A Critical Look at the Disease Model
In spite of its benefits, the disease model perspective is unable to adequately account for alcoholism and is itself beginning to fall victim to the same criticisms that it levels at the moral degeneration perspective. In particular, our cultural milieu is increasingly coming to emphasize health, nutrition, and fitness as important life-style values. In such a milieu, disease is coming to be viewed as a personal failure in adequately caring for oneself. In this way, alcoholism, viewed as a disease, is becoming increasingly defined as a personal failure that creates guilt and a denial of a problem just as surely as the moral degeneration perspective does–a theory that the disease perspective was intended to counter.
More importantly, the disease model suffers from a number of logical and theoretical flaws that not only deny its validity as a scientific model, but also limit its practicality of researching, identifying, or treating alcoholism.
Jellinek, in his model, attempts to define alcoholism in such a way as to “establish its objective reality” (1960:34). In the process, he commits the error of “reification”; he defines alcoholism into reality instead of limiting it to serve as only a term. Reification of the term means that alcoholism, while originally a label referring to some objectively defined phenomena, has become an actual condition without the proof which is derived from empirical observation (Rohan, 1976:63). In effect, Jellinek has defined alcoholism into existence and alcoholism becomes a disease simply because it is defined as a disease. There appears to be no other reason for viewing it as pathology.
Disease model proponents are at a loss to explain why alcoholism is a disease except that they maintain there are a number of biological and genetic predisposing factors serving to “mark” a portion of the population as alcoholic. Arguably, this is analogous to defining that a portion of the population will succumb to the disease of being air traffic controllers, or doctors, or miners. Because “there are certain professions and occupations which by their nature carry a higher degree of risk (of alcoholism) than the population in general” (Keyton, 1973:32), there is no reason not to conclude that similar biological or genetic factors which constitute the disease marking the person an alcoholic should also constitute the disease which marks these people for such high risk careers.
This model proceeds to claim that persons so “marked” are alcoholics even before they have their first drink and therefore, as soon as they do consume their first alcoholic beverage begin the journey down the path of alcoholism and are necessarily in need of redemption at some later point (Milam and Ketcham, 1985:34). A teleological error committed by proponents of the disease model is that they look at the effects of alcohol as proof of their theory. One of these effects is believed to be a loss of control over drinking behaviour (Jellinek, 1960:41). According the disease theorists, such loss of control is evidence of the physiological “need” for alcohol and therefore alcoholism is the product of a physiological craving for alcohol. Drinking behaviour is therefore not under volitional control and can be considered a disease, or a physiological and therefore medical problem.
However, new research is conjuring up strong opposition to this premise. In experiments manipulating the cognitions and expectations of alcoholics concerning their alcohol consumption, it has been found that the loss of control phenomenon cannot be attributed to any physiological reaction or adaptation to alcohol consumption but rather, is related to the expectations of what the person is drinking. If they are consuming alcohol but believe they are drinking a non-alcoholic beverage, the loss of control which is predicted according to the disease model is not exhibited (Marlatt, Demming and Reid, 1973).
While cross-cultural studies and twin-studies do suggest the presence of genetic factors in alcohol addiction (Goodwin, 1973; Bales, 1949; Petrakis, 1985), the claim to the existence of a “marked” population cannot be made until it can be sufficiently demonstrated that these factors alone are not only necessary but sufficient explanations to account for the development of alcohol addiction in an individual. Just as the presence of Multiple Sclerosis in a family of origin and the subsequent genetic inheritance of a disposition to contract the disease is not a sufficient explanation to account for Multiple Sclerosis in a person, there is no proof that a genetic inheritance predisposing an individual to alcoholism is a sufficient explanation to account for “contracting” alcoholism. Rather, these predisposing factors may interact with personality, environmental, cultural, social learning, health and other factors to determine the probability of alcohol addiction, just as these other factors interact to account for the contraction of MS or other diseases.
Until such time as proponents of the disease model can define what are these biological and genetic predisposing factors, propose a methodology for determining and measuring their existence, and lend tenability to the proposition that these factors constitute not only a necessary explanation, but also a sufficient explanation of alcoholism, the disease label which we have attached to alcoholism must not be considered a scientific label.
We must choose the label we use to describe alcoholism with care. The perspective from which we describe the problem will also determine which facts and components we look at and study in our attempt to better understand and explain the phenomenon:
Assuming an internal controlling condition is a preconception that interferes with the formation of an appropriate conceptual scheme. It prevents us from viewing alcohol misuse as a problem of action rather than condition, of doing rather than having, of agent rather than victim, as verb rather than noun. Such an understanding is important since our present conceptual scheme prevents us from focusing on the relevant variables in the control and modification of drinking. Our conceptual schemes influence what we select to observe, how we perceive what we select, and most importantly, how we respond. If we continue to see destructive drinking as a sign of an internal aberration, we will not only fail to assess drinking behavior and its characteristics, but we will not appreciate the relevance of external variables in the performance of drinking behavior (Rohan, 1976:64).
Additionally, alcoholism unlike genuine diseases exhibits symptoms specific to particular countries, cultures and economic classes. Whereas a particular type of cancer for instance affects the same organ in more or less the same way in all its victims, alcoholism manifests itself very differently in different cultures (Rohan, 1976). Jellinek himself admits this problem but dismisses it as unimportant (1960:13). Another criticism of disease theory is that it does not work. If penicillin was only 50% effective in controlling bacterial infections and if even in this 50% group, the infection was not cured, but only controlled or arrested, we would be reluctant to describe penicillin as a good antibiotic. In the same fashion, treatment methods using the disease perspective, such as AA exhibit a relapse rate of approximately 90% among those abstinent for one year or less and only around 40% for those abstinent for more than five years. In total, less than half the people who come to AA become “sober alcoholics” (Clinebell, 1978:144; Weisman and Robe, 1983). Surely, such a dismal figure demonstrates the need to spend some energy focusing on the other factors that contribute to the overall problem of alcoholism.
Finally, the disease theorist explains away the fact that some people who are abusive drinkers can be taught to drink in control. It argues that they are not alcoholic but only heavy drinkers. The theory thus differentiates between problem drinkers and alcoholics. Such a differentiation allows a convenient loophole for those alcoholics who wish to define themselves as merely problem drinkers (Milam and Ketcham, 1985:40). In this way, they can attempt to avoid treatment or counseling. Such a loophole does the theory no service at all. It only serves to limit the applicability of the disease perspective in excluding definite cases of alcohol abuse by labeling these cases as non-alcoholic abuse. I suggest that if alcoholism is “any use of alcoholic beverages that causes any damage to the individual or society or both” (Jellinek, 1960:35), then for the disease model to exclude such cases of alcohol abuse demonstrates a strong limitation in the model.
We can see that there are serious limitations to the disease perspective yet this model is not without its own merit. In trying to develop a new perspective, we must be careful to try and incorporate the best of the old models. In particular, the disease perspective has an advantage in that it remove the blame from the alcoholic and puts it on other factors. This effectively reduces the problem of guilt and embarrassment which compounding the problems of alcoholism. The focus that the disease perspective puts on physiology should not be disregarded, yet such a single focus is perhaps less than fair to the other factors contributing to the overall problem of alcoholism. In searching for a better paradigm to explain alcoholism, we must attempt to be fair to these other factors.