The Meaning of Addiction - 3. Theories of Addiction - Endorphins and Nonnarcotic Addiction

Written by Stanton Peele

Endorphins and Nonnarcotic Addiction

Although unsubstantiated in the case of narcotic addiction, endorphin-related explanations have proved irresistible to those considering other addictive behavior. In particular, discoveries that food and alcohol—as well as narcotics—can affect endorphin levels have prompted speculation that these substances create self-perpetuating physical needs along the lines of those the narcotics supposedly produce. Weisz and Thompson (1983) summarized these theories while noting that "At this time there is not sufficient evidence to conclude that endogenous opioids mediate the addictive process of even one substance of abuse" (p. 314). Harold Kalant (1982), a distinguished neuroscientist, was more conclusive in his rejection of the idea that alcohol and narcotics could act according to the same neurological principles. "How do you explain . . . in pharmacological terms," he queried, that cross-tolerance occurs "between alcohol, which does not have specific receptors, and opiates, which do" (p. 12)?

To date, the most active speculation by clinicians about the role of endorphins has been in the area of compulsive running and exercising (cf. Sacks and Pargman 1984). If running stimulates endorphin production (Pargman and Baker 1980; Riggs 1981), then compulsive runners are presumed to undergo narcotic-like physical states to which they become addicted. Research on the relationship between endorphin levels, mood swings, and running motivation has failed to turn up regular relationships (Appenzeller et al. 1980; Colt et al. 1981; Hawley and Butterfield 1981). Markoff et al. (1982) and McMurray and his colleagues (1984) reported that exercising subjects treated with the narcotic-blocking agent naloxone reported no differences in perceived exertion and other physiological measures from those not treated. Addicted running—defined by inflexibility and insensitivity to internal and external conditions, running until the point of harming oneself, and being unable to quit without experiencing withdrawal—is no better explained by endorphin levels than is the self-destructiveness of the heroin addict (Peele 1981).

Cigarette Addiction

Schachter (1977, 1978) has been the most vigorous proponent of the case that cigarette smokers are physically dependent on nicotine. They continue to smoke, in Schachter's view, in order to maintain habitual levels of cellular nicotine and to avoid withdrawal. Interestingly, Schachter (1971, 1977, 1978; Schachter and Rodin 1974) has proposed that different types of factors determine obesity and smoking: the former is due to an inbred predilection while the latter is due to an acquired constraint (avoidance of withdrawal). This is the same distinction drawn in traditional theories of alcohol and narcotic addiction. The distinction is necessary in order to defend biological causality in the case of excessiveness both in activities that are common to most people (eating and drinking alcohol) and activities that only some indulge in (smoking and narcotics use).

As with alcohol and narcotic use (see below), there is no prima facie reason why destructive eating and smoking habits need necessarily be dictated by separate classes of factors. Indeed, studies Schachter (1978) and his students conducted with cigarette smokers replicated results of Schachter and Rodin's (1974) work with the obese. For example, both smokers (while not smoking) and the obese were more distractible and more sensitive to negative stimuli like pain than were nonsmokers or normal-weight people. Both smokers and the obese apparently found their habits allayed anxieties and cushioned them against unpleasant stimulation (see Peele 1983b for further discussion.) Furthermore, the apparent uniformity in the addictive use of cigarettes that Schachter's model suggests is illusory. Different smokers consume different amounts of tobacco and inhale different levels of nicotine; Best and Hakstian (1978) found such variations to reflect different motivations and settings for smoking and to suggest different circumstances under which smokers can quit.

Leventhal and Cleary (1980) have pointed out how inexact the regulation of nicotine intake is in Schachter's studies: Schachter (1977) found that a 77 percent reduction in nicotine level produced only a 17 to 25 percent increase in cigarette consumption. More tellingly, these authors reflected, "Schachter's model and studies ... assume a direct and automatic step from changes in plasma nicotine level to craving and [separately] smoking and say nothing about the mechanisms and experience that give rise to either" (p. 390). For example, Schachter (1978) himself noted that Orthodox Jews regularly withstood withdrawal to give up smoking during the sabbath. People's values do not cease to operate in the face of physiological forces. Later, in the same study in which he detected a high remission rate for obesity, Schachter (1982) discovered that over 60 percent of those in two communities who had tried to quit smoking had succeeded. They had ceased smoking on the average for 7.4 years. Heavier smokers—those consuming three or more packs of cigarettes a day—showed the same remission rate as lighter smokers. It would seem that Schachter's nicotine regulation model, which he designed primarily to explain why habitual smokers cannot quit, does not take the measure of the behavior in question. Whereas his formulation of nicotine addiction had emphasized the ineluctable, overwhelming nature of withdrawal from cigarettes, he now found the ability to overcome such withdrawal "to be relatively common" (p. 436). In other words, there needs to be some additional level of explanation for why people persist in smoking as well as for why they can give it up (Peele 1984).

Alcohol Dependence

As narcotic addiction theorists have been forced by the recognition of individual variations in addiction to postulate innate neurochemical differences among people, alcoholism specialists have increasingly put forward the claim that alcohol problems are simply a function of excessive drinking. It might be said that conceptions of alcoholism and narcotic addiction not only are meeting on common ground but are passing each other going in opposite directions. The change in emphasis in alcoholism is in good part a result of the desire of psychologists and others to achieve rapprochement with disease theories (see chapter 2). It has led controlled-drinking clinicians to assert that a return to moderate drinking is impossible for the physically dependent alcoholic. Intriguingly, behaviorists have thus adopted Jellinek's (1960) formulation of the disease theory of alcoholism, in which he claimed that true (gamma) alcoholics could not control their drinking due to their physical dependence. (In his 1960 volume Jellinek was ambiguous about the extent to which this disability was inbred and irreversible, the traditional claims made by AA.)

The concept of alcohol dependence has been elaborated by a group of British researchers (Edwards and Gross 1976; Hodgson et al. 1978). In the same breath, it attempts to replace the disease theory (whose defects are more broadly agreed upon in Great Britain than in the United States) while rescuing important disease notions (see critique by Shaw 1979). The alcohol-dependence syndrome resembles the disease of alcoholism in conceiving of drinking problems as a condition that can be identified in isolation from the drinkers psychological state and situation and as one that endures beyond the alcoholic's active drinking. Severity of dependence is assessed purely in terms of how much people habitually drink and the physical consequences of this drinking (Hodgson et al. 1978), without regard for their reasons for drinking or cultural, social, and other environmental factors. Thus, those who are heavily dependent are thought to have a stable condition that makes their return to moderate drinking unlikely.