits extensive scarring and a lumpy or nodular surface—a state called cirrhosis. Many symptoms of alcoholism stem from deterioration of liver functions. Hepatic coma may occur as the liver becomes unable to produce urea, thus allowing ammonia to accumulate in the blood. Jaundice results from the liver's inability to excrete bilirubin.

Circulatory System Deteriorating liver functions exert several effects on the blood and cardiovascular system. Blood clotting is impaired because the liver cannot synthesize clotting factors adequately. Edema results from inadequate synthesis of blood albumin. Cirrhosis obstructs the hepatic portal blood circulation. Portal hypertension results, and combined with hypoproteinemia, this causes the liver and other organs to "weep" serous fluid into the peritoneal cavity. This leads to ascites11 (ah-SY-teez)—swelling of the abdomen with as much as several liters of serous fluid. The combination of hypertension and impaired clotting often leads to hemorrhaging. Hematemesis,12 the vomiting of blood, may occur as enlarged veins of the esophagus hemorrhage. Alcohol abuse also destroys myocardial tissue, reduces contractility of the heart, and causes cardiac arrhythmia.

Digestive System and Nutrition Alcohol breaks down the protective mucous barrier of the stomach and the tight junctions between its epithelial cells. Thus it may cause gastritis and bleeding. Alcohol is commonly believed to be a factor in peptic ulcers, but there is little concrete evidence of this. Heavy drinking, especially in combination with smoking, increases the incidence of esophageal cancer. Malnutrition is a typical complication of alcoholism, partly because the empty calories of alcohol suppress the appetite for more nutritious foods. The average American gets about 4.5% of his or her calories from alcohol (more when nondrinkers are excluded), but heavy drinkers may obtain half or more of their calories from alcohol and have less appetite for foods that would meet their other nutritional requirements. In addition, acetaldehyde interferes with vitamin absorption and use. Thiamine deficiency is common in alcoholism, and thiamine is routinely given to alcoholics in treatment.


Alcohol is the most widely available addictive drug in America. In many respects it is almost identical to barbiturates in its toxic effects, its potential for tolerance and dependence, and the risk of overdose. The difference is that obtaining barbiturates usually requires a prescription, while obtaining alcohol requires, at most, proof of age.

Alcoholism is defined by a combination of criteria, including the pathological changes just described; physiological tolerance of high concentrations; impaired physiological, psychological, and social functionality; and withdrawal symptoms occurring when intake is reduced or stopped. Heavy drinking followed by a period of abstinence—for example, when a patient is admitted to the hospital and cannot get access to alcohol—may trigger delirium tremens (DT), characterized by restlessness, insomnia, confusion, irritability, tremors, incoherent speech, hallucinations, convulsions, and coma. DT has a 5% to 15% mortality rate.

Most alcoholism (type I) sets in after age 25 and is usually associated with stress or peer pressure. These influences lead to increased drinking, which can start a vicious cycle of illness, reduced job performance, family and social problems, arrest, and other stresses leading to still more drinking. A smaller number of alcoholics have type II alcoholism, which is at least partially hereditary. Most people with type II alcoholism are men who become addicted before age 25, especially the sons of other type II alcoholics. Type II alcoholics show abnormally rapid increases in blood acetaldehyde levels when they drink, and they have unusual brain waves (EEGs) even when not drinking. Children of alcoholics have a higher than average incidence of becoming alcoholic even when raised by nonalcoholic foster parents. It is by no means inevitable that such people will become alcoholics, but stress or peer pressure can trigger alcoholism more easily in those who are genetically predisposed to it.

Alcoholism is treated primarily through behavior modification— abstinence, peer support, avoidance or correction of the stresses that encourage drinking, and sometimes psychotherapy. The drug disulfiram (Antabuse) is used to support behavior modification programs. It inhibits the breakdown of acetaldehyde and thus heightens its short-term toxic effects. A person who takes Antabuse and drinks alcohol experiences headache, vomiting, tachycardia, chest pain, and hyperventilation and is less likely to look upon alcohol as a means of pleasure or escape.

11asc = bag + ites = like, resembling

12hemat = blood + emesis = vomiting

Saladin: Anatomy & I 26. Nutrition and I Text I © The McGraw-Hill

Physiology: The Unity of Metabolism Companies, 2003 Form and Function, Third Edition

Chapter 26 Nutrition and Metabolism 1013

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