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Laboratory studies of the drinking behavior of alcoholics did far more
than disprove the simplistic notion of a biologically based loss of
control. The work of Mello and Mendelson (1972), Nathan and O'Brien
(1971), and the Baltimore City Hospital group (Bigelow et al., 1974;
Cohen et al., 1971) showed that alcoholic behavior could not be
described in terms of an internal compulsion to drink, but rather that
even alcoholics--while drinking--remained sensitive to environmental
and cognitive inputs, realized the impact of reward and punishment,
were aware of the presence of others around them and of their behavior,
and drank to achieve a specific level of intoxication. For example,
Mello and Mendelson (1972) found that alcoholics worked to accumulate
enough experimental credits to be able to drink 2 or 3 days straight,
even when they were already undergoing withdrawal from previous
intoxication. Alcoholics observed by Bigelow et al. (1974) drank less
when the experimenters forced them to leave a social area to consume
their drinks in a isolated compartment. Many aspects of this laboratory
portrait of the social, environmental and intentional elements in
alcoholic imbibing correspond to the picture of problem drinking that
was provided by the national surveys conducted by Cahalan and his
co-workers (Cahalan, 1970; Cahalan and Room, 1974; Clark and Cahalan,
1976).
Contemporary Genetic Research: Inherited Differences in Familial Alcoholism Rates, Reactions to Alcohol and Other Biological Traits
Recent research on genetic mechanisms in alcoholism presupposes that the genetic transmission of alcoholism has been firmly established. Support for this idea has been provided by research which found greater concordance rates in alcoholism for identical versus fraternal twins and on the greater influence of the biologic versus the adoptive family in the development of alcoholism among adoptees (Goodwin, 1979). For example, Goodwin et al. (1973) found that male adoptees with alcoholic parents were four times more likely to become alcoholics than those without, although there was no such relationship with alcohol misuse in adoptive parents. Bohman (1978) and Cadoret and Gath (1978) also found this significantly enhanced liability for alcoholism among adopted male offspring of alcoholics. Similarly, Schuckit et al. (1972) discovered that half-siblings with at least one alcoholic-biologic parent were far more likely to develop alcoholism than those without such a parent, no matter by whom they were raised.
In the absence of an indication that the inability to control drinking is inherited, researchers have begun exploring other biochemical differences that may account for alcoholism. Speculations about metabolic differences have a long history, and the metabolic process that has attracted perhaps the greatest interest recently has been the accumulation of acetaldehyde following drinking (Lieber, 1976; Milam and Ketcham, 1983). Schuckit and Rayses (1979) found that young men with familial histories of alcoholism showed levels of acetaldehyde after drinking that were double the levels of those without such histories. Other metabolic processes that have traditionally been of interest have been the more rapid onset and peak experience of physiological reactions to alcohol, as in the visible flush typical of the drinking in Oriental populations. Working from the opposite direction, Schuckit (1980, 1984b) has found the offspring of alcoholics to be less sensitive to their blood alcohol levels (BALs). This type of finding may indicate that those with a pedigree for alcoholism are not as aware of the onset of intoxication when they drink or that they have a greater tolerance for alcohol.
Since cognitive and neurological impairment have frequently been found in alcoholics, several research teams have investigated the possibility that such abnormalities precede problem drinking and can be inherited. Adolescent sons of alcoholics performed more poorly than those without alcoholic parents in perceptual-motor, memory and language-processing tasks (Tarter et al., 1984), whereas adults with alcoholic relatives did worse than those with no family alcoholism history in abstract problem solving, perceptual-motor tasks and, to a lesser extent, verbal and learning-memory tests (Schaeffer et al., 1984). The discrepancies in the latter study held for those with familial alcoholism whether or not they themselves were alcoholics. Begleiter and his co-workers (1984) found that brain-wave abnormalities that were similar to those measured in alcoholics appeared in young boys with alcoholic fathers who themselves had never been exposed to alcohol. Gabrielli et al. (1982) had found that a similar group of children showed greater fast (beta) wave activity than a group of controls.
Several teams of investigators have now also proposed that there is an important subclass of inherited alcoholism that has at its roots an antisocial personality type (ASP) (Hesselbrock et al., 1984). There is a history of findings of ASP and related traits of aggression and unsocialized power needs in alcoholics (Cox et al., 1983; Peele, 1985a). Hesselbrock and his co-workers (1984) have found that ASP may be more important to the development and progression of alcoholism than is a "positive pedigree for alcoholism." Cloninger et al. (1981, 1985) have identified a male-limited type of alcoholism with a strong hereditary component linked with impulsiveness and sensation-seeking. Adopted-out children with this variety of alcoholism had biological fathers with records of criminality as well as of alcoholism. Tarter et al. (1985) have presented the broadest argument for a severe type of alcoholism based on an inherited temperament--one characterized by extreme emotional volatility.
Difficulties Confronting Genetic Models of Alcoholism
Although hopes are high for genetic models of alcoholism, recent discoveries have not provided uniform support for any genetic proposition. Results, in particular, of two major Danish prospective studies (Knop at al., 1984; Pollock et al., 1984) and Schuckit's (1984a) ongoing comparisons of matched pairs of subjects with and without alcoholic relatives--along with results from other independent investigations-have generally not been consistent. Differences in BALs and in rate of elimination of alcohol from the blood following drinking have now been determined by all the research teams almost certainly not to characterize the offspring of alcoholics. Moreover, Schuckit and Rayses' (1979) finding of elevated acetaldehyde in these subjects has not been replicated by other groups, leading to speculation that this finding is an artifact of a difficult measurement process (Knop et al., 1981). Pollock et al. (1984) have presented only partial support for a lessened sensitivity to the effects of alcohol on alcoholic offspring, whereas Lipscomb and Nathan (1980) found that a family history of alcoholism did not affect subjects' ability to estimate blood alcohol accurately. Furthermore, brain wave abnormalities discovered by Pollock et al. (1984) in children of alcoholics do not conform to those identified by either Begleiter et al. (1984) or Gabrielli et al. (1982). It is typical of research in this area that distinctive electroencephalogram patterns have been found in each investigation of descendants of alcoholics but that no two sets of results have coincided. Lastly, Schuckit (1984a) has not discovered a special subtype of alcoholism and has not found that men from alcoholic families have antisocial personalities, while Tarter et al. (1984) found such children to be less impulsive than a group of controls.
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