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ALCOHOL AND HEALTH—

AN OVERVIEW

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ection 503(a) of the Public Health Service Act, as amended, requires that the Secretary of Health and Human Services submit to the U.S. Congress a report that contains current information on the health consequences of using alcoholic beverages and a description of current research findings on alcohol abuse and alcoholism. The Eighth Special Report to the U.S. Congress on Alcohol and Health, prepared in accordance with that requirement, focuses on research advances since publication of the Seventh Special Report in January 1990. The following overview presents some of the major highlights of the Report.

Section I-Nature and Extent of Alcohol Use and Alcohol-Related Problems

Chapter 1: Epidemiology of Alcohol Use and Alcohol-Related Consequences

Most people who choose to drink alcohol have little or no trouble limiting their intake to amounts that produce no serious health or social consequences. Some people, however, experience a number of adverse consequences from drinking. Alcohol abuse refers to patterns of problem drinking that result in health consequences, social problems, or both. Alcohol dependence, often called alcoholism, refers to a disease that is characterized by abnormal alcohol-seeking behavior that leads to impaired control over drinking. Although alcoholics and alcohol abusers may experience many of the same harmful effects of drinking, alcoholics can be distinguished by their physical dependence on alcohol and their impaired ability to control alcohol intake. In 1988, 15.3 million people in the United States met the criteria for alcohol abuse, dependence, or both, as defined by the Diagnostic and Statisti

cal Manual of Mental Disorders, Third Edition, Revised.

Apparent alcohol consumption in this country has declined from a high of 2.76 gallons of pure alcohol per capita in 1981 to 2.43 gallons in 1989. However, current consumption is still substantially higher than the relatively stable levels of about 2 gallons that prevailed during the 1950s. Between 1983 and 1988, there were significant increases in abstention and decreases in heavier drinking across a wide range of age, sex, and sociodemographic groups.

Despite the decline in per capita consumption levels, alcohol is still a factor in a substantial amount of injury and medical problems. In 1990, alcohol was involved in half of all fatal traffic crashes. Alcohol-related mortality accounted for approximately 5 percent of all deaths in the United States in 1988. Promising data have been reported for deaths from liver cirrhosis: In 1988, liver cirrhosis mortality rates fell to their lowest level since 1951. Yet, heavy drinking is associated not only with increased mortality but also with premature mortality. Estimates indicate that years of potential life lost for an individual death from alcoholic liver disease may be 9 to 22 years, compared with 2 years for an individual death from cancer and 4 years for an individual death from heart disease.

Drinking patterns vary among different populations in society. For example, studies have consistently reported that men drink more than women and experience more adverse consequences of drinking. However, a recent analysis showed that in younger age groups, rates for alcohol abuse or dependence in women more closely approximated those in men, with gender differences becoming increasingly pronounced with age.

By far, alcohol was the drug used most often by high school seniors in 1990. Within this group, 90 percent reported having tried alcohol, and 32 percent reported drinking five or more drinks consecutively during the 2 weeks prior to being

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The Epidemiological Catchment Area (ECA) survey is an important source of data on the prevalence and incidence of comorbidity in the general U.S. population. According to ECA findings, the rate at which various psychiatric disorders co-occur with alcohol use disorders exceeds rates that would be expected by chance alone. Almost 20 percent of the survey population had at least one psychiatric disorder; the rate increased to 36.6 percent among those with alcohol disorders. In general, ECA data showed that antisocial personality disorder had the strongest association with alcohol disorders.

Comorbidity appears to adversely affect the clinical course of both disorders and often predicts poor response to standard treatments for both addictive and psychiatric disorders. Accordingly, selecting appropriate treatment for patients with co-occurring illnesses is a significant concern. Studies of comorbidity treatment strategies

address such important issues as determining the disorder to be treated first, identifying whether interventions validated in non-comorbid patients work similarly for comorbid patients, and assessing the efficacy of hybrid treatment approaches compared with traditional therapies that are targeted at each disorder.

Section II-Causes of Alcohol Abuse and Alcoholism

Chapter 3: Genetic and Other
Risk Factors for Alcoholism

Findings from family, adoption, and twin studies have shown that the interaction of genetic and environmental factors determines vulnerability to alcoholism. In light of this information, researchers are pursuing systematic inquiries in population and molecular genetics and in psychological and social domains to identify the specific genes that convey susceptibility and the particular environmental determinants that interact with these genes to enhance or diminish a person's risk for developing alcohol dependence. Identifying the gene or genes responsible for susceptibility to alcoholism will enable researchers to determine the genes' actions and how they are regulated. Such knowledge has important implications in the prevention, early detection, and treatment of alcoholism.

The heterogeneous nature of alcoholism has complicated research efforts to distinguish the genetic and environmental factors that underlie the development of the disease. Adoption studies have identified two types of alcoholism— type I (milieu-limited) and type II (male-limited) -which appear to have different mechanisms of inheritance. This evidence demonstrates that various typologies of alcoholism may exist, each possibly carrying different levels of genetic influence that may be sensitive to disparate environmental

events.

The twin study paradigm has proven to be a powerful method for detecting the genetic effects of various traits. In alcohol research, twin studies have shown a greater concordance for drinking behavior and alcoholism among identical twins than among fraternal twins. Genetic processes appear to exert significant control over various behaviors that influence frequency and quantity of use and to play a role in determining vulnerability for alcoholism. In addition, genetic

factors seemingly contribute to alcoholism in both men and women.

Animal models are another tool used to study genetic determinants for alcoholism. These models enable researchers to conduct controlled analyses of genetically influenced biological characteristics, such as innate sensitivity to alcohol, that have been observed in humans. Studies using animals that are selectively bred for high or low measures of particular alcohol-related traits have shown that genetic factors affect many of the alcohol-related behaviors and responses (e.g., development of tolerance to alcohol's effects and sensitivity to withdrawal from alcohol) that are expressed in humans. Animal studies also are central to research efforts aimed at defining the underlying mechanisms of alcoholrelated behaviors.

Studies of genetic markers for alcoholism-inherited characteristics that occur with a disease more frequently than chance would dictatepromise to provide useful information about the genetic mechanisms that confer vulnerability to this disorder. Among the categories of promising markers currently being studied are electrophysiological traits (e.g., differences in event-related potentials), biochemical traits (e.g., adenylate cyclase activity), and differences in reactions to alcohol's effects.

Many potential pathways to the development of alcohol problems appear to exist. Although genes may increase risk, social and psychological elements interact with genetic factors to modulate the expression of genetic vulnerability in behavior. A promising area of study that addresses gene-environment interactions examines the possible link between the genetically based phenomenon of personality and genetic susceptibility for alcohol use disorders. These studies potentially can provide insight into why some genetically vulnerable persons never develop alcohol problems whereas others shift to problem drinking.

Chapter 4: Actions of Alcohol on the Brain

Neuroscience studies are providing increasing knowledge of alcohol's acute and chronic actions on the central and peripheral nervous systems. Using sophisticated new electrophysiological, imaging, and molecular biology techniques, researchers are examining alcohol's numerous effects on systems and regions in the brain. These studies are yielding insight into the chemical and

physiological processes that underlie the behavioral effects of acute exposure and the addiction to alcohol that can develop with chronic use.

The molecular site(s) of alcohol's action on neurons is not yet clear. Scientists have suggested several mechanisms by which alcohol may work: perturbing lipids in the cell membrane of the neuron; interacting directly with the hydrophobic region of neuronal membrane proteins; or interacting with a lipid-free enzyme protein in the membrane.

Whether alcohol acts on lipids or on proteins in the neuronal cell membrane, it is clear that alcohol alters the function of neuron-specific proteins. Acute exposure to intoxicating amounts of alcohol is associated with increased activity of the chloride ion channel that is linked to the Atype receptor of the y-aminobutyric acid neurotransmitter (GABAA). The effects of alcohol on the GABAA receptor may contribute to alcohol's anxiolytic, sedative, and motor impairment actions. Recent findings suggest that many possible GABAA receptor subtypes exist; these subtypes may be made from any combination of varying forms of five subunits. A particular gamma subunit of the GABAA receptor with a site for a phosphate molecule (phosphate is added as a posttranslational modification) appears to be needed for alcohol sensitivity.

Acute exposure to alcohol may also affect the actions of glutamate, the major excitatory neurotransmitter in the mammalian central nervous

system. Glutamate activates at least three receptor types, two of which are known as the Nmethyl-D-aspartate (NMDA) receptor and the α-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptor. Alcohol acts to inhibit glutamate receptor function. NMDA receptors are more sensitive to alcohol than are AMPA receptors. The inhibitory effect of alcohol on NMDA receptors is thought to contribute to the cognitive impairment and amnesia observed at moderate to high doses of acute alcohol exposure. Recent studies have reported that AMPAtype receptors may be formed from a variety of subunits. Although less information about NMDA structure is available, multiple subunits for this receptor are likely to be found. Knowledge of the structure of the NMDA and AMPA receptors can help scientists to develop pharmacotherapies that can selectively counteract the effects of alcohol at these sites in the brain.

Chronic exposure to alcohol can result in the development of tolerance for and physical dependence on the drug. Tolerance to alcohol

develops as a result of changes in alcohol's effects on the brain as well as an increased capacity of the body to reduce alcohol levels via metabolism. Studies have shown that animals exposed to alcohol for a period of days have diminished GABAA receptor function in neuronal tissue. This functional alteration may arise from a change in the expression of the subunit components of the receptor. Indeed, it appears that messenger ribonucleic acid coding for expression of specific GABA receptor subunits decreases with chronic exposure whereas expression of other subunits increases. Such information may be important for treating alcoholism: Pharmacological agents may be developed that target specific receptor subunits to alter alcohol tolerance at the molecular level. Changes in the function and number of G-protein-linked receptors for adenosine and norepinephrine may also be involved in the development of tolerance for alcohol.

Tolerance to alcohol develops as a result of changes in alcohol's effects on the brain as well as an increased capacity of the body to reduce alcohol levels via metabolism.

Physiological dependence is manifested by the development of various withdrawal symptoms, ranging from tremors to seizures, that occur with the cessation of alcohol intake. Researchers have begun to examine the underlying mechanisms of withdrawal seizures in an effort to gain insight into the neuronal changes that occur with physiological dependence. Findings suggest that changes in GABAA receptor subunit expression may contribute to the initiation of withdrawal seizures. Increases in NMDA receptors in various brain regions, such as the hippocampus, may also be involved in withdrawal seizures. Finally, increases in the number and function of voltage-activated calcium channels appear to play a role in withdrawal seizures.

Chapter 5: Neurobehavioral
Aspects of Alcohol Consumption

Determining why some people drink alcohol despite adverse consequences is a central issue in alcohol research. Researchers probing this question have begun to examine the role that

reinforcing properties of alcohol may play in alcohol-seeking behavior. Alcohol produces pleasurable and anxiety-reducing sensations, both of which are thought to serve as reinforcers. A theory of the biological basis for alcohol reinforcement proposes that people drink alcohol because it affects a specific reinforcement system in the brain. Researchers are using brain stimulation reward (BSR)-an experimental technique in which animals learn to self-administer small levels of electric current to specific brain areas to elicit a rewarding stimulation—to study the neurobehavioral basis of the pleasurable, or euphoric, properties of alcohol. An increase in an animal's BSR response rate after alcohol administration suggests that alcohol increases the reward experienced by the animal. Indeed, scientists have observed that alcohol enhances BSR performance in animals during the first 20 minutes after alcohol exposure, a time frame that corresponds to the period during which alcohol is absorbed into the bloodstream. BSR study findings suggest that alcohol-induced euphoria occurs soon after drinking. These findings also provide evidence for a physiological basis of alcohol reinforcement.

Substantial progress is being made in elucidating many of the neural systems responsible for alcohol reinforcement. Alcohol stimulates release of the neurotransmitter dopamine in a region of the brain involved in reinforcement. Studies suggest that alcohol may exert its reinforcing effects in the neuronal membranes at the D2 receptor, a subtype of the dopamine receptor. Serotonin, a neurotransmitter, and endogenous opiates, a class of neuropeptides, also may be associated with the reinforcing effects of alcohol.

Although people may drink to experience alcohol's euphoric effects, other factors, such as alcohol's anxiety-reducing property, may also motivate drinking. In animals, reductions in anxiety may be correlated with increased aggressiveness. One study reported that male and female rats exposed to low levels of alcohol displayed enhanced attack behavior toward male intruders. In contrast, high doses of alcohol appeared to reduce aggression. Researchers are using animal models to examine the behavioral aspects and the underlying neurophysiological mechanisms associated with the anxiety-reducing effect of alcohol.

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Chapter 6: Psychological, Social,
and Developmental Factors

Alcohol consumption is influenced by genetic determinants as well as by psychological, social, and developmental factors. Psychological influences include cognitive processes (e.g., thinking, attention, and memory) and affective factors (e.g., feelings and attitudes). Social processes are broad and encompassing, including interactions with others, media portrayals, and environmental contexts of drinking. Developmental processes, which relate to changes within individuals that occur over time and affect behavior, can result in predictable behavioral change or stability at different phases throughout life and are integrally related to psychological and social process.

Studies addressing motivation to drink alcohol, particularly in relation to alcohol's effect on negative emotional states, suggest that alcohol may be differentially reinforcing for certain individuals. Various factors—genetic influences, limited coping skills, and expectations about alcohol's ability to control stress-may increase a person's vulnerability to alcohol's reinforcing effects. Thus, chronic environmental stresses (i.e., negative life events and occupational stressors) may have more impact on some people than on others.

Researchers have suggested the concept of alcohol myopia as a possible mechanism for alcohol's stress-reducing and other perceived effects. This theory proposes that alcohol's effect on stress is controlled by the combination of alcohol's effect on information processing ability and the presence or absence of distracting elements. Through this mechanism, alcohol can decrease internal conflicts and block inhibitions, thus making social behaviors more extreme.

During the past decade, an increasing amount of research has focused on expectancies-beliefs and expectations about the effects of alcohol. Evidence suggests that expectancies about alcohol are formed at an early age, even before the actual consumption of alcohol, and can be influenced by alcohol use in the family. Studies in this area have shown that those who drink heavily tend to expect positive results from alcohol, such as improved functioning, reduced tension, and enhanced social pleasure. In addition, those who drink heavily tend to make distinctions about the effects of small and moderate doses of alcohol and about the effects of alcohol on oneself compared with its effects on others. Interpersonal influence processes, such as family and peer behavior, are important issues in

alcohol use. Parenting practices, parental alcohol use, and peer drinking can influence a person's alcohol use and the associated problems that can stem from drinking. Family appears to be a primary agent in the social control of drinking. Indeed, recent research suggests that the continuance of "family rituals" in alcoholic households can lessen the possibility of alcoholism occurring in the next generation.

Parenting practices, parental alcohol use, and peer drinking can influence a person's alcohol use and the associated problems that can stem from drinking.

Limited information currently is available about the effects of advertising and media portrayals of drinking on alcohol use. Studies examining televised portrayals of drinking have found that prime-time fictional broadcasts depicted an average of eight drinking acts per hour and that drinking characters in these broadcasts tended to be high-status individuals. Moreover, alcohol use was presented as problem free.

Alcohol problems seemingly stem from the interaction of individual differences in temperament, personality, alcohol reinforcement, stress management, family interaction, and peer relationships. Examining alcohol use and related problems from this perspective enables researchers to minimize risk through changes in environmental factors, relationships, and belief systems.

Section III-Consequences of Alcoholism, Alcohol Use and Abuse

Chapter 7: Biochemical Effects of Alcohol Metabolism

Alcohols compounds that have a hydroxyl group (e.g., an oxygen and a hydrogen molecule bonded to a carbon molecule)—abound in nature and have numerous physiological, pharmaceutical, industrial, and commercial applications. These compounds are metabolized in the body primarily by alcohol dehydrogenases, enzymes that are found in a variety of organisms, including humans. Alcohol dehydrogenases oxidize alcohols to aldehydes and ketones and

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