Dec 18, 2009

Encyclopedia of Food & Culture | Alcohol

ALCOHOL. The word "alcohol" is derived from the Arabic word al kuhul, meaning 'essence'. The favorite mood-altering drug in the United States, as in almost every human society, continues to be alcohol. One of the reasons for the significant use of alcohol and its health impact is its feature of being (along with nicotine) a legally available drug of abuse and dependence.

Our knowledge of alcohol rests on a heritage of myth and speculation. Many health benefits have been attributed to alcohol by ancient healers who saw ethanol as the elixir of life, but almost none of its positive benefits have stood the test of time. Alcoholic beverages have been revered, more than any other substance, as mystical and medicinal agents. In recent years, however, we have stripped away much of the mystery surrounding alcohol and now recognize it as a drug with distinct pharmacological effects. However, one of the reasons that beverages containing alcohol continue to be consumed is related to the folklore and history that surround its many combinations with other flavors and its many sources of fermentation and distillation.

Chemist's View

Today one thinks of alcohol and alcoholic spirits as being synonymous, yet to a chemist an alcohol is any of an entire class of organic compounds containing a hydroxyl (OH) group or groups. The first member of its class, methyl alcohol or methanol, is used commercially as a solvent. Isopropyl alcohol, also known as rubbing alcohol, serves as a drying agent and disinfectant. Ethyl alcohol or ethanol shares these functions but differs from other alcohols in also being suitable as a beverage ingredient and intoxicant. Ethanol also differs from other alcohols in being a palatable source of energy and euphoria. It is a small, un-ionized molecule that is completely miscible with water and also somewhat fat-soluble. The remainder of this article pertains to ethanol, but refers to it simply as alcohol.

Biology of Production

Making alcoholic beverages dates back at least eight thousand years; for example, beer was made from cereal mashes in Mesopotamia in 6000 B.C.E. and wine in Egypt in 3700 B.C.E.

Ethyl alcohol is actually a by-product of yeast metabolism. Yeast is a fungus that feeds on carbohydrates. Yeasts are present ubiquitously. For example, the white waxy surface of a grape is almost entirely composed of yeast. When, for example, the skin of a berry is broken, the yeast acts quickly and releases an enzyme that, under anaerobic conditions, converts the sugar (sucrose, C12H22O11) in the berry into carbon dioxide (CO2) and alcohol (C2H5OH). This process is known as fermentation (if the mixture is not protected from air, alcohol turns into acetic acid, producing vinegar). When cereal grains and potatoes are used, each requires a sprouting pretreatment (malting) to hydrolyze starch, during which diastase enzymes are produced that break down starches to simple sugars that the yeast, which lacks these enzymes, can anaerobically convert to alcohol. This process makes the sugar available for the fermentation process. The yeast then continues to feed on the sugar until it literally dies of acute alcohol intoxication.

Because yeast expires when the alcohol concentration reaches 12 to 15 percent, natural fermentation stops at this point. In beer, which is made of barley, rice, corn, and other cereals, the fermentation process is artificially halted somewhere between 3 and 6 percent alcohol. Table wine contains between 10 and 14 percent alcohol, the limit of yeast's alcohol tolerance. This amount is insufficient for complete preservation, and thus a mild pasteurization is applied.

Distillation, which was discovered about 800 C.E.in Arabia, is the man-made process designed to take over where the vulnerable yeast fungus leaves off. The distilled, or hard, liquors, including brandy, gin, whiskey, scotch, bourbon, rum, and vodka, contain between 40 and 75 percent pure alcohol. Dry wines result when nearly all the available sugar is fermented. Sweet wines still have unfermented sugar. Pure alcohol also is added to fortify wines such as port and sherry. This addition boosts their percentage of alcohol to 18 or 20 percent (such wines do not require further pasteurization). "Still wines" are bottled after complete fermentation takes place. Sparkling wines are bottled before fermentation is complete so that the formed CO2 is retained. "White" wines are made only from the juice of the grapes; "reds" contain both the juice and pigments from skins.

The percentage of alcohol in distilled liquors commonly is expressed in degrees of "proof" rather than as a percentage of pure alcohol. This measure developed from the seventeenth-century English custom of "proving" an alcoholic drink was of sufficient strength. This was accomplished by mixing it with gunpowder and attempting to ignite it. If the drink contained 49 percent alcohol by weight (or 57 percent by volume), it could be ignited. Thus, proof is approximately double the percentage of pure alcohol (an 86 proof whiskey is 43 percent pure alcohol).

Pure alcohol is a colorless, somewhat volatile liquid with a harsh, burning taste, which is used widely as a fuel or as a solvent for various fats, oils, and resins. This simple and unpalatable chemical is made to look, taste, and smell appetizing by combining it with water and various substances called congeners (pharmacologically active molecules other than ethanol, including higher alcohols and benzene). Congeners make bourbon whiskey taste different from Scotch whiskey, distinguish one brand of beer from another, give wine its "nose" and sherry its golden glow. In trace amounts, most congeners are harmless, but their consumption has been linked to the severity of hangovers and other central nervous system symptoms that include sleepiness.

Use in Food Products

Wines, liqueurs, and distilled spirits are used to prepare main dishes, sauces, and desserts, creating new and interesting flavors. The presence of alcohol in significant amounts affects the energy value of a food. Alcohol is rich in energy (29 kJ/g, or 7.1 kcal/g). It is assumed that, because of its low boiling point, alcohol is evaporated from foods during cooking. However, almost 4 to 85 percent of alcohol can be retained in foods. Foods that require heating for prolonged periods (over two hours—for example, pot roast), retain about 4–6 percent; foods like sauces (where alcohol is typically added after the sauce has been brought to a boil) may retain as much as 85 percent.

Alcohol and Malnutrition

Alcoholism is a major cause of malnutrition. The reasons are threefold. First, alcohol interferes with central mechanisms that regulate food intake and causes food intake decreases. Second, alcohol is rich in energy (7.1 kcal/g), and like pure sugar most alcoholic beverages are relatively empty of nutrients. Increasing amounts of alcohol ingested lead to the consumption of decreasing amounts of other foods, making the nutrient content of the diet inadequate, even if total energy intake is sufficient. Thus chronic alcohol abuse causes primary malnutrition by displacing other dietary nutrients. Third, gastrointestinal and liver complications associated with alcoholism also interfere with digestion, absorption, metabolism, and activation of nutrients, and thereby cause secondary malnutrition.

It is important to note that although ethanol is rich in energy, its chronic consumption does not produce the expected gain in body weight. This may be attributed, in part, to damaged mitochondria and the resulting poor coupling of oxidation of fat metabolically utilizable with energy production. The microsomal pathways that oxidize ethanol may be partially responsible. These pathways produce heat rather than adenosine triphosphate (ATP) and thereby fail to couple ethanol oxidation to useful energy-rich intermediates such as ATP. Thus, perhaps because of these energy considerations, alcoholics with higher total caloric intake do not experience expected weight gain despite physical activity levels similar to those of the non-alcohol-consuming overweight population.

Absorption and Metabolism

Unlike foods, which require time for digestion, alcohol needs no digestion and is absorbed quickly. The presence of food in the stomach delays emptying, slowing absorption that occurs mainly in the upper small intestine.

Only 2 to 10 percent of absorbed ethanol is eliminated through the kidneys and lungs; the rest is metabolized, principally in the liver. A small amount of ethanol also is metabolized by gastric alcohol dehydrogenase (ADH) [first-pass metabolism (FPM)]. This FPM explains why, for any given dose of ethanol, blood levels are usually higher after an intravenous dose than following a similar amount taken orally. FPM is partly lost in the alcoholic.This lost function is due to decreased gastric ADH activity. Premenopausal women also have less of this gastric enzyme than do men. This difference partially explains why women become more intoxicated than men when each consume similar amounts of alcohol.

Hepatocytes are the primary cells that oxidize alcohol at significant rates. This hepatic specificity for ethanol oxidation, coupled with ethanol's high energy content and the lack of effective feedback control of alcohol hepatic metabolism, results in the displacement of up to 90 percent of the liver's normal metabolic substrates.

Oxidation. Hepatocytes contain three main pathways for ethanol metabolism. Each pathway is localized to a different subcellular compartment: (1) the alcohol dehydrogenase (ADH) pathway (soluble fraction of the cell); (2) the microsomal ethanol oxidizing system (MEOS) located in the endoplasmic reticulum; and (3) catalase located in the peroxisomes. Each of these pathways produces specific toxic and nontoxic metabolites. All three result in the production of acetaldehyde (CH3CHO), a highly toxic metabolite. The MEOS may account for up to 40 percent of ethanol oxidation. Normally, the role of catalase is small. It is not discussed further here.

  1. The ADH pathway. The oxidation of ethanol by the ADH results in the production of acetaldehyde (CH3CHO) and the transformation of nicotinamide adenine dinucleotide (NAD) to nicotinamide adenine dinucleotide-reduced form (NADH). Substantial levels of acetaldehyde can result in skin flushing. Regeneration of NAD from NADH is the rate-limiting step in this ADH pathway of alcohol metabolism. It can metabolize approximately 13 to 14 grams of ethanol per hour (the amount in a typical drink). This rate is observed when blood alcohol concentrations reach 10 mg/dL. The large amounts of reducing equivalents that are generated by the alcohol oxidation overwhelm the hepatocyte's ability to maintain homeostasis and as a consequence a number of metabolic abnormalities ensue. Increased NADH, the primary form of reducing equivalents, promotes fatty acid synthesis, opposes lipid oxidation, and results in fat accumulation.
  2. MEOS. This pathway also converts a portion of ethanol to acetaldehyde. Cytochrome P4502E1 (CYP2E1) is the responsible enzyme. As other microsomal oxidizing systems, this system also is inducible, that is, it increases in activity in the presence of large amounts of the target substrate. This induction contributes to the metabolic tolerance to ethanol that develops in alcoholics. This tolerance, however, should not be confused with protection against alcohol's toxic effects. It is important to note that, even though larger amounts of alcohol may be metabolized by individuals when this capability has been induced fully, most of alcohol's harmful effects remain unabated.

Physiological Effects at Different Levels

Beneficial effects. A large variety of alcoholic beverages are available, and most people can find at least one that provides gustatory and other pleasures. Alcohol is said to reduce tension, fatigue, anxiety, and pressure and to increase feelings associated with relaxation. It also has been claimed that drinking in moderation may lower the risk of coronary heart disease (mainly among men over 45 and women over age 55), but whether that putative protection is due primarily to the alcohol or some other associated factors, such as lifestyle, remains controversial. Moderate alcohol consumption provides no health benefit for younger people, and in fact may increase risks to alcohol's ill effects because the potential for alcohol abuse increases when drinking starts at an early age.

Harmful effects. The problems of individuals who occasionally become drunk differ from those who experience drinking binges at regular intervals.

"Acute" harmful effects of alcohol intoxication: Occasional excess drinking can cause nausea, vomiting, and hangovers (especially in inexperienced drinkers). The acute neurological effects of alcohol intoxication are dose-related. These progress from euphoria, relief from anxiety, and removal of inhibitions to ataxia, impaired vision, judgment, reasoning, and muscle control. When alcohol intakes continue after the appearance of these signs and symptoms, progress to lethal levels occurs very quickly, resulting in the anesthetization of the brain's circulatory and respiratory centers.

"Chronic" harmful effects of alcohol excess: Chronic excessive alcohol consumption can affect adversely virtually all tissues. Alcoholics have a mortality and suicide rate 2½ times greater, and an accident rate 7 times greater than average. Some of the dire consequences that are associated with alcohol abuse are:

  1. Cardiovascular problems. Alcohol causes vasodilation of peripheral vessels (causing flushing), vasoconstriction (producing resistance to the flow of blood and increasing work load on the heart) and alcoholic cardiomyopathy (characterized by myocardial fiber hypertrophy, fibrosis, and congestive heart failure).
  2. Cancer. Alcohol increases the risk of alimentary, respiratory tract, and breast cancers.
  3. Liver disease. Alcohol can result in fatty liver, hepatitis, and cirrhosis.
  4. Central nervous system disorders. Alcohol causes premature aging of the brain. Blackouts may occur (for example, those affected walk, talk, and act normally and appear to be aware of what is happening, yet later have no recollection of events experienced during the blackout).
  5. Gastrointestinal disorders. Alcohol increases risk of esophageal varices, gastritis, and pancreatitis.
  6. Metabolic alterations. Alcohol increases nutritional deficiencies (primary and secondary), and adversely affects absorption and utilization of vitamins. It impairs the intestinal absorption of B vitamins, notably thiamin, folate, and vitamin B12. Wernicke's encephalopathy also may occur. This condition is the result of severe thiamine deficiency. It is characterized by visual disorders, ataxia, confusion, and coma.
  7. Immunological disorders. Alcohol decreases immunity to infections and impairs healing of injuries.
  8. Others. Alcohol causes personality changes, sexual frigidity or impotency, sleep disturbances, and depression.

Treatment

There are two major approaches that are used in the treatment of alcohol abuse: (1) correction of the medical, nutritional, and psychological problems; and (2) the alleviation of dependency on alcohol. Many sedatives or tranquilizers (for example, chlordiazepoxide) are effective in controlling minor withdrawal symptoms such as tremors. More serious symptoms include delirium tremens and seizures. For treatment of alcohol dependence, the anticraving agent naltrexone has shown promising results. Nutritional deficiency, such as lack of thiamine or magnesium, when present, must be corrected. Psychological approaches such as the twelve steps of Alcoholics Anonymous are also effective in achieving more sustained abstinence. These approaches, although helpful, too often come too late to revert the liver to its normal state. Other approaches, such as those focusing on prevention (utilizing biochemical markers), screening (through use of improved blood tests), and early detection are needed to impact on the prevalence of liver disease. The correction of nutritional deficiencies and supplementation with other substrates that may be produced in abnormally low quantities by affected patients, for example, S-adenosylmethionine (SAMe) and polyunsaturated lecithin have been shown to offset some of the adverse manifestations of alcohol's toxic effects. These and others are now being tested in humans.

Conclusion

Alcoholism, an addiction to heavy and frequent alcohol consumption, is a major public health issue. However, many believe that this condition does not attract attention that it merits from either the public or the health professions. Alcoholism is a multifaceted problem that cannot be solved by any single approach. The "consumption control approach" is a worthwhile endeavor with proven efficacy, but consumption control efforts by themselves are not sufficient. Prevention of alcohol misuse before it occurs also can be beneficial. Another prevention strategy includes establishing standards and guidelines for advertising and emphasizing responsibility and moderation in the serving and consumption of alcohol. "Behavioral" approaches focus on recognition of social and psychological factors and their correction. Finally, the "disease-control" approach provides new insights. Continued research into the pathophysiology of alcohol-induced disorders increases understanding of the condition and provides prospects of earlier recognition, and improved efforts for its early prevention and treatment, prior to the medical and social disintegration of its victims. By combining all of these approaches, chances to alleviate the suffering of the alcoholic are multiplied in a positively synergistic manner and the public health impact of alcoholism on our society can be minimized.

See also Beer; Fermentation; Fermented Beverages Other than Wine or Beer; Nutrients; Nutrition; Wine.

BIBLIOGRAPHY

Lieber, Charles S. Medical and Nutritional Complications of Alcoholism: Mechanisms and Management. New York: Plenum, 1992.

Lieber, Charles S. "Medical Disorders of Alcoholism." New England Journal of Medicine 333 (1995): 1058–1065.

Lieber, Charles S. "Alcohol: Its Metabolism and Interaction with Nutrients." Annual Reviews in Nutrition 20 (2000): 395–430.

Khursheed P. Navder Charles S. Lieber

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