associated with alcoholism (Blum et al., 1990). Although this allele is not linked to the manifestation of alcoholism, it may be associated with the severity of the disease (Cloninger, 1991). Thus there may be genetic factors that can modify the expression of alcoholism even though they are not directly linked to the etiology of the disorder.
Alcohol abuse and dependence are genetically influenced disorders, and quantification of genetic risk has begun. Studies examining psychosocial risk factors for the onset of alcohol abuse and dependence have often failed to control for family history of alcoholism or other mental disorders, especially antisocial personality disorder and depression. As psychosocial risk factor research improves, more will become known about the relative and attributable risks associated with specific factors and with clusters of factors. It appears likely that it is the accumulation of both genetic and psychosocial risk factors that increases the risk for alcohol abuse and dependence. In particular, six risk factors are strongly associated with the onset of alcohol problems:
Having a parent or other close biological relative with alcohol abuse or dependence. The mechanism may be genetic, psychosocial, or both.
Having biological markers that are highly associated with later onset of alcohol dependence: (1) a low P3 amplitude, which is a measure of a brain wave pattern (an electrophysiological marker); (2) a lower stimulated adenylyl cyclase activity or lower monoamine oxidase activity (a biochemical marker); and/or (3) a decreased sensitivity to the effects of alcohol.
Demonstrating antisocial behaviors or a combination of aggressiveness and shyness during childhood.
Having low adaptability and being unable to cope with immediate situational stresses, including adverse family conditions.
Being exposed to community, neighborhood, or peer group norms that foster alcohol use and abuse.
Having easy access to alcohol (resulting from low cost, low taxes, lenient laws, and/or minimal law enforcement).
Identification of high-risk populations should include these multiple risk factors whenever possible. Suitable preventive intervention trials could then be designed. For example, if individuals with biological markers could be identified before they use alcohol, they could be given information that might encourage them to abstain from alcohol. Also, without alcohol there would be, obviously, no alcohol abuse or depen-