The Meaning of Addiction - 3. Theories of Addiction - Global Biologic Theories of Addiction

Written by Stanton Peele

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.