Alcohol dependence: A biobehavioral perspective

Abstract

1. 1. The behaviorally based constructs of DSM-III have differentiated alcohol abuse and dependence, wherein the latter has been characterized by: (1) a history of tolerance and physical dependence; and (2) a history of pathological drinking patterns and/or problems consequent to drinking behavior (APA-DSM III 1980). In contrast, ICD-9 refers to an alcohol dependence syndrome which follows the model proposed by Edwards and Gross in 1976. The WHO memorandum on nomenclature and classification of drug and alcohol related problems has further proposed that alcohol dependence be defined along a continuum of severity, and that dependence be differentiated from severity of alcohol related disabilities (Edwards et al. 1981). In many respects, the alcohol dependence syndrome construct is consistent with Jellinek's disease concept of alcoholism which had its antecedents in medical writings of the late eighteenth and early nineteenth centuries (Lender 1979). 2. 2. Commencing in the early 1960's, many behavioral and social scientists were critical of the disease model of alcoholism. Behavioral researchers found that the drinking behavior of alcoholic subjects could be controlled by its consequences in the laboratory, suggesting that drinking behavior was like any operant. Longitudinal studies of drinking practices suggested that relapse to dependent drinking did not appear to be inevitable. In general, these researchers have utilized behavioral and epidemiological data to prove the null hypothesis: that there was no biological disease behind alcohol addiction. 3. 3. In contrast to the operant studies which served to rebut the disease construct, Ludwig and associates employed a model of Pavlovian conditioning which suggested a relationship between an alcoholic's desire to drink and an increase in autonomie arousal associated with the presence of alcohol (Ludwig et al. 1977). These investigators hypothesized that the arousal represented a subclinical conditioned withdrawal syndrome, and that the elicited psychophysiological responses were opposite from those elicited by actual alcohol consumption. Our group, Kaplan et al. 1983, at the University of Connecticut has confirmed Ludwig's findings regarding the relationship between physiological arousal and craving in the presence of alcoholic beverages (in alcoholic but not control subjects), and has further extended research in this area. The authors have postulated that dependent alcoholics experience a “state change” which may be defined on the basis of subjective and biological responses to alcohol related stimuli and beverage consumption. They have found that there is a significant relationship between severity of alcohol dependence in the last 30 days prior to admission to a treatment program and: (1) increase in skin conductance in response to the presentation of a glass which the subject presumes to contain beer; (2) likelihood of responding to a placebo beverage as though it contained real beer; (3) likelihood of choosing beverage alcohol as a reward for the completion of an operant task. Our colleagues at The University of Connecticut have also demonstrated a relationship between increase in skin conductance and increase in subjective desire to drink in alcoholics but not in control subjects; as well as a relationship between increase in desire to drink and increase in salivation in alcoholic but not control subjects (Pomerleau et al. 1983). 4. 4. In pilot studies designed to further define the biological dimensions associated with craving in the alcoholic, the authors have been examining certain endocrine responses in alcoholic and control subjects as they anticipate beer consumption, and after they consume a placebo beverage which they believe to be real beer. Alcoholics, but not controls, experience a significant decrease in serum testosterone as they hold and smell a glass of beer (Morse et al. 1985). Subsequent administration of placebo beer was followed by a return of testosterone levels to baseline, while alcoholics then demonstrated a sharp elevation in plasma insulin and a moderate increase in plasma glucose during this time period (Dolinsky et al. 1985). Changes in glucagon and Cortisol did not adequately account for the changes observed in insulin and glucose. There was a satistically significant correlation between changes in insulin and changes in craving and anxiety. 5. 5. The authors believe that the use of psychophysiological and biochemical data to assess some of the biological dimensions of craving represents a promising approach to defining the alcohol dependent state. Traditionally, alcohol dependence has been defined clinically, and more recently has been defined in the context of questionnaire data. At this writing there is a need to define biological and behavioral criteria which can be used to quantify alcohol dependence, and to clarify the relationship between the development of alcohol dependence and the various risk factors (including genetic) and consequences which influence its course.