3. Theories of Addiction
Bruce K. Alexander
In many cases, addiction theorists have now progressed beyond stereotyped disease conceptions of alcoholism or the idea that narcotics are inherently addictive to anyone who uses them. The two major areas of addiction theory—those concerning alcohol and narcotics—have had a chance to merge, along with theorizing about overeating, smoking, and even running and interpersonal addictions. Yet this new theoretical synthesis is less than meets the eye: It mainly recycles discredited notions while including piecemeal modifications that make the theories marginally more realistic in their descriptions of addictive behavior. These theories are described and evaluated in this chapter as they apply to all kinds of addictions. They are organized into sections on genetic theories (inherited mechanisms that cause or predispose people to be addicted), metabolic theories (biological, cellular adaptation to chronic exposure to drugs), conditioning theories (built on the idea of the cumulative reinforcement from drugs or other activities), and adaptation theories (those exploring the social and psychological functions performed by drug effects).
While most addiction theorizing has been too unidimensional and mechanistic to begin to account for addictive behavior, adaptation theories have typically had a different limitation. They do often correctly focus on the way in which the addict’s experience of a drug’s effects fits into the person’s psychological and environmental ecology. In this way drugs are seen as a way to cope, however dysfunctionally, with personal and social needs and changing situational demands. Yet these adaptation models, while pointing in the right direction, fail because they do not directly explain the pharmacological role the substance plays in addiction. They are often considered—even by those who formulate them—as adjuncts to biological models, as in the suggestion that the addict uses a substance to gain a specific effect until, inexorably and irrevocably, physiological processes take hold of the individual. At the same time their purview is not ambitious enough (not nearly so ambitious as that of some biological and conditioning models) to incorporate nonnarcotic or nondrug involvements. They also miss the opportunity, readily available at the social-psychological level of analysis, to integrate individual and cultural experiences.
How Is Alcoholism Inherited?
Cigarette smoking, alcoholism, and overweight—like divorce, child abuse and religion—run in families. This addictive inheritance has been most studied in the case of alcoholism. Studies endeavoring to separate genetic from environmental factors, such as those in which adopted-away offspring of alcoholics were compared to adopted children with nonalcoholic biological parents, have claimed a three to four times greater alcoholism rate for those whose biologic parents were alcoholic (Goodwin et al. 1973). Vaillant (l983) approvingly cited the Goodwin et al. and other research indicating genetic causality in alcoholism (see especially Vaillant and Milofsky 1982), but his own research did not support this conclusion (cf. Peele 1983a). In the inner-city sample that formed the basis for Vaillant’s primary analysis, those with alcoholic relatives were between three and four times as likely to be alcoholic as those without alcoholic relatives. Since these subjects were reared by their natural families, however, this finding does not distinguish effects of alcoholic environment from inherited dispositions. Vaillant did find that subjects with alcoholic relatives they did not live with were twice as likely to become alcoholic as subjects who had no alcoholic relatives at all.
Yet further nongenetic influences remain to be partialed out of Vaillant’s results. The chief of these is ethnicity: Irish Americans in this Boston sample were seven times as likely to be alcohol dependent as were those of Mediterranean descent. Controlling for such large ethnicity effects would surely reduce the 2 to 1 ratio (for subjects with alcoholic relatives compared to those without) in alcoholism substantially even as other potential environmental factors that lead to alcoholism (besides ethnicity) would still remain to be controlled for. Vaillant reported two other tests of genetic causality in his sample. He disconfirmed Goodwin’s (1979) hypothesis that alcoholics with alcoholic relatives—and hence a presumed inherited predisposition to alcoholism—inevitably develop problems with drinking earlier than do others. Finally, Vaillant found no tendency for the choice of moderate drinking versus abstinence as a resolution for drinking problems to be related to number of alcoholic relatives, although it was associated with the drinker’s ethnic group.
Proposing genetic mechanisms in alcoholism on the basis of concordance rates does not provide a model of addiction. What are these mechanisms through which alcoholism is inherited and translated into alcoholic behavior? Not only has no biological mechanism been found to date to underlie alcoholism, but research on alcoholics’ behavior indicates that one cannot be found in the case of the loss of control of drinking that defines alcoholism. Even the most severely alcoholic individuals “clearly demonstrate positive sources of control over drinking behavior” so that “extreme drunkenness cannot be accounted for on the basis of some internally located inability to stop” (Heather and Robertson 1981: 122). Intriguingly, controlled-drinking theorists like Heather and Robertson (1983) propose exceptions to their own analyses: Perhaps “some problem drinkers are born with a physiological abnormality, either genetically transmitted or as a result of intrauterine factors, which makes them react abnormally to alcohol from their first experience of it” (Heather and Robertson 1983: 141).
While it is certainly a fascinating possibility, no research of any type supports this suggestion. Vaillant (1983) found that self-reports by AA members that they immediately succumbed to alcoholism the first time they drank were false and that severe drinking problems developed over periods of years and decades. The exceptions to this generalization were psychopaths whose drinking problems were components of overall abnormal lifestyles and behavior patterns from an early age. However, these kinds of alcoholics showed a greater tendency to outgrow alcoholism by moderating their drinking (Goodwin et al. 1971), indicating they also do not conform to a putative biological model. Prospective studies of those from alcoholic families also have failed to reveal early alcoholic drinking (Knop et al.1984).
Findings like these have led genetic theorists and researchers instead to propose that the inherited vulnerability to alcoholism takes the form of some probabilistically greater risk of developing drinking problems. In this view a genetic tendency—such as one that dictates a drinker will have an overwhelming response to alcohol—does not cause alcoholism. The emphasis is instead on such biological abnormalities as the inability to discriminate blood alcohol level (BAL), which leads alcoholics to show less effect from drinking and to drink more without sensing their condition (Goodwin 1980; Schuckit 1984). Alternately, Schuckit (1984) proposed that alcoholics inherit a different style of metabolizing alcohol, such as producing higher levels of acetaldehyde due to drinking. Finally, Begleiter and other theorists have proposed that alcoholics have abnormal brain waves prior to ever having drunk or that drinking creates unusual brain activity for them (Pollock et al. 1984; Porjesz and Begleiter 1982).
All these theorists have indicated that their results are preliminary and require replication, particularly through prospective studies of people who become alcoholics. Negative evidence, however, is already available. Several studies have found that sensitivity to BAL, peak BAL after drinking, and elimination of blood alcohol are unrelated to family histories of alcoholism (Lipscomb and Nathan 1980; Pollock et al. 1984). Other negative evidence for both BAL discrimination and metabolic hypotheses is provided by the case of American Indians and Eskimos. These groups are hyperresponsive to alcohol’s effects (that is, they respond immediately and intensely to the alcohol in their systems) and yet have the highest alcoholism rates in the United States. The claim of inheritance of alcoholism from the opposite theoretical direction—that these groups succumb to alcoholism so readily because they metabolize alcohol so quickly—likewise does not succeed. Groups that share the hypermetabolism of alcohol that Eskimos and Indians display (called Oriental flush), such as the Chinese and Japanese, have among the lowest alcoholism rates in America. The disjunctive connection between obvious metabolic characteristics and drinking habits actually contraindicates significant biological determinism in alcoholism (Mendelson and Mello 1979a).
The basic problem with genetic models of alcoholism is the absence of a reasonable link to the drinking behaviors in question. Why do any of the proposed genetic mechanisms lead people to become compulsive imbibers? For example, in the case of an insensitivity to alcohol’s effects, why wouldn’t an individual who can’t reliably detect that he has drunk too much simply learn from experience (in the absence of any proposed genetic compulsion to drink) to limit himself to a safer number of drinks? Do such drinkers simply choose to drink at unhealthy levels and to experience the extreme negative consequences of drinking that, after years, may lead to alcoholism (Vaillant 1983)? If so, why? That is the question.
On the other hand, the proposed differences in metabolizing alcohol and changes in brain functioning due to drinking are extremely subtle when compared with the gross effects of Oriental flush. Yet even groups characterized by Oriental flush, like the Indians and the Chinese, can show diametrically opposite responses to the same intense physiological changes. If a given individual did indeed have an extreme reaction to alcohol, why would he not become the type of drinker who announces, “I only have a drink or two because otherwise I become giddy and make a fool of myself”? For those drinkers for whom alcohol might produce a desirable change in brain waves, why does the person prefer this state over others or other ways of gaining the same effect? The variation in behavior that is left unaccounted for in the most optimistic of these models is such as to discount the potential gain from the pursuit of as yet unestablished links between genetically inherited reactions to alcohol and alcoholic behavior. Finally, since all studies have found that it is sons and not daughters who most often inherit the risk of alcoholism (Cloninger et al. 1978), in what comprehensible ways can any of the genetic mechanisms thus far suggested for alcoholism be sex-linked?
The Endorphin-Deficiency Explanation of Narcotic Addiction
Since the primary assumption about narcotics has been that the drugs are equally and inevitably addictive for everyone, pharmacological theories of narcotic addiction have rarely stressed individual biological proclivities to be addicted. It was only a matter of time, however, before pharmacological and biological theorists began to hypothesize inherited mechanisms to account for differences in addictive susceptibility. When Dole and Nyswander (1967) introduced the ideas that narcotic addiction was a “metabolic disease” and that the tendency to become addicted outlived the actual dependence on a drug, the way was opened to suggest that “metabolic disorder could precede as well as be precipitated by opiate use” (Goldstein, cited in Harding et al. 1980: 57). That is, not only might habitual narcotic use cause a chronic and residual need for drugs, but people conceivably might already have had such a need when they started taking drugs and came to rely on them.
The discovery that the body produces its own opiates, called endorphins, presented a plausible version of this mechanism. Endorphin theorists like Goldstein (1976b) and Snyder (1977) speculated that addicts may be characterized by an inbred endorphin deficiency that leaves them unusually sensitive to pain. Such people would then especially welcome—and might even require—the elevation of their pain threshold brought on by narcotics. Heroin addicts have not yet been demonstrated to show unusual levels of endorphins. Moreover, this type of theorizing is badly strained—as are all metabolic theories of addiction—by the commonplace observations of drug abuse and addiction that were noted in chapter 1. Addicts do not in fact indicate a chronic, habitual need for narcotics. They regularly alter the type and amount of drug they use, sometimes abstaining or quitting altogether as they age. Most of the Vietnam veterans who were addicted in Asia and who then used narcotics in the United States did not become readdicted. Noting that almost none of the patients introduced to a narcotic in the hospital indicate a prolonged desire for the drug, we may wonder why so small a percentage of the general population displays this endorphin deficiency.
Endorphin deficiency and other metabolic models suggest a course of progressive and irreversible reliance on narcotics that actually occurs in only exceptional and abnormal cases of addiction. Those with inbred metabolic defects could conceivably account for only a small percentage of those who become addicted over their lifetimes. Why would the narcotic addiction that disappeared for most Vietnam veterans (or for the many other addicts who outgrow it) differ fundamentally from all other kinds of addiction, such as the kind that persists for some people? To accept this dichotomous view of addiction violates the basic principle of scientific parsimony, by which we should assume that the mechanisms at work in a large portion of cases are present in all cases. This is the same error made by psychologists who concede (without empirical provocation) that some alcoholics may indeed have constitutional traits that cause them to be alcoholic from their first drink even as research shows all alcoholics to be responsive to situational rewards and to subjective beliefs and expectations.
In his influential internal-external model of obesity, Schachter (1968) proposed that fat people had a different style of eating, one that depended on external cues to tell them when to eat or not. Unlike those of normal weight, Schachter’s overweight subjects apparently could not rely on internal physiological signs to decide whether they were hungry. As a social psychologist, Schachter originally emphasized cognitive and environmental stimuli that encouraged the obese to eat. However, his model left open the question of the source of this insensitivity to somatic cues, suggesting the probability that this was an inherited trait. Schachter’s (1971) view of the sources of overeating became increasingly physiological in nature when he began comparing the behavior of ventromedial-lesioned rats with obese humans. Several of Schachter’s prominent students followed his lead in this direction. For example, Rodin (1981) eventually rejected the internal-external model (as most researchers have by now) with an eye toward locating a neurological basis for overeating. Meanwhile Nisbett (1972), another Schachter student, proposed an extremely popular model of body weight based on an internal regulatory mechanism, called set-point, which is inherited or determined by prenatal or early childhood eating habits.
Peele (1983b) analyzed Schachter’s evolution into a purely biological theoretician in terms of biases Schachter and his students had shown all along against personality dynamics; against group, social, and cultural mechanisms; and against the role of values and complex cognitions in the choice of behavior. As a result, the Schachter group consistently failed to pick up discrepant indicators in their obesity research, some of which led eventually to the jettisoning of the internal-external model. For example Schachter (1968) noted that normal-weight subjects did not eat more when they were hungry (as predicted) because they found the type of food and the time of day inappropriate for eating. In another study that had important implications, Nisbett (1968) discovered that formerly overweight subjects who were no longer obese behaved similarly to obese subjects in an eating experiment. That is, they ate more after having been forced to eat earlier than when they had not eaten before. Nisbett interpreted these results as showing that these subjects were unable to control their impulses to overeat and could therefore not be expected to keep excess weight off.
This line of thinking was solidified in Nisbett’s set-point hypothesis, which held that the hypothalamus was set to defend a specific body weight and that going below this weight stimulated a greater desire to eat. The idea that obese people could not lose weight, based on laboratory studies and the performance of clients in weight-loss programs, had been the central tenet in all of the Schachter group’s work on obesity (cf. Schachter and Rodin 1974; Rodin 1981). Yet such pessimism seems an unlikely deduction from a study like Nisbett’s (1968), in which subjects who had been obese and who continued to display an external eating style had indeed lost weight. When Schachter (1982) actually questioned people in the field about their weight-loss histories, he found remission was quite common in obesity: of all those interviewed who had ever been obese and who had tried to lose weight, 62.5 percent were currently at normal weight.
Schachter’s serendipitous finding disputed the entire thrust of over a decade’s research—namely, that people were locked into obesity by biological forces. The idea would not die easily, however. Another Schachter student and his colleague recorded Schachter’s (1982) finding but dismissed its significance by indicating it was probably only those obese subjects who were above their set-points who had been able to lose weight in this study (Polivy and Herman 1983: 195-96). Polivy and Herman based this calculation on the estimate that from 60 to 70 percent of obese people were not obese in childhood. Their assertion requires that we believe that nearly all of the people in the Schachter study who have been overweight for reasons other than biological inheritance (and only these) had lost weight. Yet undoubtedly many in this category would remain fat for whatever presumably nonset-point reasons had caused them to become obese in the first place. Rather than being the underlying source of obesity its adherents had painted it to be, set-point now seemed not to be a major factor in most cases of overweight.
Polivy and Herman’s (1983) description of their outlook did not reflect this understanding about set-point and obesity. Instead, they argued that “for the foreseeable future, we must resign ourselves to the fact that we have no reliable way to change the natural weight that an individual is blessed or cursed with” although “perhaps, as research progresses, we will be able to imagine such biological interventions—including even genetic manipulations” that will enable people to lose weight (p. 52). Polivy and Herman furthermore attributed binge overeating—the extreme of which is bulimia—to people’s attempts to restrain their eating in the effort to go below their natural weight (see chapter 5). These researchers’ work agrees with that of popular writers (Bennett and Gurin 1982) and the dominant research approaches in the field (Stunkard 1980) in maintaining a view of human eating and overeating that is essentially the same as that held by biological theorists of alcoholism and drug addiction toward drinking and drug consumption. In all cases, people are seen to be under the sway of invariant forces that, in the long run, they cannot hope to contravene.
Meanwhile, Garn and his coworkers (1979) have shown that similarities in weight levels among people who live together are a result of similar eating habits and energy expenditure. This “cohabitational effect” holds for husbands and wives and is the largest factor in weight similarities between parents and adopted offspring. People who live together who become fat do so together (Garn et al. 1979). The longer parents and their children live together (even when the children are age 40) the more they resemble each other in fatness. The longer parents and children live separately, the less pronounced such similarities become until they approach 0 at the extremes of separation (Garn, LaVelle, and Pilkington 1984). Garn, Pilkington, and LaVelle (l984), observing 2,500 people over two decades, found “those . . . who were lean to begin with generally increased in fatness level. Those who were obese to begin with generally decreased in fatness level” (pp. 90-91). “Natural weight” may be a very variable thing, influenced by the same social values and personal coping strategies that affect all behavior (Peele 1984).
The enormity of the implications of the genetic transmission of addictive impulses is driven home by several theories claiming that people are compelled by chemical imbalances to form unhealthy, compulsive, and self-destructive interpersonal relationships. Tennov (1979) maintained that such “limerent” people, who are in every other way indistinguishable from other people, have a biological propensity to fall head-over-heels in love and create disastrous romantic attachments. Liebowitz (1983) proposed that a failure in neurochemical regulation—similar to that hypothesized to cause manic-depressive reactions leads people (almost exclusively women) to fall heatedly in love, often with inappropriate partners, and to become inordinately depressed when the relationships fail. These theories illustrate mainly the temptation to believe that compelling motivations must have a biological source and the desire to mechanize human differences, imperfections, and mysteries.
Global Biologic Theories of Addiction
Peele and Brodsky (1975), in the book Love and Addiction, also described interpersonal relationships as having addictive potential. The thrust of their version of interpersonal addiction, however, was exactly the opposite of that in Liebowitz (1983) and Tennov (1979): Peele and Brodsky’s aim was to show that any powerful experience can form the object of an addiction for people predisposed by combinations of social and psychological factors. Their approach was antireductionist and rejected the deterministic force of inbred, biological, or other factors outside the realm of human consciousness and experience. Their work signaled a burst of addiction theorizing in areas other than substance abuse, the bulk of which—paradoxically—sought to analyze these phenomena at a biological level. The result has been the proliferation of biologic theories to account both for the range of compulsive involvements people form and for the tendency some people show to be addicted to a host of substances.
Smith (1981), a medical clinician, has posited the existence of an “addictive disease” to account for why so many of those who become addicted to one substance have prior histories of addiction to dissimilar substances (cf. “The Collision of Prevention and Treatment” 1984). It is impossible to explain—as Smith attempts to do—how innate, predetermined reactions could cause the same person to become excessively involved with substances as disparate as cocaine, alcohol, and Valium. In examining the generally strong positive correlations among tobacco, alcohol, and caffeine use, Istvan and Matarazzo (1984) explored the possibilities both that these substances are “linked by reciprocal activation mechanisms” and that they may be linked by their “pharmacologically antagonistic . . . effects” (p. 322). The evidence here is rather that substance abuse exceeds biological predictability. The fact of multiple addictions to myriad substances and nonsubstance-related involvements is primary evidence against genetic and biological interpretations of addiction.
Nonetheless, neuroscientists put forward biological theories of just this degree of universality. One researcher (Dunwiddie 1983: 17) noted that
drugs of abuse such as opiates, amphetamine, and cocaine can pharmacologically stimulate many of the brain centers identified as reward centers…. On the other hand, there is considerable evidence that certain individuals have an enhanced liability for drug abuse, and frequently misuse a variety of seemingly unrelated drugs. It is interesting to speculate that for various reasons, perhaps genetic, perhaps developmental or environmental, the normal inputs to these hypothetical “reward pathways” function inadequately in such individuals. If this were the case, there may be a biological defect underlying poly-drug abuse.
While piling hypothesis upon hypothesis, Dunwiddie’s description presents no actual research findings about drug abusers, nor does it present a specific hypothetical link between deficient “reward pathways” and “polydrug abuse.” It would seem the author thinks people who get less reward from drugs are more likely to abuse them.
Milkman and Sunderwirth’s (1983) neurological model of addiction is not limited to drug abuse (as nothing in Dunwiddie’s account would so limit it). These authors believe that addiction can result from any “self-induced changes in neurotransmission,” where the more neurotransmitters that are involved “the faster the rate of firing,” leading to the “elevated mood sought by cocaine users, for example” (p. 36). This account is actually a social-psychological one masquerading as neurological explanation, in which the writers introduce social and psychological factors such as peer influence and low self-esteem into their analysis by suggesting “that the enzyme produced by a given gene might influence hormones and neurotransmitters in a way that contributes to the development of a personality potentially more susceptible to . . . peer group pressure” (p. 44). Both Dunwiddie’s and Milkman and Sunderwirth’s analyses cloak experiential events in neurological terminology without reference to any actual research that connects biological functioning to addictive behavior. These models represent almost ritualistic conceptions of scientific enterprise, and while their analyses are caricatures of contemporary scientific model building, they come unfortunately close to mainstream assumptions about how the nature of addiction is to be interpreted.
Exposure Theories: Biological Models
The Inevitability of Narcotic Addiction
Alexander and Hadaway (1982) referred to the prevailing conception of narcotic addiction among both lay and scientific audiences—that it is the inevitable consequence of regular narcotics use—as the exposure orientation. So entrenched is this viewpoint that Berridge and Edwards (1981)—while arguing that “Addiction is now defined as a disease because doctors have categorized it thus” (p. 150)—refer readers to an appendix in which Griffith Edwards declared “anyone who takes an opiate for a long enough period of time and in sufficient dose will become addicted” (p. 278). This view contrasts with conventional beliefs about alcohol that would reject the same statement with the word “alcohol” substituted for “an opiate.”
Underlying the exposure model is the assumption that the introduction of a narcotic into the body causes metabolic adjustments that require continued and increasing dosages of the drug in order to avoid withdrawal. No alteration in cell metabolism has yet been linked with addiction, however. The most prominent name in metabolic research and theory, Maurice Seevers, characterized efforts during the first sixty-five years of this century to create a model of addictive narcotic metabolism to be “exercises in semantics, or plain flights of imagination” (cited in Keller 1969: 5). Dole and Nyswander (1967; cf. Dole 1980) are the modem champions of heroin addiction as a metabolic disease, although they have provided no explicit metabolic mechanism to account for it. Endorphin theorists have suggested that regular use of narcotics reduces the body’s natural endorphin production, thus bringing about a reliance on the external chemical agent for ordinary pain relief (Goldstein 1976b; Snyder 1977).
This version of the relationship between endorphin production and addiction—like the one suggesting addicts inherit an endorphin deficiency (see above)—does not fit the data reviewed in chapter 1. Put baldly, exposure to narcotics does not lead to addiction, and addiction does not require the metabolic adjustments claimed for it. Those given the most reliable and purest supplies of narcotics, hospital patients, display—rather than an escalating need for the drug—a reduced desire for it. In an experimental trial of self-administration of morphine by hospitalized postoperative patients, subjects in the self-administration condition employed moderate, progressively declining doses of the drug (Bennett et al. 1982). That even infants and animals do not manifest an acquired hunger for opiates is the subject of chapter 4. On the other hand, compulsive street users of narcotics often do not show the expected hallmarks of addiction, such as withdrawal.
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).
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).
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.
The alcohol-dependence syndrome suffers from the tension of acknowledging the complexity of alcoholic behavior. As its supporters note, “the control of drinking, like any other behavior, is a function of cues and consequences, of set and setting, of psychological and social variables; in short, control, or loss of it, is a function of the way in which the alcoholic construes his situation” (Hodgson et al. 1979: 380). Within this framework, Hodgson et al. regard withdrawal symptoms to be a strong cue for alcoholics to return to heavy drinking. However, the appearance of withdrawal in alcoholism is itself variable and subject to drinkers’ subjective constructions. Moreover, such symptoms are regularly overcome by alcoholics in their drinking careers and in any case are limited in duration. Avoidance of withdrawal simply cannot account for continued drinking (see Mello and Mendelson 1977). There is a more basic objection yet to the alcohol dependence concept. In his critique of “the concept of drug dependence as a state of chronic exposure to a drug,” Kalant (1982) remonstrated that dependence concepts have “ignored the most fundamental question—why a person having experienced the effect of a drug would want to go back again and again to reproduce that chronic state” (p.12).
Whereas speculation about human drug dependence has been influenced greatly by generalizations from animal research (generalizations that are largely incorrect, see chapter 4), the alcohol-dependence syndrome has had to fly in the face of animal research. It is difficult to get rats to drink alcohol in the laboratory. In his seminal research, Falk (1981) was able to induce such drinking through the imposition of intermittent feeding schedules that the animals find highly uncomfortable. In this condition, the rats drink heavily but also indulge in excessive and self-destructive behavior of many kinds. All such behavior—including drinking—depends strictly on the continuation of this feeding schedule and disappears as soon as normal feeding opportunities are restored. Thus, for rats that had been alcohol-dependent, Tang et al. (1982) reported “a history of ethanol overindulgence was not a sufficient condition for the maintenance of overdrinking” (p.155).
On the basis of animal research, at least, alcohol dependence seems to be strongly state-dependent rather than a persistent characteristic of the organism. Rather than being contradicted by human behavior, this phenomenon may be even more pronounced for humans. The supposed biological basis of drinking behavior in the alcohol dependence model is thus unable to deal with major aspects of alcoholism. As one of the authors (Gross 1977: 121) of the alcohol-dependence syndrome observed:
The foundation is set for the progression of the alcohol dependence syndrome by virtue of its biologically intensifying itself. One would think that, once caught up in the process, the individual could not be extricated. However, and for reasons poorly understood, the reality is otherwise. Many, perhaps most, do free themselves.
Control of Alcohol Supply
Sociological theory and research has been the main counterpoint to disease theories of alcoholism (Room 1983) and has made decisive contributions in depicting alcoholism as a social construction, in discrediting the idea that drinking problems can be organized into medical entities, and in disproving empirical claims regarding such bedrock disease notions as inevitable loss of control and reliable stages in the progress of alcoholism (see chapter 2). Yet some sociologists have also been uncomfortable with the idea that social beliefs and cultural customs affect levels of drinking problems (Room 1976). In place of such sociocultural interpretations of alcoholism, sociology as a field has now largely adopted a supply-of-alcohol perspective based on findings that alcohol consumption in a society is distributed in a unimodal, lognormal curve (Room 1984).
Since a large proportion of the alcohol available is drunk by those at the extreme end of this skewed curve, increases or decreases in alcohol availability are believed to push many drinkers above or below what might be considered a heavy and dangerous drinking level. Alcohol supply policy recommendations thus include raising taxes on liquor to lower overall consumption. The alcohol supply model is most certainly not a biological theory and does not itself lead to theoretical derivations about alcohol metabolism. Yet as Room (1984: 304) has pointed out, it can be rationalized with the disease-theory view that those at the extreme of the curve have lost control of their drinking. In fact, the model fits best with the alcohol-dependence syndrome, where alcoholic behavior is conceived principally to be the result of excessive consumption.
At the same time, the alcohol-supply view violates a number of sociologically based findings. Beauchamp (1980), for example, propounded the alcohol-supply argument while reporting that Americans consumed from two to three or more times as much alcohol per capita in the late eighteenth century as they do today and yet had fewer alcohol problems in the colonial period. Nor does the supply model make good sense of discontinuities in consumption within a given region. Alcohol problems in France are centered in the nonwinegrowing regions that must import more expensive alcoholic beverages (Prial 1984). In the United States, fundamentalist Protestant sects consume less alcohol per capita because many of these groups abstain. However, these groups—and the relatively dry regions of the South and Midwest—also have higher alcoholism rates and incidences of binge drinking (Armor et al. 1978; Cahalan and Room 1974). How also do the Jews, located principally in the highest consumption areas in the country (urban and Eastern), maintain an alcoholism rate one-tenth or less than the nationwide rate (Glassner and Berg 1980)? On the policy side, Room (1984) noted that efforts to curtail supplies have often backfired and led to greater binges in consumption.
At a psychological level, the idea that people incur the costs of alcoholism simply because they have more alcohol available to them makes little sense. For example, what exactly is the impact on the alcoholic of making supplies harder to obtain? The result of limiting the ready medical supply of narcotics was to turn many men into alcoholics (O’Donnell 1969). Vaillant (1983) found that abstaining alcoholics were highly prone to abuse other substances or to form alternate compulsive involvements. Here the sociological level of analysis, like the metabolic, suffers from a lack of a grasp of the individual’s overall addictive ecology. The popularity of alcohol-supply ideas within a community noted for its opposition to disease ideas may make one pessimistic about whether there still can remain any intellectual resistance to metabolic theories of alcoholism and addiction.
Exposure Theories: Conditioning Models
Conditioning theories hold that addiction is the cumulative result of the reinforcement of drug administration. The central tenet of conditioning theories is that (Donegan et al. 1983: 112):
To say that a substance is used at a level considered to be excessive by the standards of the individual or society and that reducing the level of use is difficult is one way of saying that the substance has gained considerable control over the individual’s behavior. In the language of behavior theory the substance acts as a powerful reinforcer: behaviors instrumental in obtaining the substance become more frequent, vigorous, or persistent.
Conditioning theories offer the potential for considering all excessive activities along with drug abuse within a single framework, that of highly rewarding behavior. Originally developed to explain narcotic addiction (cf. Woods and Schuster 1971), reinforcement models have been applied to most popular psychoactive drugs and to nondrug addictions like gambling and overeating (Donegan et al. 1983). Solomon (1980), in a broadly influential approach he calls the opponent-process model of motivation, has extended conditioning principles to every pleasurable and compulsive activity. The complex processes that characterize learning also allow increased flexibility in describing addictive behavior. In classical conditioning, previously neutral stimuli become associated with reactions brought on in their presence by a primary reinforcer. Thus an addict who relapses can be conceived to have had his craving for the addiction reinstated by exposure to the settings in which he previously used drugs (Wikler 1973; S. Siegel 1979, 1983).
The Myth of the Universal Reinforcer: The Inherent Pleasurableness of Narcotics
Conditioning theories leave open one critical question: What is a reinforcing activity? The assumption in narcotic addiction is usually that the drug provides an inherent, biologic reward and/or that it has strong reinforcement value due to its prevention of withdrawal pain (Wikler 1973). This assumption is part of a wide range of theories of addiction (cf. Bejerot 1980; Dole 1972; Goldstein 1976a; McAuliffe and Gordon 1974; Wikler 1973). Indeed, the belief that narcotics are irresistible to any organism that, once having tried them, has free access to drugs is the epitome of the exposure model of addiction. The body of work thought best to demonstrate the truth of this belief is the observation that laboratory animals can readily be induced to ingest narcotics and other drugs. Chapter 4 shows this view to be unfounded: drug use is no more self-perpetuating for animals than it is for humans. No less a biological determinist than Dole (1980) has now declared that “most animals cannot be made into addicts…. Although the pharmacological effects of addictive substances injected into animals are quite similar to those seen in human beings, animals generally avoid such drugs when they are given a choice” (p. 142).
If the behavior of laboratory animals is not locked in by drug action, how is it possible for human beings to become addicted and lose the possibility of choice? One proposal to account for the feverish pursuit of drugs and other human involvements has been that these experiences bring in ordinate pleasure, or euphoria. The idea that pleasure is the primary reinforcement in addiction is present in several theories (Bejerot 1980; Hatterer 1980; McAuliffe and Gordon 1974) and most especially has a central role in Solomon’s (1980) opponent-process model. The ultimate source of this idea has been the supposedly intense euphoria that narcotics, particularly heroin, produce, a euphoria for which normal experience offers no near counterpart. In the popular image of heroin use and its effects, euphoria seems the only possible inducement for using a drug that is the ultimate symbol of self-destructiveness.
Some users describe euphoric experiences from taking heroin, and McAuliffe and Gordon’s (1974) interviews with addicts revealed this to be a primary motivation for continuing to use the drug. Other research contests this notion vigorously. Zinberg and his colleagues have interviewed a large number of addicts and other heroin users over several decades and have found the McAuliffe and Gordon work to be extremely naive. “Our interviews have revealed that after prolonged heroin use the subjects experience a ‘desirable’ consciousness change induced by the drug. This change is characterized by increased emotional distance from external stimuli and internal response, but it is a long way from euphoria” (Zinberg et al. 1978: 19). In a survey of British Columbian addicts (cited in Brecher 1972: 12), seventy-one addicts asked to check their mood after taking heroin gave the following responses: Eight found the heroin experience to be “thrilling” and eleven found it “joyful” or “jolly,” while sixty-five reported it “relaxed” them and fifty-three used it to “relieve worry.”
Applying labels such as “pleasurable” or “euphoric” to addictive drugs like alcohol, barbiturates, and narcotics seems paradoxical, since as depressants they lessen intensity of sensation. For example, narcotics are antiaphrodisiacs whose use frequently leads to sexual dysfunction. When naive subjects are exposed to narcotics, usually in the hospital, they react with indifference or actually find the experience unpleasant (Beecher 1959; Jaffe and Martin 1980; Kolb 1962; Lasagna et al. 1955; Smith and Beecher 1962). Chein et al. (1964) noted the very special conditions under which addicts found narcotic effects to be pleasurable: “It is . . . not an enjoyment of anything positive at all, and that it should be thought of as a ‘high’ stands as mute testimony to the utter destitution of the life of the addict with respect to the achievement of positive pleasures and of its repletion with frustration and unresolvable tension” (in Shaffer and Burglass 1981: 99). Alcoholics’ drinking does not conform any better to a pleasure model: “The traditional belief that alcoholism is maintained primarily as a function of its rewarding or euphorigenic consequences is not consistent with the clinical data” as “alcoholics become progressively more dysphoric, anxious, agitated and depressed during chronic intoxication” (Mendelson and Mello 1979b: 12-13).
The opposite picture—the rejection of positive drug rewards by those in a position to pursue more lasting satisfactions—is evident in a study of volunteer subjects’ reactions to amphetamines (Johanson and Uhlenhuth 1981). The subjects originally reported the drug elevated their moods and preferred it to a placebo. After three successive administrations of the drug over several days, however, the subjects’ preference for the amphetamine disappeared even though they noted the same mood changes from its use. “The positive mood effects, which are usually assumed to be the basis of the reinforcing effect of stimulants, . . . were not sufficient for the maintenance of drug taking, probably because during the period of drug action these subjects were continuing their normal, daily activities.” The drug state interfered with the rewards they derived from these activities, and thus, “in their natural habitat these subjects showed by their preference changes that they were uninterested in continuing to savor the mood effects” (Falk 1983: 388).
Chein et al. (1964) noted that when ordinary subjects or patients find narcotics pleasurable they still do not become compulsive drug users and that a percentage of addicts find heroin to be extremely unpleasant at first but nonetheless persist in taking drugs until they became addicted. All these examples make clear that drugs are not inherently rewarding, that their effects depend on the individual’s overall experience and setting, and that the choice of returning to a state—even one experienced as positive—depends on the individual’s values and perceived alternatives. Reductionist models have no hope of accounting for these complexities in addiction, as illustrated by the most widely deployed of such models, Solomon’s (1980) opponent-process view of conditioning.
Solomon’s model draws an elaborate connection between the degree of pleasure a given state produces and its subsequent capacity to inspire withdrawal. The model proposes that any stimulus leading to a distinct mood state eventuates in an opposite reaction, or opponent process. This process is simply the homeostatic function of the nervous system, much the same way that presenting a visual stimulus leads to an after-image of a complementary color. The stronger and the greater the number of repetitions of the initial state, the more powerful the opponent reaction and the more rapid its onset after the first stimulus ceases. Eventually, the opponent reaction comes to dominate the process. With narcotics and other powerful mood-arousing involvements such as love, Solomon proposes, an initial positive mood is replaced as the individual’s primary motivation for re-experiencing the stimulus by the desire to avoid the negative, or withdrawal state.
Solomon and Corbit (1973, 1974) constructed this model from experimental evidence with laboratory animals. As we have seen, neither the positive feelings it posits from narcotics use nor the traumatic withdrawal it imagines can account for human drug taking. Moreover, the model’s mechanistic version of neurological sources of motivation creates a Platonic ideal of pleasure as existing independent of situation, personality, or cultural milieu. The model likewise holds that a person’s response to this objective degree of pleasure (or else equally specifiable withdrawal pain) is a predetermined constant. People in fact display all sorts of differences in how ardently they pursue immediate pleasure or how willing they are to endure discomfort. For example, people vary in their willingness to delay gratification (Mischel 1974). Consider that most people find hot fudge sundaes and devil’s food cake to be extremely enjoyable and yet only a very few people eat such foods without restraint. It simply isn’t plausible that the main difference between compulsive and normal eaters is that the former enjoy the taste of food more or suffer greater withdrawal agony when not stuffing themselves.
Solomon uses the opponent-process model to explain why some lovers cannot tolerate the briefest of partings. Yet this separation anxiety seems less a measure of depth of feeling and length of attachment than of the desperation and insecurity of a relationship, which Peele and Brodsky (1975) called addictive love. For example, Shakespeare’s Romeo and Juliet prefer to die rather than be parted. This state does not result from accumulated intimacies that were eventually replaced by negative sensations, as Solomon’s model predicts. Shakespeare’s lovers cannot bear to part from the start. At the time when they both commit suicide, they have met only a handful of times, with most of their meetings having been brief and without physical contact. The kinds of relationships that lead to the withdrawal extremes of murder and suicide when the relationship is threatened rarely coincide with notions of ideal love affairs. Such couplings usually involve lovers (or at least one lover) who have histories of excessive devotion and self-destructive affairs and whose feeling that life is otherwise bleak and unrewarding has preceded the addictive relationship (Peele and Brodsky 1975).
Associative Learning in Addiction
Classical conditioning principles suggest the possibilities that settings and stimuli associated with drug use either become reinforcing in themselves or can set off withdrawal and craving for the drug that lead to relapse. The first principle, secondary reinforcement, can explain the importance of ritual in addiction, since actions like self-injection acquire some of the reward value of the narcotics they have been used to administer. Conditioned craving leading to relapse would appear when the addict encountered settings or other stimuli that were previously connected with drug use or withdrawal (O’Brien 1975; S. Siegel 1979; Wikler 1973). For example, Siegel (1983) applied conditioning theory to explain why the Vietnam soldier addicts who most often relapsed after their return home were those who had abused drugs or narcotics before going to Asia (Robins et al. 1974). Only these men would be exposed to familiar drug-taking environments when they returned home that set off the withdrawal that in turn required them to self-administer a narcotic (cf. O’Brien et al. 1980; Wikler 1980).
These ingenious conditioning formulations of human drug use have been inspired by laboratory studies of animals and human addicts (O’Brien 1975; O’Brien et al. 1977; Siegel 1975; Wikler and Pescor 1967). For example, Teasdale (1973) demonstrated that addicts showed greater physical and emotional responses to opiate-related pictures than to neutral ones. However, the conditioned craving and withdrawal such studies uncover are by the evidence minor motivations in human relapse. In the laboratory, Solomon has been able to create negative opponent-process states that last for seconds, minutes, or at most days. O’Brien et al. (1977) and Siegel (1975) have found that responses associated with narcotic injections in humans and rats that can be conditioned to neutral stimuli are extinguished almost immediately when the stimuli are presented on unrewarded trials (that is, without a narcotic).
What is more important, these laboratory findings do not appear relevant to addicted street behavior. O’Brien (1975) reported a case of an addict just out of prison who became nauseated in a neighborhood where he frequently had experienced withdrawal symptoms—a reaction that led him to buy and inject some heroin. This case has been described so often that, in its repetition, it seems a typical occurrence (see Hodgson and Miller 1982: 15; Siegel 1983: 228). Yet it is actually a novelty. McAuliffe and Gordon (1974) reported that “We have interviewed 60 addicts concerning their many relapses, and we could find only one who had ever responded to conditioned withdrawal symptoms by relapsing” (p. 803). In their thorough study of the causes of relapse, Marlatt and Gordon (1980) found heroin addicts rarely reported postaddiction withdrawal to be the reason they relapsed. None of the cigarette smokers or alcoholics Marlatt and Gordon interviewed listed withdrawal symptoms as the cause of their relapse.
Conditioned responses are particularly unlikely to account for relapse, since most former addicts do not relapse to addiction after they use a drug again. Schachter (1982) found that former smokers would smoke at a party but not return to regular smoking. Vaillant (1983) noted that “relatively few men with long periods of abstinence had never taken another drink” (p. 184). Half of the addicted Vietnam soldiers used a narcotic at home, but only a minority became readdicted (Robins et al. 1975). Waldorf’s (1983) investigation of heroin addicts who quit on their own found ex-addicts typically injected themselves with heroin after licking the habit to prove to themselves and others that they were no longer hooked. All these data point out that the unconditioned stimulus (actual drug use) is not sufficient provocation for a return to addiction. It is impossible that the weaker conditioned stimuli could provide sufficient motivation.
For Siegel and others who have analyzed the Vietnam remission data in conditioning terms, the crucial variable is simply situational change. All situational changes are equivalent in terms of this model as long as drugs have been taken in one environment and not the other, since then the new environment does not evoke conditioned withdrawal symptoms. This has prompted Siegel et al. to recommend a fresh setting as the best remedy for addiction. Yet it would certainly seem that other features of this new setting would be at least as important as familiarity for affecting addiction. Rats habituated to morphine in a diverse, social environment refused the drug in the same environment when offered a choice, while caged, isolated rats on the same presentation schedule continued to consume the morphine (Alexander et al. 1978). Zinberg and Robertson (1972) reported that addicts’ withdrawal symptoms disappeared in a treatment environment where withdrawal was not accepted, while their withdrawal was exacerbated in other environments, such as prison, where it was expected and tolerated.
The Role of Cognition in Conditioning
Addicts and alcoholics—whether treated or untreated—who achieve remission often do experience important changes in their environments. These changes frequently result, however, from self-initiated attempts to escape the addiction and other life problems. There are also those who modify addictive habits without drastically rearranging their lives. This is especially true for those addicted to less socially disapproved substances like cigarettes but also holds for a distinct minority of former alcoholics and heroin addicts. Modification of the addict’s environmental stimuli appears in these cases to be an entirely internal or psychological process. Siegel (1979) recognized this role for cognitive stimuli when he explained why some Vietnam veterans relapsed without returning to old drug haunts. He cited Teasdale (1973) and O’Brien (1975) to indicate men experienced withdrawal and craving when “talking about drugs in group therapy,” “seeing pictures of drugs and ‘works,”‘ or just “imagining themselves injecting drugs in their customary setting” (p.158).
The conditioned responses that occur with regard to subjective experience and as a result of environmental changes that addicts themselves bring about cast conditioning theories in a whole new light, where these responses seem an adjunct to individual self-control and motivation to change rather than the sources of such change. Moreover, conditioning theories in addiction are limited by their inability to convey the meaning the individual attaches to his or her behavior and environment. As a result, conditioning theories must be made so complex and ad hoc to explain the complexities of human drug taking that they lose the precision and predictive power that are their supposed scientific assets. They seem destined to suffer the same fate as did the U.S. intervention in Vietnam, the event that has prompted so much speculation about the role of conditioning in drug use. In both cases rationales become so cumbersome and counterproductive in the effort to respond to information from the field that they must collapse of their own weight.
Siegel’s utilization of cognitive variables to account for conditioning anomalies observed in heroin use is part of a venerable tradition. The first explicitly cognitive conditioning model in addiction was Lindesmith’s (1968, originally published in 1947), which contended that to be addicted the heroin user must be aware that the withdrawal pain he suffers is due to cessation of drug use and that readministering the drug will alleviate this pain. Thus so many nineteenth century narcotic users may have failed to become addicted because they simply didn’t know that narcotics were addicting! Lindesmith elaborated how cognitions affect addiction in connection with hospital patients. Patients do realize they are taking a narcotic and understand the drug’s effects, but they associate these effects with their illness. When they leave the hospital (or later when their prescription for painkillers runs out) they know any discomfort will be temporary and a necessary part of convalescence and thus they do not become addicted.
We may wonder why Lindesmith reserved the role of cognition in his model for this very limited number of ideas. For example, would not a hospital patient’s belief that continued narcotic use was harmful or that other opportunities outweighed the option of giving in to the drug’s effects be a part of the decision not to continue using narcotics? Such matters as self-conception, perceived alternatives, and values against drug intoxication and illicit activity would naturally seem to influence the individual’s choices. It is not only the decision whether to continue using a drug that cognitions, values, and situational pressures and opportunities determine, however. They also determine how the drug’s effects and withdrawal from these effects will be experienced. Contrary to Lindesmith’s scheme, people who recover from illnesses almost never acknowledge craving narcotics outside the hospital (Zinberg 1974).
Social Learning and Adaptation
Conventional conditioning models cannot make sense of drug behavior because they circumvent the psychological, environmental, and social nexus of which drug use is a part. One branch of conditioning theory, social-learning theory (Bandura 1977), has opened itself to the subjective elements of reinforcement. For example, Bandura described how a psychotic who continued his delusional behavior in order to ward off invisible terrors was acting in line with a reinforcement schedule that was efficacious despite its existing solely in the individual’s mind. The essential insight that reinforcers gain meaning only from a given human context enables us to understand (1) why different people react differently to the same drugs, (2) how people can modify these reactions through their own efforts, and (3) how people’s relationships with their environments determine drug reactions rather than vice versa.
Social-learning theorists have been especially active in alcoholism, where they have analyzed how alcoholics’ expectations and beliefs about what alcohol will do for them influence the rewards and behaviors associated with drinking (Marlatt 1978; Wilson 1981). Yet it has also been social-learning theorists who have launched the alcohol-dependence syndrome and who seem to feel subjective interpretation is far less important than the pharmacological effects of alcohol in causing drinking problems (Hodgson et al. 1978, 1979). This lacuna in their theorizing is most noticeable in the inability of modem social-learning theorists to make sense out of cultural variations in drinking styles and experiences (Shaw 1979). Whereas McClelland et al. (1972) offered an experiential bridge between individual and cultural conceptions about alcohol (see chapter 5), behaviorists have regularly rejected this kind of synthesis in favor of direct observations and objective measurements of alcoholic behavior (embodied by Mendelson and Mello 1979b).
In another area of social-learning theory, Leventhal and Cleary (1980) proposed “that the smoker is regulating emotional states and that nicotine levels are being regulated because certain emotional states have been conditioned to them in a variety of settings” (p. 391). In this way they hoped to “provide a mechanism for integrating and sustaining the combination of external stimulus cues, internal stimulus cues, and a variety of reactions including subjective emotional experience . . . with smoking” (p. 393). In other words, any number of levels of factors, from past experience to current setting to idiosyncratic thoughts, can influence the person’s associations with smoking and subsequent behavior. In creating a conditioning model as complex as this one in order to account for behavior, however, the authors may have been putting the cart before the horse. Instead of conceiving of cognition and experience as components of conditioning, it seems easier to say that addiction involves cognitive and emotional regulation to which past conditioning contributes. In this view, addiction is an effort by an individual to adapt to internal and external needs, an effort in which a drug’s effects (or some other experience) serve a desired function.
Studies that have questioned users about their reasons for continued drug-taking or that have explored the situations of street users have revealed crucial, self-aware purposes for drug use and a reliance on drug effects as an effort to adapt to internal needs and external pressures. Theoretical developments based on these investigations have focused on the psychodynamics of drug reliance. Such theories describe drug use in terms of its ability to resolve ego deficiencies or other psychological deficits—brought on, for example, by lack of maternal love (Rado 1933). In recent years theorizing of this sort has become broader: less wedded to specific child-rearing deficits, more accepting of a range of psychological functions for drug use, and including other substances besides narcotics (cf. Greaves 1974; Kaplan and Wieder 1974; Khantzian 1975; Krystal and Raskin 1970; Wurmser 1978).
These approaches developed in response to the clearcut finding that very few of those exposed to a drug, even over extended periods, came to rely on it as a life-organizing principle. What they failed to explain adequately is the great variability of reliance on drugs and addiction in the same individuals over situations and life span. If a given personality structure led to the need for an specific kind of drug, why then did the same people wean themselves from the drug? Why did others with comparable personalities not become wedded to the same substances? What was obvious in the case of narcotic addiction was its strong association with certain social groups and lifestyles (Gay et al. 1973; Rubington 1967). Efforts to incorporate this level of social reality led to higher-order theories that went beyond purely psychological dynamics to combine social and psychological factors in drug use (Ausubel 1961; Chein et al. 1964; McClelland et al. 1972; Winick 1962; Zinberg 1981).
Such social-psychological theories addressed the function of drug use in adolescent and postadolescent life stages as a way of preserving childhood and avoiding adult conflicts (Chein et al. 1964; Winick 1962). They also dealt with the availability of drugs in certain cultures and the predisposing social pressures toward their use (Ausubel 1961; Gay et al. 1973). Finally they presented the impact of social ritual on the meaning and style of use that a person in a given setting adopted (Becker 1963; Zinberg et al. 1977). What ultimately limited these theories was their lack of a formulation of the nature of addiction. While nearly all of them minimized the role of physiological adjustments in the craving and response to withdrawal that signify addiction (Ausubel 1961; Chein et al. 1964; Zinberg 1984), they provided little in the way of basic mechanisms to account for the dynamics of addiction.
As a result, the social-psychological literature exists in almost total isolation from the pharmacological and learning literature on addiction. Because they do not confront laboratory-based models directly, social-psychological theorists are forced to rely on biological concepts that their own data and ideas contradict (as illustrated by the discussion, in chapter 1, of Zinberg et al. 1978). This exaggerated deference to pharmacological constructs makes these theorists reluctant to incorporate a cultural dimension as a basic element in addiction or to explore the meaning of nonsubstance addictions—surprisingly so, given that their own emphasis on the socially and psychologically adaptive functions of drugs would seem to apply equally well to other involvements. What may curtail the social and psychological analysis of addiction most is the inappropriate meekness and limited scientific aspirations of those best suited to extend the boundaries of addiction theory in this direction. Such meekness certainly does not characterize modern conditioning and biological theorizing.
The Requirements of a Successful Theory of Addiction
A successful addiction model must synthesize pharmacological, experiential, cultural, situational, and personality components in a fluid and seamless description of addictive motivation. It must account for why a drug is more addictive in one society than another, addictive for one individual and not another, and addictive for the same individual at one time and not another (Peele 1980). The model must make sense out of the essentially similar behavior that takes place with all compulsive involvements. In addition, the model must adequately describe the cycle of increasing yet dysfunctional reliance on an involvement until the involvement overwhelms other reinforcements available to the individual.
Finally, in assaying these already formidable tasks, a satisfactory model must be faithful to lived human experience. Psychodynamic theories of addiction are strongest in their rich explorations of the internal, experiential space of their subject matter. Likewise, disease theories—while seriously misrepresenting the nature and constancy of addictive behavior and feelings—are based on actual human experiences that must be explained. This last requirement may seem the most difficult of all. One may wonder whether models built on social-psychological and experiential dynamics make any sense when confronted with the behavior of laboratory animals or newly born infants.
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