Not all studies give genetic vulnerabilities the same level of importance. Other vulnerability factors have been widely postulated. These explore the environmental and social conditions which make addiction more or less likely. Studies vary in terms of stressors (Droomers, Schrijvers, Stronks, van de Mheen & Mackenbach, 1999), social roles (Hajema & Knibbe, 1998), social influence and opportunities. (West, 2001)
Khan, Murry, & Barnes, (2002) concentrate on poverty and unemployment as predictors of alcohol abuse, although they do acknowledge that alcohol abuse has been linked to genetic, biochemical, and social causes, among others. Poverty and unemployment impose a forced financial and psychological state on an individual (Khan, Murry, & Barnes, 2002). Khan, Murry, & Barnes, (2002) feel these are important factors affecting alcohol abuse. Droomers, et al (1999) found that alcohol abuse was more common among lower educational groups, and that financial problems, deprivation, and income were stressors which lead to excessive drinking. Jones-Webb, Snowden, Herd, Short, & Hannan, (1997) found higher alcohol consumption among poor households and Singer, Valentin, Baer, & Jia, (1992 cited in Khan, Murry, & Barnes, 2002) found results for alcohol consumption being increased among unemployed individuals.
These studies argue that increased alcohol use is due to alcohol being used as an instrument of coping with stress caused by unemployment. Therefore, consumption increases with unemployment especially as it is not necessarily true that the unemployed individuals suffer reduced income, they may have savings or be given a large redundancy package. (Khan, Murry, & Barnes, 2002)
Factors other than genetics could also be in action in a familial environment: factors such as social learning from the parent(s) how to drink in such a way that alcoholism results (Eastman, 1991). Some studies claim these sorts environmental factors related with growing up and being in a high risk family (i.e. increased probability of being exposed to alcohol) could have a predominant influence on variation among individuals increasing there vulnerability (Carlson, Iacono, & McGue, 2002).
Carlson, Iacono, & McGue, (2002) estimate using a large family study that alcoholism is only moderately heritable in high risk families and therefore predominantly due to environmental factors (Carlson, Iacono, & McGue, 2002)
A Different stance posited by Temple et al. (1991 cited in Hajema & Knibbe, 1998) that changes in roles causing a more stable relation or relationships in an individual’s life lead to a decrease in alcohol consumption. Whereas changes in roles causing less stable relations would lead to an increase in consumption of alcohol. Wilsnack & Cheloha (1987 cited in Hajema & Knibbe, 1998) explained links relating to social roles and drinking behaviour as being due to the influence of multiple roles and of role deprivation. Multiple roles were expected to reduce alcohol use and role deprivation to increase alcohol consumption as social monitoring and social control of drinking will be less. (Hajema & Knibbe, 1998)
Studies indicate that alcoholism is a heterogeneous disease with various phenotypic variations. Cloninger (1987) and Babor, et al (1992 cited in Schuckit, Tipp, Smith, Shapiro, Hesselbrock, Bucholz, Reich & Nurnberger, 1995) explore this further proposing two phenotypes for alcoholism. Cloninger (1987) initially proposed two major subtypes of alcoholism, called Type I and Type II. Type II is characterized by an earlier onset of problems, high novelty seeking, low harm avoidance and low reward dependence (Cloninger, 1987). Babor, et al (1992 cited in Schuckit et al, (1995)) surgested a similar dichotomy of type A/B (Schuckit, et al, 1995). Schuckit et al, (1995) replicated this study with sucesss. Type II comparable with type B found greater genetic vulnerability with in this group than in type I or comparably Type A (Cloninger, 1987; Schuckit et al, 1995). Cloninger (1987) that women tended to be type I not type II alcoholics, and therefore environmentally predisposed not genetically.
Some studies indicate that there is a genetic contribution in male alcoholism but not in female, although this may be due to sample size or type of alcoholism. Jang, Livesley, & Vernon, (1997) argue that alcohol abuse and dependence were differentially heritable by gender. Only males were found to have significant additive genetic effects in relation to alcohol abuse and that for females, most substance use problems, including alcohol, were wholly determined by environmental factors (Jang, Livesley, & Vernon, 1997) although the results of genetic studies of gender differences in alcohol use and abuse are inconsistent (Jang, Livesley, & Vernon, 1997)
Along with different type of alcoholism some researchers have found that alcoholism may by secondary to other psychological disorders, or comorbid. Researchers now think it is likely that there is a variety of genetic factors concerned with increased the risk for developing alcoholism. Some alcoholics may have experienced severe and repetitive alcohol problems as a consequence of initial mental disorders such as schizophrenia or mania (Schuckit, et al, 1995). Studies of schizophrenics reveal a large number of substance use disorders, including alcoholism, perhaps as a consequence of bad decision making and a great deal of time spent without structured activities (McHugo, Paskus & Drake, 1993; Soyka et al., 1993; Smith & Hucker, 1994 cited in Schuckit et al., 1995). Similarly, problems related to alcohol abuse appear more widespread among individuals with bipolar manic depressive illness, especially when having manic episodes when their levels of impulsivity and poor judgment are high (Helzer & Przybeck, 1988; Winokur et al., 1993, cited in Schuckit et al., 1995). It is also thought that 20% of alcoholic individuals could have become alcoholics as a consequence of initial high level of impulsivity or an inability to form close meaningful relationships, commonly associated with antisocial personality disorder (Schuckit, Smith & Tipp, 1997). It is also thought that individuals with antisocial personality disorder have 70% chance of developing an alcohol related disorder (Hesselbrock, Hesselbrock & Workman-Daniels, 1986; Gerstley et al., 1990; Hesselbrock, Meyer & Hesselbrock, 1992, cited in Schuckit et al., 1995). As a result of this heterogeneity, it is likely that a variety of biological characteristics correlate with the vulnerability for severe alcohol-related problems (Schuckit, Smith & Tipp, 1997). Each of the major psychiatric syndromes is itself genetically influenced. This fact and these observations have led to an approach of sub grouping alcoholics based on the presence or absence of independent psychiatric disorders. (Irwin, Schuckit & Smith, 1990; Kendler et al., 1992; Cannon & Mednick, 1993 cited in Schuckit et al, 1995). The fact that such assorted disorders appear related with a greater risk towards alcoholism, possibly through different mechanisms, draw attention to the heterogeneity observed among individuals with alcoholism. (Schuckit, et al 1995) While this primary- secondary approach has the benefit of simplicity, most alcohol-dependent men and women have no pre-exsisting major psychiatric condition (Schuckit, 1985; Powell et al., 1987; Brown & Schuckit, 1988; Brown, Irwin & Schuckit, 1991 cited in Schuckit et al, 1995)
Another more resent argument is that there may be a genetic predisposition to addiction, addictive behaviour rather than substance specific addiction or abuse such as alcoholism. Although some studies argue that it is actually a genetic vulnerability to addictive behaviour and therefore not substance specific (Gorwood, et al, 2001). Recent twin and familial studies showed that the genetic factors involved in the risk for alcohol-dependence could concern dependence without substance specificity, including opiates and cocaine. The theory of familial cross-vulnerability is supported by the convergent results of twin studies (Tsuang M, Lyons M, Meyer J, et al, 1998 cited in Gorwood, et al, 2001). These studies show that genetic factors are significantly concerned in the vulnerability for any substance dependence. The candidate genes for increased vulnerability to dependence are not known, but as a number of substances that share the potential for abuse also share the ability to enhance dopaminergic activity, it is likely that there genetic roots are similar (Gorwood, et al, 2001).
Although most research acknowledges some sort of genetic contribution towards the development of alcohol abuse, not all agree to what extent this is important. It is also important to note that it is often difficult to compare studies as their definitions of alcoholism, dependence and abuse may vary. Sample size is also often an issue and the validity of some studies is contestable. These studies are usually disproving heritability of alcohol abuse. It could also be difficult to specify a specific chance of heredity as yet, as alcoholism is heterogeneous in phenotype, and until types of alcoholism (Type I/II, Type A/B, comorbidity) are studied as independent conditions with potential different levels of hereditability, if any at all. It might be the case that; Type I/A alcoholism is purely to do with social learning, mid life stressors and culture; type II/B is genetic and with ensure rapidly after first contact with alcohol, although the first contact with alcohol will still be effected by environmental factors; and that comorbid alcoholism genetically predisposed by the genetics of the pre existing mental disorder. Environmental, social, cultural aspects are obviously important, as it does not matter how inheritably a condition such as alcoholism may be, if the important initiator, alcohol, is never touched. So it is important to study all causal aspects of alcoholism. (Word count 1992)
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