O Nutrition and Health

-. 1984. Nutrient intakes: individuals in 48 states, year 1977-78. Report no. I-2. Hyatts-
ville, MD: Consumer Nutrition Division, Human Nutrition Information Service.

U.S. Department of Health, Education, and Welfare. 1972. III. Clinical, anthropometry,
dental; IV. Biochemical; V. Dietary. Ten State Nutrition Survey f%8-1970. DHEW publica-
tion nos. (HSM) 72-8131, 8132, 8133. Atlanta. GA: Centers for Disease Control.

-. 1974. Preliminary findings of the first Health and Nutrition Examination Survey,
United States, 1971-72. Dietary intake and biochemical findings. DHEW publication no.
(HRA) 741219-l. Washington, DC: U.S. Government Printing Oflice.

-. 1979a. Dietary intake source data: United States, 1971-74. DHEW publication no.
(PHS) 79-1221. Washington, DC: U.S. Government Printing Office.

-. 1979b. Hemoglobin and selected iron-related findings of persons I-74 years of age.
United States, 1971-1974. DHEW publication no. (PHS) 46. Hyattsville, MD: U.S. Depart-
ment of Health, Education and Welfare.

U.S. Department of Health and Human Services. 1983. Dietary intake source data: United
States, 1976-80. Vital and Health Statistics, series 11, no. 231. DHHS publication no. (PHS)
83-1681.

-. 1988. Surgeon General's Workshop on Health Promotion and Aging. Washington,
DC.

U.S. Department of Health and Human Services and U.S. Department of Agriculture. 1986.
Nutrition monitoring in the United States: a progress report from the Joint Nutrition Monitor-
ing Evaluation Committee. DHHS publication no. (PHS) 86-1255. Washington, DC: U.S.
Government Printing Gffice.

U.S. Senate. 1987/88. U.S. Senate SpecialCommitteeonAging--1988AgingAmerica:trends
and projections, LR 3377 (188), Dl2198. Washington, DC: U.S. Department of Health and
Human Services.

VanderJagt, D.J.; Garry, P.J.; and Bhagavan, H.N. 1987. Ascorbic acid intake and plasma
levels in healthy elderly people. American Journal of Clinical Nutrition 46:2%94.

Vatassery. G.T.; Johnson, G.J.; and Krezowski, A.M. 1983. Changes in vitamin E concentra-
tions in human plasma and platelets with age. Journal of the American College of Nutrition
4:36%75.

Vinther-Paulsen. N. 1981. Calcium and phosphorus intake in senile osteoporosis: prevention
versus cure. Federation Proceedings 40:2418-22.
Vir, SC., and Love, A.H.G. 1978. Vitamin D status of elderly at home and institutionalized in
hospital. International Journal of Vitamin Nutrition Research 48: 123-30.
Weindruch, R.. and Walford, R.L. 1988. The retardaiion of aging and disease by dietary
restriction. Springfield. IL: Thomas.

Weisman. Y.; Schen, R.J.; Eisenberg, Z.; Edelstein, S.; and Harell, A. 1981. Inadequate
status and impaired metabolism of vitamin D in the elderly. IsraelJournal of Medical Science
17:19-21.

Widgor, B., and Morris, G. 1977. A comparison of to-year medical histories of individuals with
depressive and paranoid states: a preliminary note. Journal of Gerontology 32: 160-63.
Wilson, R.S.; Weeks, M.M.; Mukhejee, S.K.; Murrell, J.S.: and Andrews, C.T. 1972. A
study of vitamin C levels in the aged and subsequent mortality. Gerontology Clinics 14: 17-20.

-. 1973. A study of the effect of vitamin C administration. Age and Ageing 3:163.

626


Aging O

Yearick, E.S.; Wang. M.S.; and Pisias, J.J. 1980. Nutritional status of the elderly: dietary and
biochemical findings. Journal of Gerontology 5:663-71.

Young, E.A.. and Rivlin, R.S. 1982. Symposia on evidence relating selected vitamin minerals
to health and disease in the elderly population in the United States. American Journal of
Clinical Nutrition 36(suppl.):977-1086.

Zauber, N.P., and Zauber, A.G. 1987. Hematologic data of healthy very old people. Journal of
the American Medical Association 257~2181-84.

627


Chapter 17

Alcohol

Inflaming wine, pernicious to mankind,
    unnerves the limbs,
   and dulls the noble mind.
         Homer
  The Iliad, VI 261 (850 B.C.)

Introduction

Alcohol (ethanol) is of importance to nutrition because it provides energy
and because its ingestion can affect the requirements for and the intake,
digestion, absorption, transport, storage, metabolism, and excretion of
many other nutrients. Few generalizations can be made regarding the
effects of alcohol on nutritional status because these depend on complex
interactions between the type, quantity, and duration of alcohol consumed
and the overall nutrient intake from the diet. These interactions are highly
dependent upon behavioral and socioeconomic factors and predisposing
genetic factors. Chronically excessive alcohol use is often associated with
symptoms, signs, and biochemical evidence of nutritional deficiencies, but
these are largely the secondary effects of reduced consumption of other
kinds of food and drink. The effect of moderate or occasional drinking is
less well documented.

Historical Perspective

Fermented beverages have been consumed in most societies since antiq-
uity, in part because fermentation provided one of the earliest methods of
food preservation (Ghalioungui 1979). In some societies, indigenous foods
that contained alcohol as a result of fermentation may have offered protec-
tion against the development of deficiencies of vitamins, amino acids, and
other essential nutrients (Steinkraus 1979; Darby 1979).

Socioeconomic factors have always affected the pattern of alcohol abuse
and its complications in different societies. In ancient Greece, for example,

629


0 Nutrition and Health

wine drinking was confined largely to the upper classes, and beer drinking
to the lower classes. In industrialized England of the 18th century, gin was
the drink of the poor, while port was drunk by the affluent, whose episodes
of gout were attributed to the contamination of port with lead.

Distilled spirits, in contrast to fermented foods and beverages, provide
concentrated sources of alcohol and calories largely without other nu-
trients. Although the process of distillation was known at least as early as
the fourth century B.C. (Ghalioungui 1979), the consumption of distilled
spirits tended for centuries to be limited to the more affluent who also had
access to varied diets. In Western Europe, distilled alcoholic beverages
were not widely available to the poor until the Industrial Revolution. In
England, government policies that liberalized controls on production and
distribution of alcoholic beverages led to the widespread "gin epidemic,"
and further legislation was then required to prohibit sales and prevent
adverse consequences (Roe 1979).

Out of this history grew a series of health and social reform movements,
including the prohibitionist movement in the United States. In their efforts
to change society's behavior, most health reform advocates focused on the
extreme consequences of alcohol abuse, using selected medical and scien-
tific data to support their arguments (Whorton 1982). This, in turn, led to
distortions in understanding the nutritional consequences of alcohol use.
For example, many studies examined the habits of accessible derelict or
vagrant alcoholics or provided descriptive reports that were easier to
obtain than biologic determinations of specific pathophysiologic mecha-
nisms.

The attitudes toward alcohol of the 19th and early 20th centuries remain
prevalent today, and many people are uncertain and misinformed about
interactions between alcohol and nutrition. Recent efforts from the U.S.
Department of Health and Human Services have focused on providing the
scientific community and the public with current information about this
area. Thus, alcohol consumption has been identified as a dietary practice in
need of change in several Federal publications. Examples include those
listed below.

Healthy People: The Surgeon General's Report on Health Promotion and
Disease Prevention, 1979. This report recommends reducing misuse of
alcohol. It includes information on prevention programs that stress the
importance of educating the public on the effects of alcohol consumption,

630


Alcohol 0

altering the social climate of its acceptability, reducing individual and social
stress factors that might increase consumption, and enforcing existing laws
(DHEW 1979).

Nutrition and Your Health: Dietary Guidelines for Americans (second
edition), 1985. One of the seven recommendations is "If you drink alcohol,
do so in moderation." The discussion of this guideline emphasizes the
caloric contribution of alcohol to the overall diet, especially for individuals
who are overweight, but notes that one to two drinks daily appear to cause
no harm in adults. It warns pregnant women that excessive alcohol con-
sumption may cause birth defects at the same time that it acknowledges that
the "level of consumption at which risks to the unborn occur has not been
established" (USDADHHS 1985).

Promoting HealthlPreventing Disease: Objectives for the Nation, 1980.
These health objectives include specific recommendations for methods to
reduce deaths due to alcohol-related behavior, accidents, and disease by
the year 1990 (DHHS 1980).

Promoting HealthlPreventing Disease: Public Health Service lmplementa-
tion Plans for Obtaining Objectives for the Nation. This report identities
priority objectives for prevention of alcohol misuse and outlines Federal
efforts in education, grant support, technical assistance, economic incen-
tives, and research and surveillance measures aimed at achieving them. It
also assigns to specific agencies the primary responsibility for each of the
implementation steps and provides data on the anticipated date of initiation
of each step (DHHS 1983).

The Sixth Special Report to the U.S. Congress on Alcohol Abuse and
Health from the Secretary of Health and Human Services. This report
provides the most comprehensive statement to date of current knowledge
in the epidemiology of alcohol abuse and alcoholism; the genetics, psycho-
biologic effects, and medical consequences of alcoholism; the effects of
alcohol on pregnancy outcome; the adverse social consequences of alcohol
abuse; trends in treatment, research, and practice; and perspectives on
prevention (DHHS 1987).

The 1990 Health Objectives for the Nation: A Midcourse Review, 1986.
This report provides data on progress toward achieving the 1990 objectives
for prevention of deaths due to alcohol misuse. Although it notes im-
pressive achievements in reducing alcohol-related motor vehicle accident

631


O Nutrition and Health

fatalities and deaths due to cirrhosis, it stresses the importance of multi-
disciplinary approaches to prevention of the adverse health consequences
of individual behavior associated with alcohol consumption (DHHS 1986).

Significance for Public Health

Although the nutritional elements of the public health impact of alcohol
abuse are still being defined, in and of itself, misuse of alcohol is one of the
most preventable health problems in the United States. As mentioned
above, prevention of the adverse consequences of alcohol misuse is a major
health objective for the year 1990 (DHHS 1986). Excessive alcohol intake is
a prominent contributor to 4 of the 10 leading causes of death in the United
States-cirrhosis of the liver, motor vehicle and other accidents, suicides,
and homicides (NCHS 1986). As discussed in the cancer chapter of this
Report, chronic alcohol abuse also increases the risk for oral, esophageal,
liver, and other types of cancer.

In 1980, it was estimated that nearly 20,000 deaths could be directly
attributed to alcohol use, from alcoholic liver disease, alcoholism, alco-
holic psychosis, alcoholic cardiomyopathy, alcoholic gastritis, alcoholic
polyneuropathy, nondependent use of alcohol, and accidental poisoning by
alcohol. Almost 78,000 fatalities could be indirectly attributed to alcohol
use (Ravenholt 1984). In 1983, about 42 percent of all motor vehicle deaths
were alcohol related. Problems such as homicides and automobile acci-
dents that are indirectly related to alcohol consumption have the highest
rates among young adult males ages 18 to 24. Excessive alcohol intake
during pregnancy is estimated to cause birth defects in 1,400 to 2,000 babies
annually. The costs of the medical and social consequences of excessive
alcohol intake were estimated to be $117 billion in 1983 (DHHS 1987). In
the late 1970's, 19 percent of adolescents reported problems related to
drinking alcohol. Among adults over age 18, approximately 10.6 million are
alcohol dependent and another 7.3 million experience alcohol-related ad-
verse consequences (DHHS 1986).

Recent trends suggest that both the intake of alcohol and its adverse health
consequences are declining in this country. Overall per capita ethanol
consumption increased annually from 1977 to 1980, reached a plateau in
1980 and 1981, and then began an annual decline until 1985, when it was
slightly below the 1977 level (Laforge et al. 1987). Beer consumption in 1985
was 3 percent above the 1977 level; wine consumption per capita increased
over the entire period of 1977 to 1985, and in 1985 it was 31 percent higher
than in 1977. Per capita consumption of spirits, however, declined over this

632


Alcohol O

entire period, and in 1985 was 15 percent below the 1977 level (Laforge et
al. 1987). There has also been a slow decline in deaths attributable entirely
to alcohol-related causes since 1980 (Berkelman et al. 1986).

Scientific Background

Quantitative Aspects of Alcohol Consumption Among Individuals
Different units are used to record the quantity of alcohol intake among
individuals. Commonly used units are grams or ounces of pure alcohol.
There are approximately 15 g of alcohol in each of the following standard-
sized drinks: I-% oz of 80 proof liquor, 5 oz of table wine, and 12 oz of beer
(Bennington and Church 1985).

Consumption of Alcoholic Beverages

The proportion of U.S. adults who drink alcoholic beverages depends on
both the region of the country and sociocultural background. Estimates of
the various categories of drinkers in the population are usually based on
survey information, and the estimated quantities consumed are often based
on self-reports. Such surveys indicate that about 33 percent of the general
population say they do not drink alcohol at all; 34 percent are light drinkers,
who say they drink from one to three drinks per week; 24 percent are
moderate drinkers, who report consuming fewer than two drinks a day; and
9 percent are heavy drinkers, who average two drinks a day or more (Moore
and Gerstein 1981). In studies ofthe heaviest drinkers (i.e., alcohol abusers
and alcoholics), the quantity of alcohol consumed is very difficult to
ascertain, and clinical criteria for the diagnosis of alcoholism usually must
depend on factors other than alcohol intake information (Task Force on
Nomenclature and Statistics 1980).

Although this classification into light, moderate, and heavy drinkers seems
reasonable and is used in this chapter, it is arbitrary and not universally
accepted. For example, in the Honolulu Heart Study, consumption of two
to three drinks per day was considered moderate, but, according to the
above classification, it would be considered heavy consumption. The use of
the Michigan Alcoholism Screening Test (a short questionnaire shown to be
efficient in identifying alcoholics) and other alcoholism screening tests
such as the Self-Administered Alcoholism Screening Test (Swenson and
Morse 1975) may prove important in separating alcoholic from non-
alcoholic persons by standard criteria rather than by self-reports.

Surveys also reveal wide regional variations, especially among the percent-
age of individuals who say they abstain completely from alcohol (e.g., 14

633


0 Nutrition and Health

percent in western New York State, 32 percent in San Francisco). The
percentage of heavy drinkers, adults who report drinking two drinks or
more a day, ranges from 9 percent nationwide to 23 percent in Boston and
24 percent in western New York State (Barnes and Russell 1978; Wechsler,
Demone, and Gottleib 1978).

The frequency of alcohol consumption reported by high school students
differs from that reported by adults in national surveys. In a 1985 nation-
wide survey of about 17,000 high school seniors conducted by the National
Institute on Drug Abuse, only 8 percent of seniors said they had never used
alcohol. Nearly 5 percent of seniors drank every day, and 37 percent
reported episodes of heavy drinking (five or more drinks per occasion)
during the previous 2 weeks (DHHS 1987).

Categories of Beverages Consumed and Types of Drinkers

Since 1934. the consumption of alcohol in the United States, based on
statistics from commodity sales, has increased almost continuously, and in
1984 the annual per capita intake in terms of absolute alcohol was 2.65 gal/
person 14 years of age or older (DHHS 1987). As one-third of the U.S. adult
population abstains from alcohol, those who drink consume an average of
1.3 oz of absolute alcohol per day. These distinctions become even more
important when examined more closely: the heaviest drinking 5 percent of
the population accounts for about 50 percent of total alcohol consumption,
and the heaviest drinking 33 percent accounts for over 95 percent of total
alcohol consumption. Given the presumed absence of impact of alcohol on
the nutrition of the one-third of the population who abstain, and negligible
impact on that of the one-third who are light drinkers, the group of primary
interest from this perspective is this latter group.

Over time, consumption of the various types of alcoholic beverages has
changed. Beer is now the most prevalent alcoholic beverage consumed,
accounting for almost 50 percent of the alcohol consumption in the United
States. Distilled spirits account for nearly 39 percent and wine for 12
percent. The wine industry was virtually dismantled as a result of Prohibi-
tion but has recently made significant advances in recapturing part of the
market and appears to be continuing to increase its share of sales. The
types of distilled spirits consumed have also changed with time; in recent
decades, there has been a shift from whiskey to other forms of distilled
spirits, such as gin and vodka.

Alcohol Abuse and Alcoholism
The essential feature of alcohol abuse is a pattern of pathologic moderate to
heavy alcohol use for at least a month that causes impairment in social or

634


Alcohol O

occupational functioning. The accepted diagnostic criteria, as defined in
the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) of
the American Psychiatric Association, are useful for such patterns of
chronic, pathologic alcohol consumption (Task Force on Nomenclature
and Statistics 1980). DSM-III criteria describe three main patterns of
alcohol abuse: (1) regular drinking of large amounts, (2) regular heavy
drinking but limited to weekends, and (3) episodic binges of heavy daily
drinking lasting weeks or months, interrupted by long periods of sobriety.
These criteria for the diagnosis of alcoholism also include either a pattern of
pathologic alcohol use or impairment in social or occupational functioning
and either central nervous system tolerance or withdrawal symptoms.

The number of Americans with alcohol problems is estimated to be as high
as 18 million (DHHS 1987). In an outpatient medical setting using the Self-
Administered Alcoholism Screening Test, the prevalence of abstainers was
13 percent and the prevalence of possible or probable alcoholism was 5.4
percent (Hurt, Morse, and Swenson 1980). The prevalence of alcoholism in
general hospitals, estimated by using the Michigan Alcoholism Screening
Test, was 18 percent for men and 5.5 percent for women (Moore 1971). In
emergency room patients, the prevalence of alcoholism may be as high as
30 percent of patients during the evening hours (Rund, Summers, and
Levin 1981). However, precise statistics for the prevalence of alcoholism
are not available now, nor are they likely to become so in the near future,
because alcoholism is diagnosed infrequently, especially in its earlier
stages.

Physiology of Alcohol Use

Absorption. Alcohol is readily absorbed from all levels of the gastroin-
testinal tract, and blood concentrations rise rapidly after ingestion. Overall
absorption of alcohol depends partly on the rate of gastric emptying. Food,
particularly fat, delays gastric emptying and stimulates gastric secretion,
thereby diluting the concentration of alcohol and blunting its rapid absorp-
tion into blood.

Absorption across the gut mucosa appears to occur as a result of passive
diffusion. The rate of absorption varies as a function of the concentration
gradient, the area and permeability of the absorbing surface, and the
volume of regional blood flow (Kalant 1971). During the first 15 minutes
after oral administration, maximum alcohol levels are rapidly found in the
stomach, duodenum, and proximal jejunum; at 90 minutes, peak levels are
found in the mid-jejunum. Alcohol levels in the ileum parallel those in the
blood, suggesting that the ileal concentration results from passage of alco-
hol from the blood back into the lumen rather than from transit along the

635


O Nutrition and Health

small bowel (Halsted, Robles, and Mezey 1973). Infusion of alcohol directly
into the duodenum, the first segment of the small intestine where most
nutrients are absorbed, causes blood levels of alcohol to rise as high as
those following direct intravenous administration, and these levels rise
much more rapidly than those that occur when alcohol is infused into the
stomach.

Distribution. Once absorbed, alcohol diffuses rapidly across capillary and
other cell membranes and is distributed uniformly throughout all extra-
cellular and intracellular body water. At equilibrium, the concentration of
alcohol in all tissues is proportional to the tissue water content, so that
differences in the volume of body water among people can help to explain
why some individuals are apparently more susceptible than others to the
pharmacologic and toxic effects of alcohol. Smaller, lighter people are more
susceptible to the effects of alcohol than larger, heavier people simply
because their fluid volume is less. For a given body weight, the volume of
body water is less in females than in males, and less in older people than in
younger people; therefore, a given dosage of alcohol can be expected to
produce higher blood concentrations in women and older persons and to
affect them more (Vestal et al. 1977).

Metabolism. Alcohol is metabolized by the liver first to acetaldehyde, then
to acetate, and, finally, to carbon dioxide and water. Three separate enzyme
systems can account for the initial oxidation of alcohol to acetaldehyde
(Badawy 1978; Lieber 1984; Pirola 1978). Quantitatively, the most impor-
tant system is that involving alcohol dehydrogenase, an enzyme found in
the cytoplasm of liver cells. The acetaldehyde produced is rapidly oxidized
to acetate by the enzyme acetaldehyde dehydrogenase, resulting in little
accumulation of acetaldehyde in either the liver or blood.

Alcohol and acetaldehyde dehydrogenases exist in several forms, which
oxidize alcohol and acetaldehyde at different rates. These enzyme varia-
tions may account in part for observed differences in rates of alcohol
metabolism among individuals of different genetic backgrounds and may
help explain, for example, why some people of Oriental or American Indian
heritage have lower tolerances for alcohol consumption (DHHS 1985).

A second enzyme system located in the liver, called the microsomal eth-
anol-oxidizing system (MEOS), probably plays a relatively minor role in
alcohol metabolism, at least at low concentrations, but it has significant
activity at higher concentrations of alcohol. This system can be stimulated
by chronic exposure to high levels of alcohol. This is associated with cross
induction of the metabolism of other drugs, such as the anticonvulsants

636


Alcohol 0

hydantoin and phenytoin, the barbiturates, the sedative meprobamate, the
tricyclic antidepressants, the phenothiazine tranquilizers, and oral anti-
coagulants (Pirola 1978). The inducibility of this system results in interac-
tions between alcohol and other drugs that may alter the rate of disappear-
ance of alcohol and other drugs from the body (see chapter on drug-nutrient
interactions) and may activate a variety of hepatotoxic agents and carcino-
gens.

A third enzyme system, the catalase system, appears to be of minor
importance in the metabolism of alcohol and is not stimulated by chronic
consumption of alcohol. Several other minor metabolic pathways, such as
glucuronide and sulfate conjugation and fatty acid esterification, have been
identified, but their importance remains unclear.

Some of the metabolic consequences of alcohol consumption can be ex-
plained by shifts in oxidation-reduction balance that occur as a conse-
quence of ethanol oxidation. Reduced nicotinamide-adenine dinucleotide
(NADH) is produced as a result of the oxidation of ethanol by the alcohol
dehydrogenase enzyme system and by the further oxidation of
acetaldehyde to acetate. An increased supply of NADH relative to NAD
may affect carbohydrate, lipid, and protein metabolism and account for
alterations in the hepatic metabolism of steroids, biogenic amines, some
drugs, and, perhaps, even some toxins. Other deleterious effects of alcohol
ingestion have been attributed to aldehyde or its cytotoxic interactions with
body proteins (Wickramsinghe, Gardner, and Barden 1987).

Excretion. More than 95 percent of the alcohol ingested is oxidized in the
liver to carbon dioxide and water, and the remainder is excreted in the
urine, feces, perspiration, and expired air.

Key Scientific Issuesa

o Effect of Alcohol on Nutritional Status and Energy Balance
0 Role of Alcohol in Diseases of the Liver
0 Role of Alcohol in Diseases of the Nervous System
o Role of Alcohol in Cardiovascular Diseases
o Role of Alcohol in Reproductive Disorders

aThe role of alcohol in cancer, diabetes, and osteoporosis is not covered here but is
reviewed in the chapters devoted to those conditions.

637


O Nutrition and Health

Effect of Alcohol on Nutritional Status and Energy Balance

Whether alcohol injures organs directly because of its toxic effects on
tissues or indirectly because of the nutritional deficiencies it causes has
been a subject of debate for decades. In the mid-18th and 19th centuries,
alcohol was considered a toxin and was classified with other poisons, such
as arsenic, mercury, and ergot. The discovery of vitamins in the 20th
century gave momentum to studies of the association between alcohol
consumption and nutritional status, especially between 1920 and 1940.
Similarities between complications of alcoholism such as those affecting
the nervous system and various vitamin deficiency states led to the belief
that most physical manifestations of alcoholism had a nutritional basis.

The malnutrition observed in alcoholics was proposed as the primary
reason for the organ and tissue damage found so frequently in this popula-
tion. Patients with severe alcoholic liver disease and ascites who were
given a diet high in protein and B-complex vitamins had a better prognosis
than those provided with a regular diet, and there was a significant associa-
tion between the occurrence of nutritional deficiency and the occurrence of
alcoholic cirrhosis (Patek and Post 1941). This finding suggested that eating
a diet high in protein and B-complex vitamins would protect an individual
from the effects of alcohol. Because so many nutritional deficiencies were
observed in derelict alcoholics, the assumption naturally was made that
similar but milder nutritional deficiencies were present in all other alco-
holics.

By the early 1960's, however, many of the clinical consequences of alco-
holism were shown to be the direct toxic effects of alcohol itself (Lieber
1966). Most recent evidence points to the toxic effect of alcohol or its
metabolic byproducts as the primary mode of liver injury. In addition,
possible genetic differences in predisposition to the direct toxic effects of
alcohol have been recognized. The effects of alcohol on the nutritional
status of nonalcoholic social drinkers remains to be defined.

Excessive alcohol intake increases the risk for malnutrition through a
variety of pathophysiologic mechanisms, including direct and indirect
alterations in both nutrient intake and requirements, digestion, absorption,
transport, storage, metabolism, and excretion. For any nutrient, alcohol
may affect one or more of these processes. The following sections summa-
rize what is known about the most important interactions between alcohol
and each major nutrient. The reported effects of alcohol vary greatly,
depending on how much and how long it is consumed. In some cases,

638


Alcohol O

marked differences among animal species have led to apparently contradic-
tory and confusing experimental results.

Energy

At the turn of this century, Atwater determined that ethanol provides 7
kcal/g, and ever since then this amount has been used as the basis for
calculating the contribution of alcohol to total energy intake (Passmore
1979). The use of this conversion factor assumes that the energy in alcohol
is fully available to the body. Based on this conversion factor, only 3 to 7
percent of the calories consumed by all Americans over the age of I4 are
derived from alcohol, but if nondrinkers are excluded, alcohol provides
over IO percent of the calories consumed by adult drinkers in the United
States (Williamson et al. 1987).

Many observations suggest that the caloric contribution of alcohol is more
complex than can be explained by the Atwater conversion values, and
therefore, the concept of alcohol and energy balance has recently been
revised. If, for example, alcohol provides an average of 20 percent of the
calories in the diet of the average drinking American adult, then many
alcoholics consuming much larger amounts ought to be obese. Instead,
national data indicate that despite higher energy intakes, drinkers are no
more obese than nondrinkers (Gruchow et al. 1985). Alcoholics tend to lose
weight over time, and abstinence is commonly associated with a gain in
weight (Morgan 1982). In one study, eight malnourished alcoholic patients
lost an average of 9 lb while they were consuming at least 200 g (about 1,400
kcal) of ethanol daily for a minimum of 3 weeks. They then gained an
average of 7 lb after abstaining from alcohol for 2 weeks and eating an
adequate diet (Halsted, Robles, and Mezey 1971). In another study, alcohol
was associated with a substantial reduction in weight among women (Wil-
liamson et al. 1987). The conclusion usually drawn from such studies is that
alcoholics do not consume an adequate diet, which is often true.

Increasing alcohol intake while maintaining an adequate diet, however,
does not necessarily lead to a weight gain. For example, when 56 alcoholic
patients were admitted to a hospital and fed a diet of 2,600 kcal, those who
received an additional 256 g, or 1,800 kcal, of alcohol each day experienced
no greater weight gain than those who received the diet of 2,600 kcal alone
(Mezey and Faillace 1971). Similarly, when alcoholic patients were fed diets
supplemented with 2,000 kcal of alcohol, no consistent change in body
weight occurred, but when the 2,000 extra kcal were provided as chocolate,
there was a consistent weight gain (Pirola and Lieber 1972). This study
showed that substitution of an equal number of kcal of alcohol for carbohy-

639


O Nutrition and Health

drate at a level of 50 percent of total kcal was followed by weight loss, and
the same result was obtained at 25 percent of total kcal (McDonald and
Margen 1976).

The mechanisms accounting for the apparent inefficiency in conversion of
potential energy from alcohol are complex and incompletely understood
(World et al. 1984). Metabolic rate, as measured by oxygen consumption, is
higher in rats fed alcohol than in those fed the same number of calories as
carbohydrate (Pirola and Lieber 1972). Alcohol increases oxygen con-
sumption in normal human subjects and is reported to increase it even more
in alcoholic persons (Lieber 1984).

Several mechanisms have been proposed to explain how the oxidation of
alcohol could result in "inefftcient" energy transfer. The MEOS pathway of
alcohol oxidation requires a reducing equivalent, from nicotine adenine
dinucleotide phosphate (NADPH), and results in the production of heat
rather than high-energy phosphate bonds. Subsequent reduction of NAD to
NADH during the oxidation of acetaldehyde to acetate would result in no
net change in total reducing equivalents. Furthermore, the alteration in the
ratio of NADH to NAD in the cell cytoplasm might temporarily shift
various substrates to the more reduced state and thereby impair the flux of
reducing equivalents into the mitochondria for subsequent oxidative phos-
phorylation. A third mechanism could result from abnormalities in mito-
chondrial membranes, but this would be more likely to occur in alcoholic
individuals and therefore would not explain the acute increase in metabolic
rate following alcohol ingestion in normal drinkers (Lieber 1984).

Recent studies on nonshivering and postprandial thermogenesis (Rothwell
and Stock 1986) may cast some light on another possible mechanism to
explain the observed rise in oxygen consumption following alcohol inges-
tion. Landsberg and Young (1984) have shown that sympathetic nervous
activity plays a central role in the increased heat production following
feeding and the reduced heat production associated with starvation. Alco-
hol ingestion, especially in large amounts, has been associated with in-
creases in catecholamine levels, specifically norepinephrine (Beilin and
Puddey 1984).

The caloric value of alcohol (at least when ingested in large amounts)
cannot be regarded as equivalent to the caloric value of other dietary
sources of energy, as measured by the synthesis of high-energy phosphate
bonds. Loss of weight when alcohol is substituted isocalorically for carbo-
hydrate and the failure to gain weight when an otherwise adequate diet is
supplemented with alcohol have led to the suggestion that alcohol-derived


Alcohol 0

calories should be disregarded completely as an energy source in predict-
ing dietary-induced changes in weight (World et al. 1984). but the factors
may work differently by pattern of alcohol use.

For moderate drinkers, another factor that must be considered is the effect
of alcohol on caloric intake from other foods, especially in individuals who
are chronically dieting. Recently, the concept of the "restrained eater" has
been developed (Herman and Polivy 1980). Briefly stated. the restrained
eater attempts to maintain body weight at a lower-than-set-point level by
chronically undereating. When obligated toeat, or when the self-restraint is
temporarily suspended, rebound overfeeding occurs. This hypothesis is
supported by studies in which volunteers were asked to taste an appealing
food after some of them had been provided a preliminary dose of alcohol.
Among restrained eaters, alcohol increased the amount of food consumed,
but alcohol did not affect the subsequent intake of unrestrained eaters
(Polivy and Herman 1976a, 1976b).

These findings are consistent with the frequent clinical observation that
obese people have greater difficulty dieting and maintaining lower body
weights if they continue to drink alcohol. Whether the signals involved are
psychologic or biologic remains to be determined. Animal studies suggest
that biologic signals may be responsible because similar overeating can be
demonstrated in animals who have been underfed before testing (Herman
and Polivy 1980).

Lipids

Abnormalities in lipid metabolism are common in both alcoholics and mild
to moderate drinkers (Janus and Lewis 1978). Body fat stores usually are
depleted when weight loss results from poor diets. Alcoholics with chronic
pancreatitis and pancreatic insufficiency may not digest fat efficiently
because of a reduced output of pancreatic lipases, the primary enzymes for
digesting lipids. Hepatic insufficiency can also cause fat malabsorption due
to impaired secretion of the bile salts that emulsify fats and make them
more digestible and absorbable. In addition, abnormalities in intestinal
mucosal cells have been found to occur as a direct result of alcohol toxicity
and, more commonly, as an indirect result of malnutrition (Green 1983).

Carbohydrate

Differences among animal species and differences in experimental condi-
tions have led to apparently conflicting results regarding the effects of
alcohol on carbohydrate metabolism (Marks 1978). Two major syndromes
warrant discussion: (1) impaired glucose tolerance and (2) alcohol-induced

641


(3 Nutrition and Health

hypoglycemia. These effects are of special concern in patients with di-
abetes mellitus.

Impaired Glucose Tolerance. Impaired glucose tolerance is most easily
demonstrated if the dosages of alcohol are sufficient to increase sympathet-
ic nervous system activity and, perhaps, to decrease peripheral uptake of
glucose. Doses of alcohol sufficient to produce blood alcohol levels of
approximately 80 mg of alcohol per 100 ml of blood and mild euphoria do
not activate the sympathetic nervous system and do not greatly affect blood
glucose concentrations (Marks 1978). Indeed, some studies have shown an
improvement in glucose tolerance following alcohol ingestion. Mild fasting
hyperglycemia has been observed in more than 20 percent of middle-class
alcoholics at the time of admission for alcoholism treatment (Hurt et al.
1986). It appears that the conditions under which alcohol is consumed, the
associated dietary intake, the level of alcohol consumption, the history of
alcohol consumption, and the presence of organ pathology such as hepatic
insufficiency are responsible for the wide variation in the effects of alcohol
on glucose tolerance.

Hypoglycemia. A rare but often fatal complication of alcohol abuse is
profoundly low blood sugar (Williams 1984). This condition usually occurs
in the context of acute alcohol ingestion after minimal food intake for
several days or more. Victims are found stuporous or deeply comatose,
with blood glucose levels below 20 mg/lOO ml of blood. It has been pro-
posed that alcohol blocks gluconeogenesis by metabolic shifts that result in
reduced conversion of gluconeogenic precursors into glucose and
glycogen. In the absence of glycogen stores, profound hypoglycemia oc-
curs. Alcohol-induced hypoglycemia can be produced experimentally in
normal healthy volunteers by inducing them to fast for 36 to 72 hours before
administering alcohol (Freinkel et al. 1965). Obesity, or pretreatment with
corticosteroids, tends to blunt the hypoglycemic effect of alcohol. In
contrast, malnutrition, adrenocortical insufficiency, thyrotoxicosis, and
consumption of diets high in protein and low in carbohydrate increase
sensitivity to the hypoglycemic effects of alcohol ingestion.

Diabetes Meflirus. The effects of alcohol on the management of diabetes
have been reviewed (McDonald 1980). Of particular importance are altera-
tions in the metabolism of oral hypoglycemic drugs. Sulfonylurea com-
pounds stimulate insulin release from the pancreatic beta cells and, in turn,
inhibit hepatic gluconeogenesis, thus augmenting the hypoglycemic effects
of alcohol. Prolonged alcohol ingestion can stimulate hepatic metabolic
pathways responsible for drug metabolism and thereby shorten the half-life

642


Alcohol 0

of certain drugs (see chapter on drug-nutrient interactions). In such cases,
the effectiveness of these drugs diminishes with prolonged alcohol inges-
tion.

For example, alcohol can impair the action of oral hypoglycemic agents.
Both phenformin-a drug no longer available in the United States, but used
elsewhere-and alcohol inhibit the decarboxylation of pyruvate to acetyl-
CoA and favor the reduction of pyruvate to lactic acid, which would tend to
increase the risk for lactic acidosis. Patients who take chlorpropamide
experience flushing and other symptoms similar to those induced by disul-
firam (Antabuse) when alcohol is consumed. Evidence indicates that there
are genetic predispositions to this drug-alcohol interaction. Finally, alco-
hol-related deteriorations in judgment may be especially serious for per-
sons with insulin-requiring diabetes if inebriation leads to errors in insulin
dosage, administration, and diagnosis. In rare cases, profound hypo-
glycemia with permanent neurologic deficit has occurred.

Protein

Data from animal studies suggest that low-protein diets, sufficient to pro-
duce protein malnutrition, affect the biosynthesis of the alcohol de-
hydrogenase enzyme system and the availability of other cofactors re-
quired for alcohol oxidation (Orten and Sardesai 1971). Furthermore, the
ability of rats, and possibly humans, to oxidize alcohol varies with both the
amount of dietary protein and the types of protein ingested. For example,
egg and milk proteins have been found to be more beneficial in maintaining
normal rates of alcohol oxidation than proteins from cereals or other plant
sources. When measured by indicators such as degree of inebriation and
incidence of death due to alcohol intoxication, however, a mixture of
proteins from vegetable sources has been shown to provide protection
comparable to that from animal protein alone (Lucas, Ridout, and
Lumchick 1%8).

Water-Soluble Vitamins

Thiamin. Poor dietary intake and poor selection of foods, frequently seen
in alcoholics, reduce thiamin intake. Alcohol may interfere with absorption
of thiamin, with its activation to thiamin pyrophosphate, or with the ability
of thiamin pyrophosphate to combine with the enzymes for which it is a
cofactor (Hoyumpa 1983). In addition, hepatic storage of thiamin may be
reduced due to fatty infiltration of the liver, hepatocellular damage, or
cirrhosis. Increased losses of thiamin from the body, as well as increased
requirements due to increased metabolic demands, especially following

643


O Nutrition and Health

refeeding with carbohydrates, have been reported. Wemicke-Korsakoffs
syndrome caused by thiamin deficiency in the alcoholic population is
discussed later in this chapter.

Riboflavin and Niacin. Riboflavin deficiency has been documented in
alcoholics, but the mechanism for this deficiency, other than a presumed
inadequate intake, has yet to be delineated.

In the 1940's, reductions in mortality rates from 90 to 14 percent following
therapy with niacin (nicotinic acid) were reported in a large series of
alcoholic patients who presented with impaired consciousness, delirium, a
particular type of muscular rigidity called cogwheel rigidity, and uncontrol-
lable grasping and sucking reflexes (Jolliffe 1940, 1941). In some patients,
paralysis of the eye muscles and memory defects developed during therapy.
Although these symptoms were attributed to niacin deficiency, deficiencies
of other nutrients, especially thiamin, were probably present as well.

Vitamin B,. Evidence suggests that alcohol inhibits the absorption of
vitamin B, (Baker et al. 1975) and its release from the liver (Sorrel1 et al.
1974). Alcohol also increases the rate of degradation of pyridoxal-5-phos-
phate, one of the active forms of vitamin B,. However, the magnitude of
vitamin B, deficiency, its contribution to morbidity, and the precise mecha-
nisms involved in its effects on alcoholic persons are unknown.

Folate and Vitamin B,,. Folate deficiency is probably the most common
vitamin deficiency observed in alcoholics. Conversely, alcoholism is prob-
ably the most common cause of folate deficiency in the U.S. adult popula-
tion. As with other nutrients, many factors contribute to folate deficiency
in alcoholics, although poor dietary intake is undoubtedly the major cause.
Alcoholics with good diets are less likely to have a folate deficiency than
alcoholics with poor diets. The type of alcoholic beverage typically con-
sumed may be significant because beer contains considerably more folate
than wine or distilled spirits.

Folate malabsorption has been reported to occur among alcoholics, but this
condition may be secondary to the toxic effects of alcohol or to malnutri-
tion, both of which can damage the intestinal mucosa and impair nutrient
absorption. Accordingly, correction of folate deficiency has been followed
by improved absorption both of folate and other vitamins and minerals.

Urinary excretion of folate is increased by alcohol intake. and its tissue
utilization is decreased (Russell et al. 1983). Alcohol may directly inhibit

644


Alcohol 0

enzymes involved in folate metabolism. Several investigators (Sullivan and
Herbert 1964; Lindenbaum 1977) have shown that alcohol antagonizes the
ability of folate to reverse the megaloblastic bone marrow changes seen in
deficiency states, but larger doses of folate can overcome this antagonism.
The suppressive effects of alcohol have been shown to be present whether
folate is given intravenously or orally, suggesting that a metabolic function
subsequent to absorption is involved.

Others have observed that macrocytosis (large red blood cells) occurs
frequently in alcoholics and that this symptom persists despite folate
supplementation unless alcohol intake is curtailed. Because of the high
prevalence of folate deficiency and related anemia in derelict alcoholics,
some investigators have proposed that low concentrations of folate be
added to inexpensive domestic wine and spirits as a way of preventing this
deficiency (Kaunitz and Lindenbaum 1977). However. it should be noted
that even though folate deficiency can cause macrocytosis, the mac-
rocytosis often seen in heavy drinkers is usually not related to folate
deficiency and is not corrected by administration of the vitamin. Instead,
this macrocytosis appears to be due to the direct effect of alcohol on the
architecture of the red cell and is correctable only with abstinence. Be-
cause this kind of macrocytosis is usually unaccompanied by anemia, the
presence of macrocytosis without anemia is a useful clue to alcohol abuse.

Symptoms of vitamin B,2 deficiency are much less common than those of
folate deficiency in alcoholics. Among malnourished alcoholics with liver
disease, the prevalence of vitamin B,, deficiency is similar to that seen
among randomly selected municipal hospital patients. Indeed, in some
studies, the circulating levels of vitamin B,, have been found to be higher in
alcoholics than in normal controls (Bonjour 1980).

The major manifestation of either folate or vitamin B,, deficiency is mac-
rocytic megaloblastic anemia. Macrocytic anemia, without mega-
loblastosis, is also seen in chronic liver disease. Megaloblastic changes in
the intestinal mucosal cells of persons with folate or vitamin B,, deficiency
may further impair nutrient absorption and bioavailability.

Ascorbic Acid (Vitamin C). Serum ascorbic acid levels have been found to
be lower in alcoholics than in nonalcoholics, probably because of inade-
quate diets. However, some data suggest that even when diets are adequate,
increasing levels of alcohol consumption are associated with lower serum
levels of ascorbic acid. Whether ascorbic acid affects alcohol metabolism is
uncertain, as is knowledge of the extent to which this interaction may have
clinical significance (Bonjour 1979).

645


O Nutrition and Health

Fat-Soluble Vitamins

Vitamin A. Vitamin A, as a fat-soluble vitamin, requires for its absorption a
certain level of fat in the diet and adequate quantities of pancreatic lipid-
digesting enzymes (lipases) and bile salts in the small intestine. Some
complications of alcoholism, such as pancreatic insufficiency and biliary
insufftciency, can therefore lead to malabsorption of vitamin A. In addi-
tion, alcoholics with liver disease may have impaired storage or transport
of vitamin A because of an inadequate synthesis of retinol-binding protein,
the protein formed in the liver that transports vitamin A in the blood. Even
moderate alcoholic liver disease is associated with severely decreased
vitamin A concentrations, and these levels are reduced in the liver even
when blood levels of vitamin A, retinol-binding protein, and prealbumin are
normal (Leo and Lieber 1982).

The storage form of vitamin A, retinol, is oxidized to its active form,
retinal, by retinol dehydrogenase, an enzyme similar to alcohol de-
hydrogenase. Impairments in the metabolism of vitamin A have been
reported in alcoholics, and some evidence suggests that retinol and ethanol
compete for the alcohol dehydrogenase enzyme in the liver, testes, and
retina (Shaw and Lieber 1983). Experimental deficiencies of several nu-
trients, including vitamin A, have been shown to enhance carcinogen-
induced tumors in laboratory animals. Whether vitamin A deficiency plays
a role in the reported association between alcohol intake and certain types
of tumors remains to be determined (Committee on Diet, Nutrition, and
Cancer 1982).

Vitamin D. Vitamin D and its metabolites are involved in regulating calcium
and phosphorus metabolism, bone formation and resorption, and various
other physiologic functions, including some aspects of immune function.
Alcoholics have been reported to have low circulating levels of vitamin D,
especially 25hydroxyvitamin D, the metabolite formed in the liver. Not
surprisingly, alcoholic persons with liver disease have lower levels of this
metabolite than persons without liver disease. Higher rates of osteomalacia
and osteoporosis have been reported in alcoholics (see chapter on skeletal
diseases). The specific mechanisms to account for these findings remain
unclear. Certainly, conditions associated with fat malabsorption may lead
to malabsorption of vitamin D. In addition, some evidence suggests that
alcohol induces enzymatic changes in the liver that favor the production of
inactive metabolites of vitamin D. As discussed below in the section on
minerals, the actions of vitamin D are closely linked with the metabolism of
calcium and phosphorus, the levels of which may be altered in response to
heavy alcohol ingestion.


Alcohol 0

Vitamin E. Alcoholic persons may develop severe malabsorption of vi-
tamin E due to pancreatic or biliary insufficiency, but actual reports of
vitamin E deficiency in alcoholics have been uncommon (Losowsky and
Leonard 1967). Available data suggest that vitamin E malabsorption occurs
most commonly in the presence of cirrhosis and steatorrhea, or fat malab-
sorption (Leevy, Tanribilir, and Smith 1971). Whether antioxidants such as
vitamin E protect against alcohol-induced fatty changes in the liver remains
uncertain (French 1971).

Vitamin K. Evidence suggests that at least half of the vitamin K required by
humans is normally synthesized by bacteria in the intestine. In rare cases,
vitamin K deficiency may occur with fat malabsorption, which is common
in alcoholics. In addition, persons with alcoholic liver disease demonstrate
a variety of impairments in the synthesis of vitamin K-dependent and other
blood clotting factors. Bleeding disorders are, therefore, common in alco-
holics. Alcohol also has been shown to affect blood platelets, coagulation
inhibitors, and tibrinolysis (Larkin and Watson-Williams 1984).

Minerals

Iron. Iron deficiency in alcoholics may occur as a result of repeated
gastrointestinal bleeding or clotting disorders. Iron overload, with hemo-
siderosis, may occur because of increased iron intake, either from alcoholic
beverages (especially certain wines) or from iron-containing vitamin-min-
eral supplements that are often taken because of otherwise unexplained
anemia. Iron absorption may be increased due to the increased solubility of
ferric iron in the small intestine caused by stimulation of gastric acid
secretion by alcohol. Increased iron absorption has also been reported in
persons with pancreatic insufficiency, folate deficiency, and cirrhosis. In
addition, disorders in heme synthesis can result in iron deposition in bone
marrow and other organs. Alcoholics may develop sideroblastic anemias,
characterized by the presence of ringed sideroblasts, in which iron is
deposited between the membrane folds of the mitochondria (Eichner and
Hillman 1971). Such anemias may result from vitamin B, deficiency, usu-
ally in association with folate deficiency or other impairments in activity of
enzymes involved in heme synthesis (Larkin and Watson-Williams 1984).
Hepatic hemosiderosis also appears to occur more frequently in alcoholics
and may be exacerbated by coexisting hemolysis, blood transfusion, or the
prolonged administration of therapeutic iron. In most such cases, it is not
possible to separate the causes from the consequences of iron deposition in
the development of hepatic failure (Larkin and Watson-Williams 1984).

647


0 Nutrition anti Health

Magnesium. Low magnesium levels have been demonstrated in the blood,
skeletal muscle, and heart muscle of alcoholics (Wheeler et al. 1977).
Chronic alcohol use can result in both reduced intake and malabsorption of
magnesium. Alcohol ingestion acutely increases the urinary excretion of
magnesium. Because magnesium is necessary for certain thiamin-depen-
dent enzymes, there has been speculation that magnesium plays a role in
the development of some of the neurologic complications of alcohol abuse,
including Wemicke-Korsakoff's syndrome (discussed later in this chapter).
However, the data are inconsistent, and the precise role, if any, of magne-
sium remains to be determined (Thomson 1978). Finally, magnesium insuf-
ficiency can be associated with hypocalcemia, perhaps because hypomag-
nesemia causes resistance to parathyroid hormone and impairment of its
secretion.

Calcium and Phosphorus. Alcohol ingestion increases urinary calcium
excretion, but the mechanisms for this action have yet to be determined.
The possible roles of magnesium, parathyroid hormone, and vitamin D in
this effect are unclear. Chronic alcoholics may have low serum calcium
levels, usually secondary to reduced serum albumin levels from malnutri-
tion, liver disease, or acute pancreatitis. As noted above, vitamin D intake,
absorption, and metabolism may also be impaired in alcoholics, resulting in
abnormalities in phosphorus, calcium, and magnesium metabolism. For
example, low levels of vitamin D impair calcium absorption. Low levels of
dietary calcium result in increased urinary retention of calcium and in-
creased urinary excretion of phosphate. By whatever combination of mech-
anisms, hypophosphatemia occurs in some alcoholics and is easily detect-
able by routine laboratory testing at the time of admission to the hospital,
although its symptoms are similar to those seen in other syndromes associ-
ated with alcohol abuse. In some groups of alcoholics, mild hyper-
phosphatemia has been observed more frequently than hypophosphatemia
(Hurt et al. 1986).

Zinc. Reduced concentrations of zinc have been found in the plasma, red
blood cells, and liver of humans and rats following chronic alcohol inges-
tion. Alcohol appears to increase the urinary excretion of zinc, perhaps
because of increased release of zinc from hepatic stores. Protein catabolism
is also associated with increased urinary zinc losses. The effect of zinc
deficiency on alcohol metabolism has not been established, but prelimi-
nary evidence suggests that zinc-dependent enzymes, such as those in-
volved in vitamin A metabolism, may be inhibited by alcohol (Thomson
1978). Some alcoholic men with night blindness have required both zinc and
vitamin A treatment to correct visual dysfunction (McClain et al. 1979), but

648


Alcohol O

whether the origin of this problem is liver dysfunction or nutrient malab-
sorption is as yet uncertain.

Nutritional Status of Alcoholics

Three types of malnutrition may be observed in alcoholics (Lieber 1983):
(I) primary malnutrition due to a decreased intake of nutrients, (2) second-
ary malnutrition caused by an impairment in the digestion and absorption
of nutrients due to the effects of alcohol, and (3) tertiary malnutrition due to
an alteration in the ability to convert nutrients to their active coenzyme
forms, resulting in nutritional complications that potentiate the direct toxic
effects of alcohol.

The nutritional status of alcoholics remains ill defined because of variations
in the types of studies performed and the groups of alcoholics that have
been studied. The derelict alcoholic has a different baseline nutritional
status than the middle-class alcoholic, and findings derived from studying
one group cannot necessarily be extrapolated to the other.

The preponderance of studies have examined indigent alcoholics who are
readily available and willing to cooperate at least temporarily with re-
searchers. These individuals are probably as different in the type and
amount of alcohol and food consumed as they are in every other aspect of
day-to-day living when compared with nonindigent and middle-class alco-
holics. Although indigent alcoholics make up less than 5 percent of the total
alcoholic population, there is a persistent misconception that this group is
representative of the alcoholic population at large. The almost total exclu-
sion of women in this population is an indication that indigent alcoholics are
not representative of all alcoholics.

Because of the association of alcoholism with serious medical illnesses
such as liver cirrhosis or pancreatic insufficiency, another tendency is to
study the nutritional status of persons with these conditions rather than the
much larger-and healthier-portion of the alcoholic population. A clear
distinction needs to be made between each of these groups. For example,
the dietary intake of a large group of hospitalized alcoholic patients has
been reported to be poor when judged by "traditional standards" (Patek et
al. 1975). The mean daily energy intake in this group was over 3,000 kcal,
but more than 50 percent was derived from alcohol. All of these patients
were hospitalized for the treatment of medical complications ofalcoholism,
and two-thirds had cirrhosis, a much higher prevalence than expected for
the general alcoholic population (Lelbach 1975).

649


O Nutrition and Health

Individuals hospitalized in alcoholism treatment centers may also have
severe alcohol-associated medical problems, but the primary reason for
their hospitalization is alcoholism. Therefore, these patients are probably
more representative of the overall alcoholic population. Despite the high
proportion of caloric intake from alcohol in this group, only a few studies
have reported evidence of malnutrition. Among a small group of male
alcoholics in an inpatient alcoholism treatment program, total caloric in-
take was estimated to be 2,600 to 2,700 kcal, with alcohol providing 22 to 36
percent of calories (Neville et al. 1968). In a similar group of middle-class
alcoholics, the mean intake measured by diet history at admission to an
alcoholism treatment unit was 3,100 kcal, with alcohol accounting for 35
percent of the daily energy intake (Hurt et al. 1981). No severe nutritional
deficiencies were found using anthropometric measurements and blood
studies of protein status in a small group of alcoholic patients hospitalized
in a veterans hospital alcoholism treatment program (Dickson et al. 1983).
Despite adequate protein intake, alcoholic patients, with and without liver
disease, had significantly lower body weights, triceps skin folds, and arm
muscle circumferences than abstainers (Simko, Connell, and Banks 1982),
but no assessment of the socioeconomic status of this group was included.
Thirteen percent of nonindigent alcoholics in another study were mal-
nourished, but because of the method used to analyze the anthropometric
data, the percent was probably higher (Tomaiolo and Kraus 1980). In yet
another study, 13 percent of low-income alcoholics and 10 percent of
middle-income alcoholics were judged to be malnourished, but obesity
occurred in 2 percent and 4 percent, respectively. This latter research
suffered from the vagueness of the nutritional data, which was based on the
overall medical status of the subjects. In a group of 179 middle-class males,
47 of whom were alcoholic inpatients, the consumption of alcohol was
associated with a decrease in energy intake from other sources and a
reduction in the nutrient density of the diet at both moderate and high levels
of alcohol consumption (Hillers and Massey 1985).

A comparison of alcoholics of lower socioeconomic status with those of
higher socioeconomic status showed small but clear differences in the ratio
of height-to-weight, triceps skin fold, mid-arm muscle circumference, and
hematocrit (Goldsmith, Iber, and Miller 1983). Only 8 percent of this
middle-income group were moderately malnourished, compared with 24
percent of the low-income group. In the low-income group, 8 percent were
severely malnourished. Thus, socioeconomic class is an important factor
that often is not taken into full account in nutritional studies of alcoholics.
Furthermore, very few studies have been conducted on middle-income
alcoholics, although these indicate that the nutritional status of this group is

6.50