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Causes Of Alcoholism Essay, Research Paper
Alcoholism is considered to be a chronic illness or disease that is marked by an uncontrolled consumption of alcoholic beverages despite its interference with one’s physical or mental health, and social, family, or occupational responsibilities. It is actually a drug addiction, which is also referred to as alcohol dependence, as by the American Psychiatric Association (APA). The APA’s DSM-III-R requires that at least three of the following conditions be present in order for an individual to be classified as an alcoholic: alcohol is often taken in larger amounts or over a longer period than the person intends, the individual has a persistent desire or one or more unsuccessful efforts to cut down or control their alcohol use, the person often consumes alcohol to relieve or avoid withdrawal symptoms, the individual suffers from characteristic alcohol withdrawal, or the person exhibits a marked tolerance, which is at least a fifty percent increase in the amount of alcohol needed in order to achieve intoxication or the desired effect, or a markedly diminished effect occurs from continued consumption of a constant amount of alcohol (Silverstein, 1990). The development of alcoholism usually occurs over a period of between five and twenty-five years, and generally follows a fairly consistent pattern of progression. Although the statistics vary, studies do show that the incidence of alcoholism is increasing, and that about seven percent of adults in the United States alone are affected by it (Malik, 2000). However, research for a cure for alcoholism is slowed by the fact that experts still dispute what individual or combination of factors actually cause the disease. This paper will attempt to present and analyze the major possible causes of alcoholism, genetics and environment, and then discuss the conclusion reached through the evidence presented, that alcoholism is caused by a complicated interaction of both genetic and environmental factors.
Alcoholism as a Family Trait
The observation that alcoholism tends to run in families has been confirmed by numerous reports in the modern scientific literature. For example, N. S. Cotton, in a frequently cited review, analyzed thirty-nine familial alcoholism studies published over a ten-year period. In doing so, she found substantial agreement among the studies that an alcoholic is much more likely than a nonalcoholic to have a parent or other relative who is also an alcoholic. In fact, two-thirds of the studies found that at least twenty-five percent of the alcoholics studied had alcoholic fathers. Therefore, based on her review, Cotton estimated that, on average, one-third of any sample of alcoholics has at least one parent who is also an alcoholic (Jang & Vernon, 2000). However, this does not account for the possibility that a parent could be a carrier of alcoholic genes, and yet not be an alcoholic. No studies were found on alcoholism in individuals who were at high-risk due to having an alcoholic grandparent, so the results of this influence on alcoholism are not yet know. However, the evidence that alcoholism runs in families is not necessarily evidence for a strictly genetic cause of the disease. For, traits that are familial may be passed down from generation to generation by genetic factors or by environmental factors caused by close social contact and cohabitation.
Alcoholism as Caused by an Interaction of Genetic and Environmental Factors
Research has produced evidence that both genetic and environmental factors contribute to alcoholism, and that the interaction of genetic and environmental factors is emerging as a fundamentally important issue in the search for the cause of alcoholism. As yet, the specific gene or genes involved have not been identified and the mechanisms by which genetic transmission occurs have yet to be defined (Vaillant, 1983). Likewise, the specific environmental risk factors are not known, although research does suggest possible childhood antecedents of alcoholism as well as potential psychological and social mechanisms related to drinking behavior and to the process of becoming dependent( McCarty, 2000). It is most plausible that the relative contribution of genetics or environment to the expression of alcoholism in any given individual will vary depending on a number of factors including the subtype of alcoholism. For example, one form of alcoholism appears to be highly dependent on genetic factors, another form appears to require both specific genetic and environmental factors, and there are also cases of alcoholism without any obvious genetic factors (Secretary, 1990).
Genetics as a Cause of Alcoholism
Numerous studies have demonstrated that alcoholism tends to run in families and that the pattern is consistent with genetically transmitted susceptibility. Other explanations, however, are possible, because the social environment shared by members of the same family could also predispose to alcoholism. For this reason, studies assessing the role of genetics in alcoholism must minimize or control for environmental variable.
Approaches to Studying the Genetic Cause
Several different approaches to studying this role are possible, including the study of twins and adoptees. Twin studies are based on the principle that if a trait such as alcohol dependence has genetic determinants, then people who are genetically identical, such as identical twins, should tend to develop more similar drinking patterns and problems than those who are genetically no more alike than ordinary siblings or fraternal twins. Adoption studies are based on the principle that children born to alcoholics but adopted at an early age and raised by others, even in a nonalcoholic environment, may have a greater tendency to abuse alcohol or become alcohol dependent if they have inherited genes that make them vulnerable.
One of the earliest studies of alcoholism in twins was by L. Kaij, who found a seventy-four percent concordance rate of alcoholism between identical twins. In contrast, he found the concordance of alcoholism between fraternal twins to be only thirty-two percent (Valliant, 1983). A higher concordance rate among identical than among fraternal twins was also found by Hrubec and Omenn, who reported a twenty-six percent concordance rate of alcoholism in identical twins and only a rate of thirteen percent in fraternal twins (Bellinir, 2000). The higher concordance of alcohol dependence rates among identical twins compared to fraternal twins suggests that genetic factors are involved in predisposition to alcoholism.
An environmental explanation is also possible. For example, Partanen suggested that part of the concordance of alcohol abuse patterns between twins arises from their tendency to be socially closer than non-twin siblings and, therefore, presumable more imitative (Landes, Jacobs, & Foster, 1993). Other studies by Kaprio have found that the frequency of social contact is especially high between identical twins (Bender, 1997). A study conducted by Clifford of twin brothers in the United Kingdom found evidence suggesting that at least twenty percent of the variance in alcohol consumption could be attributed to the shared family experiences of the twins (Secretary, 1990). The issue of the effects of social contact between twins was again addressed in a recent Finnish study of the concordance of alcohol use patterns in adult twin brothers between the ages of twenty-four and forty-nine. This study, involving virtually the entire population of twins in that age group in Finland (over 2,800 pairs, nearly one-third of whom were identical twins), is the largest to date on the concordance of drinking patterns among twins. Subjects were given a questionnaire to determine drinking habits and frequency of social contact between the twins, including cohabitation. Analysis of the data showed that cohabitation or frequent social contact between the twins was indeed correlated with the concordance in their drinking patterns, that identical twins had more social contact with each other during adulthood than fraternal twins, and that the concordance of drinking patterns was greater between identical twins than between fraternal twins (Ketchan & Asbury, 2000).
However, greater social interaction did not fully explain the strongly similar drinking habits if identical twins, and analytical methods that adjusted for the contribution of cohabitation and social contact variables revealed a significant genetic contribution to the concordance. One of the most recent twin studies conducted by Heath was also quite large, obtaining drinking information from a population of more than 1,200 identical and more than 750 fraternal female twin pairs located through the Australian National Twin Register. These sample sizes were large enough to permit a detailed analysis of the interaction of genetic and environmental factors in determining alcohol consumption levels. In addition to questions about alcohol consumption, the respondents, whose average age was about thirty-five, were asked for information about their marital status and the amount of social contact between the twins. Unlike the study of Finnish male twins, analysis of the Heath data gave no evidence that concordance of drinking habits in these female twin pairs was influenced in any way by either their frequency of social contact with each other or by their cohabitation (Silverstein, 1990). This finding might reflect gender differences in social influences on drinking habits or cultural differences between Finland and Australia. The most significant finding, however, was a significant interaction between genetics and environment in relation to marital status, which was found to be a major modifier of genetically influenced drinking habits. For purposes of statistical analysis, living together with a man was considered the equivalent of marriage. In the younger groups (age 30 and under), genetic differences accounted for sixty percent of the variance in drinking habits in twins who were not married, but for only thirty-one percent of the variance in married twins. Likewise, in the older groups (age 31 and older), genetic factors accounted for seventy-six percent of the variance in drinking habits in the unmarried women, but for only forty-six percent of that variance in the married respondents (Silverstein, 1990).
Adoption studies are important because they allow genetic and environmental factors to be assessed independently of each other. Thus the effects of environmental factors can be estimated by comparing individuals with different genetic backgrounds who were raised in the same home (adoptees and their nongenetic siblings), and genetic influences can be assessed by comparing genetically related individuals who were raised in different environments. In adoption studies conducted in Sweden by Bohman, which examined the backgrounds of both adoptive and biological parents in relation to the existence and extent of alcohol abuse and alcohol dependence in the adopted offspring, led to the recognition of two types of alcoholism having different patterns of inheritance: type 1, milieu-limited; and type 2, male-limited. As with earlier studies in Denmark by Goodwin , the Swedish studies found no correlation of alcohol dependence between adoptive parents and adoptees (Bellinir, 2000). It must be noted however that some researchers have found previous twin and adoption studies unconvincing. Criticisms involve possible biases introduced by adoption agency practices that match adoptees and adoptive parents and by the effects of use of subject groups spanning several decades. In addition, generalizability concerns were expressed based on both the use of nonstandard definitions of alcoholism and on possible differences between people who place their children up for adoption and people who do not (Jang & Vernon, 2000).
Genetic Evidence — Markers of Alcoholism
An important aspect of genetics research on alcoholism is the study of potential behavioral, physiological, and biochemical markers of genetic susceptibility to alcoholism. Such markers may be of two general types: factors that predispose individuals to alcohol dependence and are directly involved in its development, and factors that are not themselves predisposing but are correlated with those that are (Secretary, 1990).
Many studies have focused on the electrical brain wave known as the P3 component or P3 wave. This brain wave normally appears during the performance of cognitive tasks. The strength of the P3 wave is measured by its amplitude on an EEG. In a study conducted by Begleiter, reduced amplitude of the P3 component of the event-related potential was found in young boys who had never drunk but were considered to be at risk of alcoholism because their fathers were alcoholic, and similar findings have been reported by numerous other investigators (Bender, 1997). In a recent study, Porjesz replicated their previous findings of reduced P3 amplitudes in which abstinent alcoholics were presented with a task requiring them to discriminate a single designated visual stimulus occurring infrequently in a series of other visual stimuli occurring frequently. A difference between this study and the earlier ones was that the abstinent alcoholics were presented with more than one meaningful visual stimulus in a series of extraneous stimuli. The meaningful stimuli had equal probabilities of occurring and were task relevant and motivationally significant because of a $1 award for timely pressing of a switch in response to the stimulus and a $1 fine for tardiness. Despite the incentives, the P3 waves evoked by this test had lower amplitudes in the alcoholics than in the nonalcoholic control subjects (Malik, 2000). As with the earlier P3 studies by these investigators, the results suggest multiple deficits in cortical brain areas involved in the generation of the P3 wave, particularly in motivational and cognitive systems involved in information processing. Electrophysiological studies have also continued with alcohol-na ve boys who are at risk for alcohol dependence because their fathers are alcoholic. The finding of Begleiter that young boys who had never used alcohol or other drugs showed significantly reduced P3 amplitudes like those seen in abstinent alcoholics suggests that the trait precedes the development of alcoholism and might be a genetic marker of predisposition (Landes, Jacobs, & Foster, 1993).
Beta Wave Activity
EEG studies also have demonstrated differences between people with and without a family history of alcoholism. Gabrielle found that both alcoholics and their male children have been found to have excessive beta wave activity in their EEGs compared to nonalcoholics and children without a family history of alcoholism (McCarty, 2000).
Numerous reports have been published on the enzyme monoamine oxides (MAO) as a potential marker of predisposition to alcoholism. MAO, which is involved in the metabolism of biogenic amines (a class of chemicals that includes neurotransmitters), exists in two forms, designated A and B. Both forms of MAO are found in the brain, but blood platelets contain only type B. Several investigators, such as Tabakoff and Faraj have reported lower platelet MAO levels in alcoholics than in controls (Ketchan & Asbury, 2000).
Other Biological Markers
Other proteins have been investigated as potential markers of predisposition to alcoholism. For example, the frequency of an antigen, CW3, part of a group called human leukocyte antigens (HLA), has been observed more frequently in alcoholics than in controls as found in a study conducted by Shigeta (Secretary, 1990). A study of 11 serological (blood) markers in alcoholics by Hill also found a higher frequency of particular blood group factors among alcoholics and their first-degree relatives ( Bellinir,2000).
Biological factors can increase the risk of becoming dependent on a drug such as alcohol, but only in the context of environmental factors that are themselves predisposing. A number of large studies, including those done by Chassin and by Long and Scherl, have identified several factors that consistently predict initiation of alcohol dependency in young people. These include alcohol and drug use by peers or parents, delinquency, sociopathy in the parents, poor self-esteem, social nonconformity, and stressful life changes (Vaillant, 1983). The use of alcohol is “social,” or merely casual during the initiation stage, and for most individuals it never goes beyond that stage. The factors responsible for transition from social drinking to eventual dependence, in studies done by Donovan and by Galizio and Maisto, indicate that factors likely to be involved in the intensification and transition to dependence are the pharmacologic effects of alcohol, or those chemical effects that alcohol has on the body, the psychological state of the user, especially the user’s expectations about alcohol’s effects’, as well as the characteristics of the setting in which the alcohol is used (Landes, Jacobs, & Foster, 1993).
A major feature of alcohol and other drugs is that they initially produce pleasant effects that reinforce continued consumption. Reinforcement is widely believed to play a major role in alcohol abuse and dependence. Although there is much research still to be done in this area, it is know through both animal and human research that alcohol produces reinforcement in at least two ways: by producing mild euphoria and by reducing anxiety. The two effects probably vary from one individual to another, with one effect acting as the predominant reinforcer (Bender, 1997).
It is often difficult to know whether personality factors are antecedents or consequences of alcohol abuse. However, as discovered by Marlatt, a history of antisocial behavior and high levels of depression or low self-esteem have been found in many studies of alcohol abusers (McCarty, 2000). Some researchers are skeptical about personality as a determining factor in alcohol abuse, however, partly on the grounds that, although many early behaviors reported to be predictive of later abuse are very prevalent in the general population, although most people do not become dependent on alcohol. In particular, they questioned the predictive value of early antisocial behavior, arguing that a large number of abusers have never displayed antisocial behavior and that many people who show that behavior early in life do not become addicts (Ketchan & Asbury, 2000).
There is evidence that direct pharmacological effects alone may not be sufficient for either the development or the maintenance of alcohol and drug abuse. Social learning, in which information about the consequences of behavior is transmitted through observation of others as well as through one’s own experiences, also plays an important role. Such nonpharmacological contributors include expectations about the direct pharmacological actions of alcohol on the individual, as well as expectations about its indirect effects on their behavior and social functioning (Malik, 2000). According to Marlatt and colleagues, the most notable and most widely held belief, and therefore expectation, about alcohol is that it is something of a “magic elixir” that can enhance social and physical pleasure, sexual performance and responsiveness, power and aggression, and social competence (Ketchan & Asbury, 2000). The power of expectancy is suggested by research showing that people can experience alcohol-like effects when they only think they have consumed alcohol but have instead consumed a placebo beverage, as shown in Abrams’ and Wilson’s study (Bellinir, 2000).
There is even evidence that people can acquire expectations about alcohol long before they take their first drink and that these early expectancies are strong predictors of alcohol dependence in adulthood. In comparing adolescent alcohol abusers with demographically similar non-abusing peers, Brown found that the alcohol abusers expected more positive effects from alcohol (Vaillant, 1983). A subsequent study by Mann examined alcohol expectancies among adolescents at high and low risk of future alcoholism and found that high-risk adolescents expected enhanced cognitive and motor functioning and reduced tension, whereas low-risk adolescents expected altered social behavior ( Jang & Vernon, 2000).
To test the role of expectancies in a controlled manner, Newlin and colleagues have developed an experimental approach in which subjects are divided into two groups, one receiving an alcohol placebo and the other receiving a nonalcoholic beverage that is not purported to be alcoholic. Thus two conditions are created: expectation of alcohol but none received, and no expectation of alcohol and none received. The design allows an alcohol expectancy effect to be measured against a control condition in which alcohol is neither expected nor received. The expectancy effect measured in these studies was the heart rate. The pharmacological action of alcohol normally accelerates the heart rate, but it was confirmed in young college men that alcohol expectancy decreased the heart rate. This effect, called the antagonistic placebo response, was not found in women, however. Expectancy of receiving alcohol increased the heart rate in women as alcohol itself would do (Bender, 1997). The same experimental design was also used in a study of sons of alcoholics to test the hypothethesis that they would show a greater antagonistic placebo response than sons of non-alcoholics. It was confirmed that an alcohol placebo produced significantly greater reduction of the heart rate in the sons of alcoholics. The reductions could not be attributed to differences in baseline heart rate, drinking practices, or personality measures. The sons of alcoholics also reported feeling more “intoxicated” after consuming the placebo drink than the sons of non-alcoholics, suggesting the possible existence of some fundamental differences in the two groups in their ability to perceive drug states (Jang & Vernon, 2000).
Levenson also tested a hypothesis that individuals at greater risk for alcoholism tend to get greater reinforcement from drinking because they find it more rewarding. The hypothesis was supported in a comparison of alcohol-induced stress attenuation in high- and low-risk subjects in which the effects of a high dose of alcohol on both physiological (cardiovascular and motor responses) and self-reported psychological effects for stress from aversive stimulation were measured. Although all subjects received the same amount of alcohol on a body weight basis, those judged at risk for alcohol dependence (because they had an alcoholic parent or matched a personality pattern thought to be associated with the development of alcoholism) experienced a smaller response to the stressor after drinking than control subjects who had neither risk factor. The enhanced stress reduction was evident in subjects with either type of alcoholism risk factor, but no additional stress attenuation was seen in subjects who had both risk factors. There were no differences in the responses of male and female subjects at risk (Secretary, 1990).
Finn and Pihl also measured the effects of alcohol on cardiovascular responses to aversive stimulation. The subjects, all males, were in three groups: those judged at high risk because they had alcoholic fathers and a multigenerational family history of alcoholism, those judged at moderated risk because there was no alcoholism in the generation preceding that of their alcoholic fathers, and those judged at low risk because they had no family history of alcoholism. Before drinking, the high-risk group was found to have greater cardiovascular reactivity to the stressor than the moderate-risk group. After drinking, however, the high-risk group showed a dramatic reduction of cardiovascular response to the stressor, while the moderate- and low-risk groups shoed increased reactivity. The evidence suggested that the greater baseline reactivity to stress and the heightened stress-dampening effect of alcohol in individuals at high risk of alcoholism may make them more disposed to use alcohol in adverse situations (Landes, Jacobs, & Foster, 1993). The similar reactivity of the moderate- and low-risk groups in contrast to the high-risk group indicated a need to look more closely at the frequency of alcoholism in an alcoholic family history before judging the risk of alcoholism in any one family member. In a subsequent study by the same investigators, that replicated the findings of the first, it was concluded that investigators should ascertain that familial alcoholism has existed for at least two successive generations before judging an individual to be at risk because of family history. The researchers, however, observed that the majority of high-risk studies published have apparently not gone beyond one generation in describing family history of alcoholism (Landes, Jacobs, & Foster, 1993).
Longitudinal Studies on Environmental Factors
Longitudinal studies of the children of alcoholics have explored childhood factors and their relationship to the development of alcoholism in adulthood. One such study of children focused on factors that allow some offspring of alcoholics to go through childhood and adolescence without developing any serious problems. Asian and Polynesian natives of Hawaii having at least one alcoholic parent and having experienced alcohol-related family problems as children were selected for study; control subjects were from the same cohort of native Hawaiians. Serious problems at home, school, work, or in the community had developed by age eighteen in forty-one percent of the children of alcoholic parents, and thirty percent had records of repeated or serious delinquency. A striking contrast was found with respect to contacts with social services and mental health agencies – thirty-seven percent of the children of alcoholics had made such contacts during their teens, compared with only seven percent of the children without alcoholic parents. The frequency of adjustment problems associated with parental alcoholism was significant in this study (Silverstein, 1990).
Nevertheless, nearly sixty percent of the offspring of alcoholics had not developed such problems by age eighteen. Interviews and community records indicated that the members of the resilient group did well in school, at work, and in social life and that they had realistic goals and expectations for the future. Further evaluation of the resilient and nonresilient children of alcoholics indicated differences in the two groups in temperament, communication skills, and locus of control (the belief as to whether one’s life is controlled by oneself or by external factors). Characteristics differentiating the problem-free offspring of alcoholics from others included relative intelligence, achievement orientation, early social skills, responsible and caring attitude, positive self-concept, and belief in their own effectiveness. One of the factors that most strongly influenced outcome in the children was the presence or absence of alcoholism in the mother; 25 percent of the nonresilient offspring had an alcoholic mother, compared with only 3.5 percent of resilient offspring (Silverstein, 1990).
There is a wealth of evidence, especially due to twin and adoption studies, that one of the greatest risk factors for becoming an alcoholic is to be the son, daughter, or sibling of one. This familial nature of alcoholism has stimulated a great deal of research to identify the causes and mechanisms of the transmission of alcoholism in families. In general, these investigations focus on either genetics, psychological and social factors, or the interaction of the two. The studies presented here indicate that both genetics and environmental factors are involved in the development of alcoholism. For, although genetics is certainly a cause of the disease, there must be other contributing factors as the majority of individuals genetically predisposed to alcoholism never suffer from it. Psychological and social factors such as the pharmacological effects of alcohol, the psychological state of the user, and the user’s expectations about alcohol’s effects on them influence drinking behaviors, and research is continuing on the environmental factors involved in the development of alcoholism. Therefore, it can be determined that the interaction of genetics and environment is a fundamental cause of the dedetermined that the interaction of genetics and environment is a fundamental cause of the development of alcoholism, and future research on the disease will no doubt focus increasingly on this interaction.
Bellenir, K. (2000). Alcoholism Sourcebook. 81-86.
Bender, D. (1997). Chemical Dependency: Opposing Viewpoints. 49-79.
Jang, K. & Vernon, P. (2000). Personality Disorder Traits, Family Environment, and Alcohol Misuse: a Multivariate Behavioral Genetic Analysis. Addiction. 95. 6. 873-888.
Ketcham, K. & Asbury, W. (2000). Beyond the Influence: Understanding and Defeating Alcoholism. 28-39.
Landes, A., Jacobs, N., & Foster, C. (1993). Illegal Drugs and Alcohol – America’s Anguish. 39-53.
Malik, K. (2000). The Gene Genie. New Statesman. 13. 612. 53-54.
McCarty, D. (2000). Detoxification Centers: Who’s in the Revolving Door? The Journal of Behavioral Health Services
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