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Here, in brief, is a description of one way genetic and experiential factors may interact to produce alcoholism.


The potential alcoholic must be able to drink a lot (i.e., lack an intolerance for alcohol).


Some people experience more euphoria from alcohol than others do (Goodwin et al. 1979). This factor is also quite possibly under genetic control. Because euphoria is a positive reinforcer, presumably people who experience the most euphoria are the ones most likely to drink.


Like most drugs of abuse, alcohol is quickly absorbed and eliminated; the effects occur rapidly and disappear rapidly. Experimental studies indicate that alcoholics experience dysphoric as well as euphoric effects from alcohol (Mello 1975). Those individuals who experience the most euphoria (because of genetic factors) quite possibly also experience the most dysphoria, the cure for which is more alcohol. After a few drinks, these people may drink more to relieve the dysphoria than to restore the euphoria. In any case, during a single drinking period there may be two reinforcers involved: production of euphoria and reduction of dysphoria. This peak-valley effect may explain loss of control. The height of the peak and the depth of the valley may be genetically controlled.


For reasons described above, alcohol in genetically susceptible individuals may be massively reinforcing. The reinforcements occur during individual drinking periods and most strikingly "the morning after," when the "hair of the dog" swiftly relieves that formidable dysphoria known as a hangover. When loss of control leads to binge drinking, withdrawal symptoms occur (a super hangover).


After periods of abstinence, binge drinkers often relapse. This is one of the mysteries of alcoholism. If it is true that alcoholics continue heavy drinking mainly to curb dysphoriant effects, and if it is true that alcohol is a relatively weak euphoriant compared, say, to cocaine or amphetamines (May field and Allen 1967), then why should a binge drinker start drinking again after experiencing horrendous effects from previous binges? Some alcoholics are sociopaths, and in their case relapse may be explainable as another instance of "not learning from experience." Most alcoholics, however, seem to learn from most experiences as well as the next person. Why relapse?

Stimulus generalization may be the answer. As noted, alcohol in genetically susceptible individuals is a massively reinforcing agent. Both the positive (euphoriant) and negative (dysphoriant) effects resemble mood states and physical feelings experienced in sobriety. The terms "euphoriant" and "dysphoriant" are used here as shorthand for "positive reinforcer" and "negative reinforcer," respectively. The former may resemble any type of rewarding experience, e.g., sex or the pleasure of receiving a gift. The latter may resemble hunger, fatigue, or feelings of loneliness, anxiety, and depression.

Through the process of stimulus generalization, the ups and downs introduced by alcohol become cued to a wide variety of internal states and external circumstances. Even heavy drinkers drink more on some occasions and in certain settings. These occasions and settings become associated with both the highs and the lows of drinking. They become conditioned stimuli, just as do the internal feelings that resemble the highs and lows of drinking.

Relapse represents a conditioned response to these conditioned stimuli. Since relapse is usually erratic and unpredictable, it is quite likely that a combination of "interoceptive" and "exteroceptive" conditioned stimuli are required to produce relapse. The necessary combination very likely differs between individuals and even in each individual from time to time. As Keller (1972) wrote,

For any alcoholic there may be several or a whole battery of
critical cues or signals. By the rule of generalization, any
critical cue can spread like the tentacles of a vine over a
whole range of analogs, and this may account for the growing
frequency of bouts, or for the development of a pattern of
continuous inebriation. An exaggerated example is the man
who goes out and gets drunk every time his mother-in-law
gives him a certain wall-eyed look. After a while he has to
get drunk whenever any woman gives him that look.

The conditioning theory is not new. Wikler, Ludwig, and their associates (Ludwig and Wikler 1974; Ludwig et al. 1974) have described it in much detail. It remains a theory, and not an easy theory to test, at that. Combined with the genetic data, it has the advantage of showing how genetic factors may interact with learning (conditioning) to produce problem drinking. As Ludwig and Wikler (1974) have pointed out, social and psychological "modifiers" obviously influence the "addictive cycle." For example, studies indicate that alcoholics differ from nonalcoholics in having a dominant mother and a weak, passive father (Barry 1974). There is also evidence that ordinal birth position influences who becomes alcoholic (Barry et al. 1969). A host of other psychological and social modifiers have been described in the alcoholism literature; few would dispute the importance of some or all of these modifiers in promoting or discouraging the hypothetical geneticconditioning sequence proposed above.


Assuming the above hypothesis has some validity for alcoholism, to what extent can it explain other forms of substance abuse? Attempting to shown Common features in alcoholism and drug abuse in general, 1 will break down the problem into the traditional triad of agent, host, and environment.


Commonly abused psychotropic substances have, I propose, some features in common. First, they are short acting, that is, rapidly assimilated and rapidly eliminated. Nicotine perhaps better meets this definition than any other compound widely used and abused today (and some believe nicotine is the most abused of readily available substances). Historically. phenobarbital, a long-acting drug, was not considered addictive, but with the introduction of short- and intermediate-acting barbiturates in the 1930s, the addiction problem with this class of drugs became quickly apparent. Alcohol (which is rapidly absorbed and eliminated at about the rate of 15 ml per hour), opiates, newer barbiturates and their analogs, amphetamines and other stimulants, and nicotine rank among the most abused substances in the world. There is still some doubt about marijuana, which, if smoked, is rapidly assimilated but has metabolites with very long half-lives. Its abuse potential in Western countries still remains controversial, but all the other drugs listed above have the common feature of being short acting.


Genetic factors could operate in two ways to increase or decrease the possibility of an individual becoming dependent on a substance or substances.

First, many individuals are "protected" from developing specific substance abuses because they develop aversive physiological and subjective effects from the drug or drugs in small quantities. There are many anecdotal reports of individuals who can never smoke cigarettes, drink alcohol, use sleeping pills, or tolerate amphetamines or opiates, and the reason appears to be genetic. In the case of alcoholism, many millions of people are thus protected; how many are protected from use or abuse of other substances is not known.

A second means by which peak-and-valley drugs, such as those described earlier, may produce dependence in "unprotected" individuals is probably also under genetic control and involves varying degrees of positive reinforcement from the substance followed quickly by aversive effects which can only be relieved by reuse of the substance that produced the reinforcement-aversive sequence in the first place. If, for example, after many years of not smoking, a former chain smoker smokes a cigarette, he or she receives some reinforcing effects. From that point on, however, the need to smoke is based more on a "drug hunger" or craving produced by that first cigarette than it is on a desire to obtain whatever gratification the first cigarette produced. The initial reinforcing effect, by the way, obviously is not the same for all commonly abused substances. The euphoria from amphetamines and cocaine is apparently much stronger than that produced by alcohol, and the reinforcer that drives the cigarette habit clearly is not euphoria.

To recapitulate, a drug of abuse is one that quickly enters and leaves the body, producing aversive effects during the second stage which can only be relieved by reintroduction of the substance (a chocolate bar, a tranquilizer, or even a pipe cannot truly substitute for a cigarette in the chain smoker who has started the addictive cycle).

One last word about the host: However available the agent, and however susceptible the host, it must be remembered that the host is also born with other traits and susceptibilities, and in the intricate byplay of genetic and environmental factors, forces may emerge which oppose or nullify tendencies to use or abuse a particular substance. These countervailing forces must always be taken into account in evaluating individuals at risk.


There is no question that availability influences use. During Prohibition, hospitalizations for drinking problems and cirrhosis rates dropped precipitously. This was also true during the Second World War in countries like France and England where wine and beer were scarce, expensive, and often rationed. But it is important to note that more is involved than legality and commercial availability. Prices, ages of buyers, prevailing attitudes toward the substance, and a multitude of other factors will influence use.

Interactive Models of
Nonmedical Drug Use

Richard L. Gorsuch, Ph.D.

Gorsuch and Butler (1976a,b) developed a multiple-model theory of nonmedical drug use in an attempt to provide relatively concrete and detailed descriptions of factors leading to specific types of nonmedical drug use. The primary focus of the models is on illicit "hard" drug abuse, such as abuse of heroin and cocaine. The models, however, are not restricted solely to "hard" drug abuse but probably apply to the nonmedical use and abuse of several types of substances. The first section below provides the theoretical background for the models' development. The second section outlines the models themselves.

The research upon which the models were based was detailed previously (Gorsuch and Butler 1976a,b) and is not repeated here. While occasional studies will be referenced to illustrate major conclusions, the point of the present paper is to explain the models and their perspectives rather than to review the literature. Other recent research reviews (e.g., Sadava 1975; Jessor 1979) have identified the same empirically established characteristics as we did. Recent research programs have continued to document these conclusions (e.g., Jessor 1976; Nail et al. 1974; Sadava and Forsyth 1977; Kandel 1978b).



The theory presented here is psychological, focusing upon the individual, with drug behavior as the dependent variable. Groups are important only insofar as they influence the behavior of the members of that group.

The author gratefully acknowledges the research assistance of Pat
Rose in the preparation of this paper.

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