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16—
Alcohol

Alcohol consumption is difficult to quantify accurately, and there is no universally acceptable classification system or standard for the safe level of drinking. In 1862, the British established a daily upper limit of 1.5 oz as the safe level of alcohol consumption  (O'Brien and Chafetz, 1982). The equivalence in drinks can be calculated from Table 16-1 (Baum-Baicker, 1985a). The Fourth Special Report of the U.S. Congress on Alcohol and Health considered the moderate drinker as one who consumed 0.22 to 0.99 oz of ethanol per day and the light drinker as one who consumed 0.01 to 0.21 oz/day (NIAAA, 1981). Accordingly, Turner et al. (1981) proposed that to qualify as moderate, one's alcohol consumption should not exceed 0.8 g/kg of body weight (bw) per day (an absolute limit of 80 g of alcohol) or an average of 0.7 g/kg bw in a 3-day period, as shown in Table 16-2 (Baum-Baicker, 1985a). People exceeding these limits are considered heavy drinkers (Klatsky et al., 1979). By this standard, 24% of all adults in the United States can be considered moderate drinkers, one-third as light drinkers, 9% as heavy drinkers, and about one-third as abstainers (NIAAA, 1987).

The best indicator of drinking is the blood alcohol level (BAL) at any time. At a BAL of 0.05 (5 parts of alcohol to 10,000 parts of blood), generally reached after one or two drinks, many people experience positive sensations such as relaxation, euphoria, and well-being (Hales and Hales, 1986). Above this mark, a person starts feeling worse and gradually loses control of speech, balance, and emotions. When BAL reaches 0.1, a person is considered to be drunk (i.e., experiences symptoms of frequent headaches, nausea, stomach pain, heartburn, gas, fatigue, weakness, muscle cramps, irregular or rapid heartbeats, dramatic mood swings, and depression and paranoia); at 0.2, some people pass out; at 0.3, some collapse into a coma; and at 0.4, a person can die (Hales and Hales, 1986).

Patterns of Alcohol Consumption in the United States

In 1985, 18 million adults 18 years of age and over had problems with alcohol use (NIAAA, 1986). Forty-one percent of these (7.3 million) were alcohol abusers, defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as drinkers who experienced at least one severe or moderately severe consequence of alcohol abuse, such as job loss, arrest, or illness, during the previous year. The remaining 59% (10.6 million) were alcoholics, defined as drinkers who, during the past year, experienced at least one symptom of alcohol withdrawal or one loss-of-control symptom plus one other symptom of de-



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Page 431 16— Alcohol Alcohol consumption is difficult to quantify accurately, and there is no universally acceptable classification system or standard for the safe level of drinking. In 1862, the British established a daily upper limit of 1.5 oz as the safe level of alcohol consumption  (O'Brien and Chafetz, 1982). The equivalence in drinks can be calculated from Table 16-1 (Baum-Baicker, 1985a). The Fourth Special Report of the U.S. Congress on Alcohol and Health considered the moderate drinker as one who consumed 0.22 to 0.99 oz of ethanol per day and the light drinker as one who consumed 0.01 to 0.21 oz/day (NIAAA, 1981). Accordingly, Turner et al. (1981) proposed that to qualify as moderate, one's alcohol consumption should not exceed 0.8 g/kg of body weight (bw) per day (an absolute limit of 80 g of alcohol) or an average of 0.7 g/kg bw in a 3-day period, as shown in Table 16-2 (Baum-Baicker, 1985a). People exceeding these limits are considered heavy drinkers (Klatsky et al., 1979). By this standard, 24% of all adults in the United States can be considered moderate drinkers, one-third as light drinkers, 9% as heavy drinkers, and about one-third as abstainers (NIAAA, 1987). The best indicator of drinking is the blood alcohol level (BAL) at any time. At a BAL of 0.05 (5 parts of alcohol to 10,000 parts of blood), generally reached after one or two drinks, many people experience positive sensations such as relaxation, euphoria, and well-being (Hales and Hales, 1986). Above this mark, a person starts feeling worse and gradually loses control of speech, balance, and emotions. When BAL reaches 0.1, a person is considered to be drunk (i.e., experiences symptoms of frequent headaches, nausea, stomach pain, heartburn, gas, fatigue, weakness, muscle cramps, irregular or rapid heartbeats, dramatic mood swings, and depression and paranoia); at 0.2, some people pass out; at 0.3, some collapse into a coma; and at 0.4, a person can die (Hales and Hales, 1986). Patterns of Alcohol Consumption in the United States In 1985, 18 million adults 18 years of age and over had problems with alcohol use (NIAAA, 1986). Forty-one percent of these (7.3 million) were alcohol abusers, defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as drinkers who experienced at least one severe or moderately severe consequence of alcohol abuse, such as job loss, arrest, or illness, during the previous year. The remaining 59% (10.6 million) were alcoholics, defined as drinkers who, during the past year, experienced at least one symptom of alcohol withdrawal or one loss-of-control symptom plus one other symptom of de-

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Page 432 TABLE 16-1   Amount of Ethanol in a Drinka   Ethanol Content (%) Unit of Measure Ethanol in a Drink [oz and (ml)) Beverage Type       Whiskey (80 proof) 40 1-oz shot (30 ml) 0.40 (11.83) Table wine 12.1b 3.5-oz glass (104 ml) 0.42 (12.42) U.S. beer 3.5c 12-oz bottle (355 ml) 0.42 (12.42) a From Baum-Baicker (1985a). b Most table wines contain 11 to 13% ethanol. Fortified wines, such as sherry and port, contain approximately 20% ethanol. c Most U.S. brands contain 3.2 to 4.0% ethanol. pendence. Although alcohol abusers and alcoholics were defined as separate groups, they were not considered to be mutually exclusive. Many alcoholics also reported consequences of alcohol abuse, and some counted as alcohol abusers may have had alcohol dependence. Alcohol consumption peaks in the 20- to 40-year age group; alcohol abuse is most frequent in youth and middle age. A national study by Schoenborn and Cohen (1986) showed that 70% of people between the ages of 20 and 34 consumed alcohol. In a 1985 survey, 66% of the high school seniors interviewed reported that they had consumed alcohol in the past month and 5% described themselves as daily drinkers. Thirty-seven percent of them had had five or more drinks on at least one occasion during the 2 weeks before the survey (NIAAA, 1987). Alcohol use decreases in the elderly. Among those 65 to 74 years of age, 43% consumed alcohol. The percentage fell to 30% after age 75. The national survey of Cahalan et al. (1967) showed that 15% of those under 40 years and 5% of the elderly were heavy drinkers. The lower percentage of alcoholics among the elderly is believed to be the consequence of attrition, as younger alcoholics die from accidents, cirrhosis, or other medical complications. It is also more difficult to define alcohol abuse among the elderly, because many of the criteria for such a classification (e.g., inability to hold a job, drunken driving, or other consequences of drinking) are less likely to apply to the elderly. Furthermore, family members may underreport excess alcohol use to protect the dignity of their elderly relatives. Alcoholism affects nearly 18% of the institutionalized elderly (Schuckit and Miller, 1976), who are more likely to have medical problems. As many as 28% of the elderly residents of psychiatric institutions have had problems with alcohol use. Blose (1978) also found that 40 to 60% of nursing home patients had a history of alcohol-related problems. These figures are especially important in light of the increasingly high percentage of older people in the U.S. population. Males are more likely to drink alcohol (Table 16-3) and to drink more heavily than females. Nevertheless, the proportion of women who drink has increased in the past 25 years. Through the 1970s, more women than men were abstainers and light drinkers, and fewer women were heavy drinkers. By 1981, the percentage of women who were TABLE 16-2  Upper Limits of Allowable Daily Alcohol Consumptiona Weight of Individual 0.8 g/kg bw per dayb   0.7 g/kg bwb   (kg) (lb) Ethanol (g) 80-Proof Spirits (oz) 12% Table Wine (oz) 3.6%c Beer (oz) Ethanol (g) 80-Proof Spirits (oz) 12% Table Wine (oz) 3.6%c Beer (oz) 50 110 40 4.3 14 38 35 3.7 13 33 60 132 48 5.1 17 46 42 4.5 15 40 70 154 56 6.0 20 53 49 5.2 18 47 80 176 64 6.9 23 61 56 6.0 20 53 90 198 72 7.7 26 69 63 6.7 23 60 100 220 80 8.6 29 76 70 7.5 25 67 a From Baum-Baicker (1985a). Conversions: 1 oz = 23.34 g or 29.574 ml. b Turner et al. (1981) defined moderate intake as no more than 0.8 g/kg bw per day or an average of 0.7 g/kg bw over a 3-day period. See text. c By weight, or 4.5% volume.

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Page 433 TABLE 16-3   Estimated Numbers of Adult Alcohol Abusers and Alcoholics, 1985a   Alcohol Abusersb Alcoholicsb Total   Percent of Groups Number Percent of Population Number Percent of Total Number Sex             Male 5.61 4,849,810 8.40 7,296,979 14.01 12,146,789 Female 2.53 2,446,354 3.50 3,327,213 6.03 5,773,567 Both 3.97 7,296,164 5.79 10,624,192 9.76 17,920,356 a From NIAAA (1986). b See definitions in text. heavy drinkers and the percentage of women ages 35 to 44 who were drinkers had increased (Wilsnack et al., 1984). Rates of excessive drinking and self-reported drinking problems for the adult black population are similar to rates in the general U.S. population (NIAAA, 1987). Black youths have higher abstention rates and lower rates of heavy drinking than white youths. Native Americans, on the average, are more likely to be heavy drinkers than the general population. Some tribes have lower percentages of drinking adults than the U.S. population (30% versus 67%), whereas the percentage of drinkers in other tribes reaches 80% (NIAAA, 1987). Little is known about drinking practices or alcohol-related problems among Asian Americans, although they are generally believed to have a lower prevalence than found in other groups (see Chapter 4 of this report). Genetics and Alcoholism Studies of families, twins, adoptees, and animals suggest that alcoholism results from an interaction between heredity and environment (NIAAA, 1987). Research is now focused on identifying physiological, psychological, and biochemical markers for susceptibility to alcohol (see Chapter 4). Cultural Aspects of Alcohol Use Historical Perspective Ethnographic Review Ancient Egyptians believed that beer (or bouza) was invented by the goddess Osiris (Ghalioungui, 1979). Beer, produced by malting, was considered food and drink and was the beverage of common people at festivals. Wine was also produced in ancient Egypt and used in religious celebrations and as a medicine. In contrast with beer, wine was considered an aristocrat's drink (Ghalioungui, 1979). In Mesopotamia 3000 years B.C., beer was the drink of the cereal-growing south, whereas wine was the choice of the vine-growing north (Ghalioungui, 1979). Accounts of drunkenness in ancient Greece and Rome are well documented (Roe, 1979). Greeks ate cabbage to avoid inebriety—a custom later adopted by the Arabs ( Ghalioungui, 1979). In the Bible, however, the beneficial references to drinking appear to be related to unfermented grape juice (Wilkerson, 1978). In pre-Islamic Arabia, beer, fermented dates, milk, and wine were commonly consumed (Gawad, 1968). Drinking took place in houses, taverns, and dancing places and along caravan routes. With the advent of Islam, abstinence became the rule in Arabia. In other Middle Eastern cities, such as Baghdad, Cairo, Damascus, and Tehran, drinking was not banned but was unpopular, and today it is barely tolerated (Ghalioungui, 1979). Chicha (beer made from maize) played important religious, economic, and political roles in the Andean South American society during the Incan empire (Morris, 1979). Alcohol had a similar place among the Aztecs of Mexico (Paredes, 1975) and the Mayans of Central America (Gonçalves de Lima et al., 1977). In medieval Europe, drunkenness was prevalent among the lower orders of clergy (Roe, 1979). In medieval England, wine became plentiful after grapes were imported from France at the end of the fourteenth century. Throughout the Middle Ages, drunkenness was largely associated with revelry, feasting, and religious celebrations. Alcoholism did not become a social problem until distilled beverages became available around 1100 A.D. (Singer et al., 1956). Until the sixteenth century, fortified wine was produced only on a small scale in monasteries. Franciscus Sylvius, a seventeenth-century professor of medicine at the University of Leiden, may

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Page 434 be the first to have distilled alcohol from grain and to have named the result aqua vitae (Lucia, 1963). The English, who called it gin, imported it during the reign of William III. By 1700, gin was produced from excess corn (Dorothy George, 1931) to compete with French liquors (Hirsch, 1949). In the first half of the eighteenth century in England, especially 1720 to 1750, lower-income people drank large quantities of alcohol, and the adverse nutritional consequences of alcoholism were first recognized at that time (Roe, 1979). The Gin Act of 1751 imposed a duty on spirits and stopped distillers, chandlers, and grocers from retailing liquor. This legislation brought excessive alcohol consumption under control several years later (Webb and Webb, 1903). Rum was developed in the Caribbean in 1650 as a by-product of the sugarcane industry and was distributed to the British Royal Navy in 1892. It was believed to confer strength and offer protection against scurvy (Chalke, 1976). Puritans in the American colonies believed that alcoholic drinks were wholesome and strengthening. In the eighteenth century, when rum and whiskey became available, alcohol abuse became evident. Black slaves and American Indians were considered too irresponsible to be trusted with the alcohol (Roe, 1979), but the colonists nevertheless used alcoholic beverages to appease the Indians and to motivate the slaves to perform unpleasant tasks. Alcohol and Nutritional Disorders The relationship between alcohol abuse and nutritional disorders was reported as early as the eighteenth century (Sedgewick, 1725). In the United States, Benjamin Rush observed in 1809 that approximately 4,000 people died annually from the use of rum (Rush, 1818). He described such effects of hard drinking as loss of appetite, jaundice, dropsy, diabetes, redness of face, fetid breath, epilepsy, gout, and madness. Bynuum (1968) observed that the concept of chronic alcoholism as a disease, instead of as a vice or a cause of other diseases, began about the turn of the eighteenth century, when the phrase habitual drunkenness, the equivalent of today's chronic alcoholism, was coined. Fuchs (1848) described alcohol as a poison. Huss (1852) attributed the effects of chronic alcohol abuse to tissue damage and believed that alcohol's toxic effects were similar to those caused by intoxicating foods. Jolliffe (1940) described the role of alcohol in the development of nutritional deficiencies. Alcohol in Medicine In the middle of the nineteenth century, alcohol was commonly used to treat certain diseases and to alleviate symptoms (Roe, 1979). In 1864, a committee of the National Academy of Sciences, in response to a request from the Surgeon General of the U.S. Army, recommended that in military hospitals whiskey be replaced with alcohol, medicated with additives appropriate for the intended objective (Parker, 1978). A  strong reaction to its use as a drug occurred early in the nineteenth century and paralleled the growth of the temperance movement (Horsley and Sturge, 1915). From antiquity, wine, beer, and, later, spirits were considered to be food for the sick when solid foods could not be tolerated (Roe, 1979) and, in many societies, to have nutritional value (Steinkraus, 1979). Although alcohol has been used clinically as an appetite stimulant, as a sedative-hypnotic drug, and as a calorie source for intravenous administration, these uses have not been subjected to controlled medical evaluation (Becker et al., 1974). Ethanol is unusual among drugs in that it has a biphasic impact on the nervous system. In small amounts, it stimulates; but as it accumulates in the body it depresses, and the amount that makes the difference is minute for most people. Many effects of drinking are determined less by the quantity consumed than by one's expectations (Heath, in press). Transcultural Anthropological Perspective Alcohol and drinking are perceived differently among Western and non-Western cultures. Some insights into the cultural role of alcohol can be discerned by comparing these cultures. Western Societies In Western societies, the frequency of alcoholism is not uniform among various ethnic groups. For example, most Jews drink, but few become alcoholics; ascetic Protestants rarely drink, but those who do so generally drink heavily (Heath, 1975). Bales (1946) explained that Jews regard drinking as a family sacrament, since wine is introduced to children in a sacred ritual context. In contrast, the Irish perceive drinking in a convivial secular context whereby adult men prove their manhood. Since the 1970s, however, Jews have been showing patterns of alcohol abuse (Heath, 1987), presumably because of growing

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Page 435 distance from traditional orthodoxy and from the moral authority of their faith (Douglas, 1987). Comparative ethnic studies also show changes in drinking patterns among Italians, Poles, and Portuguese after they migrated to America (Heath, 1987). Non-Western Literate Societies Among non-Western literate societies, there are wide differences in consumption of alcoholic beverages. For example, although prohibition of alcoholic beverages is supposed to characterize the Islamic world, alcohol-related problems are now recognized in Saudi Arabia (Al-Qthami, 1978) and in Bahrein (Alsafar, 1974). In India, some groups of Hindus espouse drunkenness as religious duty, whereas others practice complete abstinence (Heath, 1975). Nonliterate Societies Among nonliterate societies, the Camba of eastern Bolivia esteem drunkenness and actively pursue it, but there is no alcoholism in the sense that they do not suffer any alcohol-related economic, social, or psychological problems nor do they engage in aggressive behavior (Heath, 1975). Among African tribal societies, beer drinking is an integral part of most social activities among men. Beer is used as an offering to appease the gods, as a pledge of agreement between parties following adjudication, as a reward for help in working one's land in a system of reciprocal labor exchange, and as a medicine. Pathological addiction or aggressive behavior does not occur in these groups (Heath, 1975). North American Indians also vary widely in their reactions to alcoholic beverages and have changed their attitudes over time. In the first decades of contact with whites, the Iroquois of upstate New York and southeastern Canada consumed distilled liquors in moderation and drinking became an integral part of their religion. In the early eighteenth century, however, aggression became part of their drunken behavior, following the example of white trappers and traders. By 1800, drunkenness had become a serious problem and eventually led to abstinence (Dailey, 1968). Kunitz et al. (1971) suggest that cirrhosis mortality rates are much higher among the Navaho than among the Hopi because the Hopi condemn drinking and reject the drunk, whereas the Navaho expect young men to be heavy drinkers and never force them into isolation or fail to welcome them  back into the community. Some populations show no reactions to alcohol such as hangovers, blackouts, and addiction, even when drunkenness is commonplace, e.g., among the Peruvian Quechua, Bolivian Camba, Salish, Polynesians, and Tarahumara (Heath, 1975). It is not known whether this lack of reaction is due to differences in thresholds to pain, physiological reactions to alcohol, attitudes toward or expected effects of alcohol, or other biologic or cultural factors. Cross-Cultural Studies Alcoholic beverages have been used to foster social integration in many societies, such as Finnish Lapps, Bolivian Camba, and many American Indian and South African tribes (Heath, 1975). In other societies, they have been used to appease gods, to pay fines or taxes, to mobilize agricultural labor, to overcome shyness and gain courage, to symbolize social unity, to promote social cohesion or conviviality, to relieve anxieties and pressures due to conflict with a dominant culture, to enhance social status and prestige, to mark personal identity and boundaries between ethnic groups, and to serve as a mode of recreation (Douglas, 1987; Heath, 1975, in press). Social problems are related more frequently to consumption of alcohol in Western societies than non-Western societies. Alcoholism is rare in non-Western societies, even where most adults of at least one sex drink regularly and where drunkenness is valued (Heath, 1975). Several generalizations can be derived from cross-cultural studies: · In most societies, drinking is a social act embedded in a context of values, attitudes, and other norms, all of which influence the expression of effects, regardless of biochemical, physiological, or pharmacokinetic factors. · Drinking is governed by rules tied to strong emotions and sanctions, determining such things as who may or may not drink, how much of what they may drink, in what context, and with whom. · Alcohol promotes relaxation and sociability in various populations. · Physical, economic, psychological, social, or other problems associated with drinking are rare in many cultures. · When alcohol-related problems occur, they are linked with modalities, attitudes, and norms regarding drinking. · Attempts at prohibition are not successful unless embedded in sacred or religious values (Heath, 1987).

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Page 436 Evidence Associating Alcohol Consumption with Chronic Diseases Assessment of Alcohol Consumption The accurate assessment of alcohol consumption is difficult in population-based studies, and evidence regarding validity and reliability of the estimates has rarely been obtained. Some people are likely to underreport actual consumption, and the frequency of such underreporting varies with the social undesirability of consuming alcohol. In many epidemiologic studies, particularly the earlier ones, participants were simply asked to report an average number of drinks of beer, wine, and liquor or cocktails per day without regard for the complexities of drinking behavior or for the interview techniques needed to obtain information. Investigators have reported alcohol consumption in different units (e.g., number of drinks per day or volume of alcohol per month) and have used different formulas for converting the reported drinking behavior into these units. As a result, it is often difficult to summarize the results of such studies. Some writers have tried to circumvent this problem by using such terms as light, moderate, and heavy drinking, but such descriptive words are not satisfactory for scientific purposes. Where possible, alcohol consumption is reported herein as grams of ethanol per week, but these figures should be considered approximations and interpreted cautiously. Difficulties in assessing published statistics related to alcohol and drug abuse have been highlighted in a recent editorial (Barnes, 1988). Obesity Ethanol may contribute to obesity because, depending on the level of intake, it can serve as an important energy source. The carbohydrate content is negligible for whiskey, cognac, and vodka; however, it is 2 to 10 g of carbohydrate/liter for red or dry white wine, 30 g/liter for beer or dry sherry, and as much as 120 g/liter for sweetened white or port wines (Pekkanen and Forsander, 1977). National consumption data show that, on the average, alcohol contributes 4.5% of total calories to the energy intake of Americans (Scheig, 1970). The heavy drinker may derive as much as half, or more, of the daily calories from ethanol. Although the combustion of ethanol in a bomb calorimeter yields a value of 7.1 kcal/g, its biologic value may be less when compared in vivo to an equivalent carbohydrate intake. Metabolic ward  subjects given additional calories as alcohol failed to gain weight (Lieber et al., 1965). No additional weight was gained by 17 hospitalized alcoholics who were given 1,800 alcohol-derived calories in addition to their 2,600-calorie diet (Mezey and Faillace, 1971). In metabolic ward studies, isocaloric substitution of ethanol for carbohydrates as 50% of total calories in a balanced diet resulted in a decline in body weight, and when given as additional calories, ethanol caused less weight gain than did calorically equivalent carbohydrates or fats (Pirola and Lieber, 1972). Crouse and Grundy (1984) reported variable responses to additional calories given as ethanol: no weight gain in lean individuals and some weight gain in half the obese individuals. The view that ethanol increases metabolic rate is supported by the observation that ethanol ingestion increases oxygen consumption in normal subjects and that this effect is much greater in alcoholics (Tremolieres and Carre, 1961). Substitution of ethanol for carbohydrates increases the metabolic rate of humans and rodents (Stock and Stuart, 1974; Stock et al., 1973). A 15% increase in thermogenesis was seen in rats fed ethanol for 10 days (Stock and Stuart, 1974). In humans, diet-induced thermogenesis was also increased (Stock and Stuart, 1974). In rats, some, but not most, of the energy wastage was attributable to brown-fat thermogenesis (Rothwell and Stock, 1984). One postulated mechanism of energy wastage is oxidation without phosphorylation by the microsomal ethanol-oxidizing system (Pirola  and  Lieber, 1972). This pathway was induced by chronic ethanol consumption (Pirola and Lieber, 1975, 1976). Israel et al. (1975) explained energy wastage as the uncoupling of mitochondrial nicotinamide adenine dinucleotide (NADH) reoxidation, perhaps abetted by catecholamine release or a hyperthyroid state. However, the implication of the hyperthyroid state is unresolved (Teschke et al., 1983). As a calorie source, alcohol is not as efficient as carbohydrates, especially when consumed chronically in large amounts. Thus, ethanol may contribute to excess energy intake, but is not a common primary cause of obesity. Moderate alcohol intake (i.e., 16% of total calories) was associated with a slightly elevated energy intake (Gruchow et al., 1985a). Despite comparable levels of physical activity there was no weight gain, perhaps because of the metabolic considerations discussed above. This and a slightly higher level (23%) of alcohol intake

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Page 437 (Hillers and Massey, 1985) were associated with a substitution of alcohol for carbohydrates as a source of calories. When the percentage of calories from alcohol exceeds 30%, large decreases in protein and fat intake occur. Cancer Epidemiologic Studies Because the associations between alcohol consumption and cancer vary by site, the committee considered the evidence separately for each site. Oral Cavity and Pharynx Mortality from oropharyngeal cancer is higher among people in occupations providing ready access to alcohol and among alcoholics, whereas risks are lower among alcohol abstainers such as Seventh-Day Adventists and Mormons in the United States (de Lint and Levinson, 1975; Lyon et al., 1976). In 14,000 Danish brewery workers who were not alcoholics, but who did have an above-average consumption of beer, the incidence of pharyngeal cancer was twice as high as that in the general population (Jensen, 1979). In a study of 543 men with cancer of the lip, oral cavity, and pharynx and 207 controls, Wynder et al. (1957a,b) found an association of these cancers with alcohol drinking. Rothman and Keller (1972) reanalyzed information on consumption of alcohol and use of tobacco obtained by Keller and Terris (1965). The risk for oropharyngeal cancer increased with increasing alcohol consumption at every level of smoking. In agreement with the findings of Wynder et al. (1957b), the analysis showed multiplicative interactions between alcohol and tobacco in their effects on oral-cavity cancer. Evidence for the role of alcohol and tobacco in cancer of the oral cavity also comes from a study in France (Schwartz et al., 1962). The average daily consumption of alcohol was significantly increased in patients with cancers of the tongue, buccal cavity, oral pharynx, and hypopharynx. Case-control studies in Puerto Rico (Martinez, 1969) and in the United States (Graham et al., 1977) have confirmed the role of alcohol in cancer of the oral cavity. Larynx Early clinical and occupational studies showed an association between access to alcoholic beverages or heavy alcohol drinking and laryngeal cancer (Kennaway and Kennaway, 1947; Kirchner and Malkin, 1953). Most studies of alcoholics indicate an excess of laryngeal cancer (Monson and Lyon, 1975; Schmidt and de Lint, 1972). The risk of laryngeal cancer among male Danish brewery workers was twice as high as expected (Jensen, 1979). Several case-control studies have examined the interaction of alcohol and tobacco. Wynder et al. (1957a) reported that the risk of laryngeal cancer increased with the amount of whiskey consumed, even after adjusting for tobacco. Later, Wynder et al. (1976) confirmed the dose-response relationship, although the increase in risk was less than in the earlier studies. Other studies in the United States (Graham et al., 1981), Denmark (Olsen et al., 1985), and Canada (Burch et al., 1981) confirmed the dual role of alcohol and tobacco in increasing the risk of laryngeal cancer. In most of these analyses, the two factors were found to have a synergistic effect. Esophagus A high prevalence of alcoholism has been found among patients with esophageal cancer (Piquet and Tison, 1937). Furthermore, the incidence of esophageal cancer was greater among people employed in the production or distribution of alcoholic beverages than in the general population (Jensen, 1979). Wynder and Bross (1961) reported a dose-response relationship between esophageal cancer and consumption of whiskey and beer by smokers of 16 to 34 cigarettes per day. The risk was approximately 25 times higher among drinkers of seven or more units of whiskey per day than among light whiskey consumers. A dose-response relationship was also found among beer consumers. In Paris, Schwartz et al. (1962) found that average alcohol consumption was much higher among patients with esophageal cancer than among traffic accident victims. Martinez (1969) reported a clear dose-response relationship between esophageal cancer and daily consumption of alcohol in Puerto Rico. In France, Tuyns et al. (1977, 1979, 1982) found dose-response associations between the consumption of alcohol, after adjusting for tobacco, and the risk of esophageal cancer. Alcohol and tobacco combined had a synergistic effect: There was a very high risk among people who both drank and smoked heavily. Those studies also indicated that the risk of esophageal cancer was pronounced for consumers of apple cider distillates. In a later study, Tuyns (1983) examined the risk associated with alcohol con-

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Page 438 sumption among 74 men and women with esophageal cancer who never smoked. In both sexes, the risk increased with increased daily alcohol consumption. Similar associations were also found in Singapore (De Jong et al., 1974). A case-control study of black men in Washington, D.C., by Pottern et al. (1981) indicated that risk was higher among consumers of hard liquor than among beer drinkers (relative risks of 7.3 and 2.7, respectively). Stomach Although no increased stomach cancer risk was found among Finnish alcoholics or Danish brewery workers (Hakulinen et al., 1974; Jensen, 1979), Sundby (1967) reported a mortality ratio of 1.6 for stomach cancer among alcoholics in Norway. Studies in France (Audigier and Lambert, 1974) and in Japan (Hirayama, 1972) also suggested that alcohol may be associated with cancer at this site. One case-control study showed an association between stomach cancer and wine drinking (Hoey et al., 1981), but other case-control studies have not supported such an association (Acheson and Doll, 1964; Graham et al., 1972; Haenszel et al., 1972; Schwartz et al., 1962; Tuyns et al., 1982). Colon and Rectum Breslow and Enstrom (1974) reported an association between beer sales and rectal cancer in 41 states in the United States and in 24 countries. However, when consumption data for fats were taken into account, the correlation with colon cancer disappeared, whereas the positive correlation between beer consumption and rectal cancer remained (Schrauzer, 1976). In Denmark, no increased risk of either colon or rectal cancer was found among brewery workers (Jensen, 1979), but a similar study among brewery workers in Ireland showed a doubling of the risk of rectal cancer (Dean et al., 1979). There was a moderately nonsignificant increased risk of rectal cancer in one case-control study by Tuyns et al. (1982). In a case-control study conducted in Australia, Kune et al. (1987) found little evidence of an association of any alcoholic beverages with colon cancer, but beer was a risk factor for rectal cancer. The effect was more marked in males than in females. The relative risk for the highest consumption levels in quartiles compared to the lowest was approximately 2. The risk of rectal cancer varied with beer-drinking patterns in the previous 15 to 20 years. Nevertheless, in other case-control studies, either no association or only a weak association was found between the risk of colorectal cancer, colon cancer, or rectal cancer and the consumption of alcohol or beer (Dales et al., 1979; Graham  et al., 1978; Miller et al., 1983). By contrast, in cohort studies conducted in Norway (Bjelke, 1978) and in Hawaii (Pollack et al., 1984), there was a dose-response relationship between risk of rectal cancer and consumption of alcohol, especially with regard to frequency of beer consumption. Pancreas Some studies suggest an association between pancreatic cancer and alcohol consumption (Burch and Ansari, 1968; Cubilla and Fitzgerald, 1978); however, most studies of alcoholics have not shown an increased risk for cancer at this site (Hakulinen et al., 1974; Monson  and Lyon, 1975). Similarly, no cohort or case-control studies have confirmed an increased risk (Jensen, 1979; MacMahon et al., 1981; Tuyns et al., 1982). Liver In North America and western Europe, cirrhosis of the liver is related mainly to alcohol consumption, and there is a firm association between cirrhosis of the liver and primary liver cancer (Tuyns, 1982). However, not all studies of alcoholics suggest an increased risk of primary liver cancer (Nicholls et al., 1974; Schmidt and de Lint, 1972). Studies of male Danish brewery workers, however, provide a clear association between primary liver cancer and cirrhosis of the liver (Jensen, 1979). In Finland, a significant excess (p < .05) of primary liver cancer was found among alcohol abusers (Hakulinen et al., 1974). Some studies suggest that primary liver cancer may be increased in alcoholics, even in the absence of cirrhosis (Lieber et al., 1979). Accumulating evidence links viral hepatitis and hepatocellular carcinoma in alcoholics. Serologic markers of viral hepatitis are more frequent in alcoholics (Chevilotte et al., 1983; Gluud et al., 1982; Hislop et al., 1981; Mills et al., 1979; Orholm et al., 1981). Prevalence of anti-HBV (hepatitis virus B) antibodies was also found to be higher in an unselected outpatient alcoholic population (Gluud et al., 1984). Bréchot et al. (1982) reported that 19 of 51 subjects with various stages of alcoholic liver disease had one or more serologic markers of HBV in their serum. Eight of the 51 subjects had HBV-DNA in their livers. In five of these subjects, the DNA was integrated into the genome. Whether this increased incidence of pos-

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Page 439 itive cases is due to the socioeconomic status of the alcoholic, increased exposure to hepatitis infection from blood transfusions, or enhanced susceptibility to infection remains to be determined. Bréchot et al. (1982) evaluated 20 subjects with alcoholic cirrhosis and hepatocellular carcinoma for evidence of HBV infection. Only 9 of 16 tested serologically had markers of HBV infection, but in all 20 subjects, HBV-DNA was integrated into the genome of the neoplastic liver cells. However, among alcoholic cirrhotics, Omata et al. (1979) found no difference in the frequency of hepatitis infection between those with and those without hepatocellular carcinoma. Goudeau et al. (1981) reported HBV markers in 31% of 125 asymptomatic alcoholics, 55%  of 163 alcoholics with cirrhosis, and 22% of 46 with hepatocellular carcinoma. Yarrish et al. (1980) noted similar rates of HBV infection in both alcoholic and nonalcoholic subjects with hepatocellular carcinoma. Of their alcoholic subjects with hepatocellular carcinoma, 88% were seropositive for HBV markers, compared to 69% of nonalcoholic subjects with hepatocellular carcinoma. In summary, most studies indicate an increased prevalence of HBV infection among alcoholics with cirrhosis and an association between the infection and a high frequency of liver cell cancer. Breast Most of the studies conducted on this subject suggest that breast cancer risk is related to alcohol consumption (Graham, 1987; Schatzkin et al., 1987). There was a positive correlation between alcohol consumption and breast cancer in 41 states in the United States, but not in 24 other countries (Breslow and Enstrom, 1974). Breast cancer mortality was twofold higher among 2,070 people admitted to mental hospitals in the United Kingdom with a diagnosis of alcoholism (Adelstein and White, 1976). The Third National Cancer Survey in the United States indicated a relative risk of 1.5 for breast cancer from consumption of hard liquor and wine. There was also a dose-response relationship with total alcohol consumption (Williams and Horn, 1977). In one case-control study, Rosenberg et al. (1982) found increased risk of breast cancer for drinkers compared with nondrinkers; the association was evident for beer, wine, and spirits. In another, conducted in France by Lê et al. (1984), there was an increased risk of breast cancer in subjects who consumed alcoholic beverages with meals. The association was significant for beer (relative risk, 2.2) and for wine (relative risk, 1.5). In a cohort study of more than 96,000 women in a multiphasic health examination program in the United States, breast cancer incidence was increased in those who had reported consuming more than three drinks a day (Hiatt and Bawol, 1984). In a 4-year follow-up study of nearly 90,000 U.S. nurses ages 34 to 59, a significant dose-response relationship was found between alcohol consumption and breast cancer risk (Willett et al., 1987). Among women consuming 5 to 14 g of alcohol daily (about 3 to 9 drinks/week), the age-adjusted relative risk of breast cancer was 1.3 (95% confidence interval, 1.1-1.7). Among those consuming 15 g of alcohol or more per day, the relative risk was 1.6 (range, 1.3-2.0). Adjustment for known breast cancer risk factors (e.g., parity, age at first birth, history of maternal breast cancer, prior breast disease, and relative weight) and a variety of nutritional variables (including estimated consumption of total calories, total fat, saturated fat, polyunsaturated fat, cholesterol, carotene, preformed vitamin A, and vitamin E) did not alter this association. Several other studies, however, have provided no evidence of an association between alcohol and breast cancer (Byers and Funch, 1982; Webster et al., 1983) or only limited evidence (Begg et al., 1983). These conflicting findings are not easy to reconcile, but could be partly explained by methodological differences. For example, although nutritional variables were evaluated in the study by Willett et al. (1987), the data were obtained from a self-administered questionnaire, and it was not possible to evaluate confounding by variables, which may have masked an association. In that study, therefore, increased alcohol consumption could have been a marker for other factors that increase the risk of breast cancer. In a detailed review of the epidemiologic findings concerning alcohol consumption and breast cancer, Longnecker et al. (1988) concluded that there was sufficient evidence to support an association. Animal Studies Over the past 20 years, animal studies have shown that ethanol, either applied topically or administered as part of the diet, has cocarcinogenic effects. Examples of these experiments include the enhanced carcinogenesis of 7,12-dimethylbenzanthracene applied either to the cheek epithelium of young hamsters (Elzay, 1966, 1969) or to the skin of mice (Stenbäck, 1969), esophageal tumors induced in rats by diethylnitrosamine

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Page 440 (DEN) (Gibel, 1967), liver tumors induced by vinyl chloride (Radike et al., 1981), nasopharyngeal cancers initiated in pair-fed hamsters by nitrosopyrrolidine (McCoy et al., 1981), and rectal cancers initiated by dimethylhydrazine in rats (Seitz et al., 1984). However, the simultaneous addition of DEN and ethanol in drinking water (25%) did not modify DEN induction of hepatocarcinogenesis (Habs and Schmähl, 1981), nor did consumption of diets containing ethanol (35% total calories) affect the number of liver tumors induced by dimethylnitrosamine (DMN) (Teschke et al., 1983) or modify the development of preneoplastic hepatic foci by aflatoxin B1 in rats (Misslbeck et al., 1984). Similar results were obtained by Schwarz et al. (1983) using DEN or N-nitrosomorpholin as carcinogens and 10% ethanol in drinking water. The association of alcohol consumption with cancers at sites that do not come into contact with high ethanol concentrations suggests that mechanisms other than, or in addition to, the direct cytotoxic effects of ethanol play a role in carcinogenesis. These are discussed in the following sections. Activation of Chemical Carcinogens Ethanol may act as a cocarcinogen at remote sites through its capacity to induce the microsomal cytochrome  P450-dependent biotransformation system. Ethanol administration to rats increases hepatic benzpyrene hydroxylase (Rubin et al., 1970). Likewise, activation of nitrosopyrrolidine was substantially increased (Farinati et al., 1985a). Ethanol induces microsomal DMN N-demethylase activity, which functions at low DMN concentrations (Garro et al., 1981). This effect contrasts with those of other microsomal enzyme inducers and may be due to the induction by ethanol of a specific form of cytochrome P450 (Koop et al., 1982; Ohnishi and Lieber, 1977), which differentially affects the activation of various carcinogens. Indeed, a selective affinity for DMN has been demonstrated with the ethanol-induced form of cytochrome P450 (Yang et al., 1985), and an active form of this isozyme (now called P450 IIE1 ) has been purified from human liver (Lasker et al., 1987). Furthermore, in studies using microsomes of ethanol-fed animals, enhanced mutagenicity was demonstrated at low DMN concentrations (Garro et al., 1981). A growing body of evidence indicates that ethanol acts as a cocarcinogen. For example, the combined action of DMN and alcohol increased the incidence of olfactory neuroepitheliomas in mice (Griciute et al., 1981). Takada et al. (1986) noted neoplastic changes in the liver of rats treated with alcohol and DEN or with phenobarbital and DEN, suggesting that ethanol, as well as phenobarbitol, is a promoter of hepatocarcinogenesis. The intestinal metabolism of xenobiotic substances may also be altered by ethanol consumption. Elevated cytochrome P450 levels and microsomal enzyme activities have been observed in the esophagus (Farinati et al., 1985a) and in the upper small intestine of rats after chronic ethanol ingestion (Seitz et al., 1979). In the Salmonella typhimurium test system, chronic ingestion of ethanol enhanced the capacity of intestinal microsomes to activate benzo[a]pyrene to a mutagen (Seitz et al., 1978) and the capacity of intestinal microsomes to activate 2-aminofluorene and tryptophan pyrolysate (Seitz et al., 1981). Enhanced activation of benzo[a]pyrene to mutagenic derivatives has been mediated by lung microsomes in ethanol-fed rats (Seitz et al., 1981). Ethanol also enhanced the induction of nasopharyngeal tumors in hamsters treated with nitrosopyrrolidine (McCoy et al., 1981) and increased the activation of nitrosopyrrolidine to a mutagen by microsomes isolated from hepatic, pulmonary, and esophageal tissues (Farinati et al., 1985a; McCoy and Wynder, 1979). In the rats treated with 1,2-dimethylhydrazine (DMH), chronic ethanol consumption enhanced the appearance of rectal tumors but not tumors in the distal or proximal colon (Seitz et al., 1984). This effect did not relate to the cytochrome P450-dependent oxidizing system in the liver or in the colonic mucosa or to changes in the fecal bile acids. However, colonic mucosal alcohol dehydrogenase (ADH) was increased by 47% in rats fed ethanol, but it is not clear whether this local increase is associated with the observed enhancement of carcinogenesis. Effects of Ethanol on DNA Metabolism Obe and colleagues reported that acetaldehyde, the first metabolite of ethanol, induces sister chromatid exchanges (SCEs) in cells grown in tissue culture (Obe and Beck, 1979; Obe and Ristow, 1977) and concluded that there is an elevation of chromosome aberrations in alcoholics (Obe and Ristow, 1979). Alcohol may also inhibit the capacity of cells to repair carcinogen-induced DNA damage. O6-methylguanine transferase (O6-MeGT) is the enzyme responsible for repairing O6-methylguanine (O6-MeG) and O6-ethylguanine adducts. After 4 weeks on a diet containing

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Page 441 ethanol as 36% of total calories, O6-MeGT activity was reduced by approximately 40% relative to controls. In other experiments in rats, 50 mM of ethanol, a concentration corresponding to blood levels in alcohol abusers, directly inhibited O6-MeGT activity (Farinati et al., 1985b). Even minute amounts of acetaldehyde noticeably inactivate the enzyme (Espina et al., 1988). Since alkylation at the O6 position of guanine is associated with both mutagenesis and carcinogenesis (Kleihues et al., 1979; Lewis and Swenberg, 1980; Newbold et al., 1980), the apparent decrease in O6-MeGT activity in alcohol-fed rats could be a mechanism of cancer induction. Some studies failed to detect an effect of dietary ethanol in the repair of DMN-induced O6-MeG adducts (Belinsky et al., 1982; Schwarz et al., 1982). In one of these, however, O6-MeG levels were examined only until 4 hours after DMN administration (Schwarz et al., 1982). The differences in experimental results may be due to differences in feeding protocols. Local Effects of Ethanol on Cancer Induction Ethanol ingestion produced overt tissue damage in the mucosa of the stomach (Dinoso et al., 1976; Eastwood and Kirchner, 1974; Gottfried et al., 1978) and the small intestine (Baraona et al., 1974; Perlow  et al., 1977). The damage was followed by cell proliferation when the administration of alcohol was stopped (Baraona et al., 1974; Willems et al., 1971). Ethanol also stimulated cell proliferation in the germinative epithelium of the rat esophagus in the absence of overt mucosal damage (Mak et al., 1987). Stimulation of cell replication would sensitize the esophagus to chemical carcinogens. Congeners In addition to the local effects of ethanol, some congeners (nonalcoholic components) in alcoholic beverages may play an etiologic role in the development of cancer. Esophageal cancer has been produced in animals by administering relatively large amounts of nitrosamines, which may occur as congeners in some alcoholic beverages (Lijinsky and Epstein, 1970; Lowenfels, 1974). Ethanol catalyzes the production of nitrosamines from nitrites and secondary amines under conditions present in the upper gastrointestinal tract (Pignatelli et al., 1976). Alcoholic beverages contain a variety of carcinogens such as polycyclic aromatic hydrocarbons (e.g., phenanthrene, fluoranthrene, benzanthracene, benzopyrene, chrysene) (Masuda et al., 1966). Asbestos fibers derived from filters have been detected in beer, wine, sherry, and vermouth (Bignon et al., 1977; Biles and Emerson, 1968; Cunningham and Pontefract, 1971). Carcinogenic Effects of Dietary Deficiencies Combined with Alcohol Abuse Ethanol consumption combined with vitamin A deficiency increases the incidence of squamous metaplasia of the trachea (Mak et al., 1984). Drugs that induce liver microsomes decrease hepatic vitamin A (Leo et al., 1984). A similar effect was also observed in baboons and rats given ethanol (Sato and Lieber, 1981) and other xenobiotic substances, including carcinogens, that interact with liver microsomes (Innami et al., 1976; Kato et al., 1978; Reddy and Weisburger, 1980). Similar observations have been made in humans. For example, patients with alcoholic liver disease had very low hepatic vitamin A levels at all stages of their disease (Leo and Lieber, 1982). Retinol can compete with DMN for its activation (presumably to carcinogens) in liver microsomes (Leo et al., 1986b). Lowering hepatic vitamin A  by diminishing this inhibition may indirectly favor chemical carcinogenesis. Ethanol also may exert a direct stimulatory effect on cell proliferation independent of vitamin A status (Mak et al., 1987). A Plummer-Vinson-like syndrome was observed among female patients with oral cancer (Wynder et al., 1957a). Hyperplasia was observed on the skin of riboflavin-deficient mice (Wynder and Chan, 1970). Vitamin B6 plays an important role in the production of antibody response to various antigens (Axelrod and Trakatellis, 1964). This effect may influence tumor development indirectly by affecting the consequences of exposure to HBV. Wynder (1976) reported that pyridoxine deficiency is associated with enhanced liver tumor formation. Vitamin E and other antioxidants, such as butylated hydroxytoluene (BHT), propylgallate, and ethoxyquin, have reduced the induction of tumors by certain carcinogens in several target organs (Ulland et al., 1973; Wattenberg, 1972a,b). The protective effect of BHT against chemically induced carcinogenesis may be offset, at least in part, by its potentiation of ethanol-induced vitamin A depletion (Leo et al., 1987b).

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