DQ WK 1

Almost everyone has an easy answer to the question: Why do people use drugs? According to Stewart (1987), heroin addicts use “junk” the first time because they are curious. Heroin has a mystique. It is used by pop stars, writers, and glamorous people, and they like its effect. For those who find daily life to be fairly humdrum, heroin can be the ultimate filler of gaps—it can substitute for career, religion, romance, or virtually anything else. Weil and Rosen (1993) believe that drug use (and addiction) results from humans’ longing for a sense of completeness and wholeness, and searching for satisfaction outside of themselves. As noted author (and addict) William S. Burroughs (1977) indicated in Junky, “Junk wins by default. I tried it as a matter of curiosity. I drifted along taking shots when I could score. I ended up hooked” (p. xv). This notion of drift is a recurrent theme in theories of addiction.

People begin using cocaine for some of the same reasons. According to Baum (1985), his clients provided these excuses for using cocaine:

“The mystical reputation aroused my curiosity.” . . .

“It’s available and being offered all the time.” . . .

“It gave me a sense of well-being, like I was worth something.” . . .

“It felt good to be a part of a group.” . . .

“It was a great way to escape.” (pp. 25–42)

The reasons why people continue to use drugs to the point of becoming physically and/or psychologically dependent on them are more complex. Some have attempted to explain this phenomenon as a deficit in moral values, a disease, conditioning or learned behavior, or as a genetic propensity. Still others see it as a “rewiring” of the brain (see Chapter 3). At this point, there is no one single theory that adequately explains addiction.

Jacobs (1986) attempted to develop a general theory of addiction, drawing on his experience and research with gamblers. In his view, addiction is a dependent state acquired over time to relieve stress. Two interrelated sets of factors are required to predispose persons to addiction: an abnormal physiological resting state, and childhood experiences producing a deep sense of inadequacy. He argues that all addictions (drugs, sex, alcohol, etc.) follow a similar three-stage course of development.

Most models of addiction assume that an addiction is an “addictive disease” (Washton, 1989, p. 55). As such, it continues to exist whether or not the addicted person continues to use the drug. Even if a person who has the disease is abstinent for a long period of time, the symptoms of addiction will appear again from renewed contact with the drug. The disease model of addiction rests on three primary assumptions: predisposition to use a drug, loss of control over use, and progression (Krivanek, 1988, p. 202). Johnson (1973) put it somewhat differently in saying, “The most significant characteristics of the disease [alcoholism] are that it is primary, progressive, chronic, and fatal” (p. 1). There are others, such as Peele (1985), who question the validity of this model. Speaking of the complex nature of addiction, he rejects all strictly biological explanations and says that addiction cannot be resolved biologically because “lived human experience and its interpretation are central to the incidence, course, treatment, and remission of addiction (see Preface).” An adequate theory would have to synthesize pharmacological, experiential, cultural, situational, and personality components.

Drummond (2001) provides an interesting perspective on theories of drug craving, most of which can be classified into three categories:(1) phenomenological models, which are based on clinical observation and description; (2) conditioning or cue-reactivity models, which are useful in the exploration of craving and relapse; and (3) cognitive models, which are based on social learning theory. He concludes that no one theory provides an adequate explanation of the phenomenon of craving. Addiction, drug dependence, and craving are all terms used to identify the phenomenon of loss of control over drug-taking behavior, although each has a slightly different meaning.

Etiological Theories

Addiction is not easily defined. For some, it involves the “continued, self-administered use of a substance despite substance-related problems, and it results in tolerance for the substance, withdrawal from the substance, and compulsive drug-taking behavior due to cravings” or drives to use the substance (Schuckit, 1992, p. 182). However, the American Psychiatric Association’s criteria for dependence do not require that tolerance or withdrawal be present (see Chapter 5).

There are at least as many explanatory theories of addiction as there are definitions. We will focus on three broad theoretical categories—psychological theories, biological theories, and sociocultural theories—as well as discuss some alternative explanations. These theories are not mutually exclusive, and divisions sometimes seem quite arbitrary. None is presented as the correct way of explaining this phenomenon. We do have preferences, and we lean more toward certain models than others, but no single theory adequately describes the etiology of addiction or dependence. (For a more comprehensive treatment of etiology, see Ott, Tarter, and Ammerman [1999].) As social workers, it seems fitting to suggest that the “person-in-environment” model may ultimately provide the best mechanism for an understanding of addiction. We will return to this perspective at the end of the chapter.

The Moral Model

One of the earliest theories offered to explain the etiology of addiction is humankind’s sinful nature. Since it is difficult to show empirical evidence of a sinful nature, the moral model of addiction has been generally discredited by modern scholars. However, the legacy of treating alcoholism and drug addiction as sin or moral weakness continues to influence public policies regarding alcohol and drug abuse. Perhaps this is why needle/syringe exchange programs have been so strongly opposed in the United States.

Psychological Theories

Another explanation for the origins of craving alcohol and mind-altering drugs lies in the psychological literature—that is, the literature that deals with one’s mind and emotions. Psychological models define addiction as an individual phenomenon but do not necessarily exclude or minimize social factors or other elements in the development of an addiction. There are actually several different psychological theories of alcoholism and drug addiction; they include cognitive-behavioral, learning, psychodynamic, and personality theories, among others.

Cognitive-Behavioral Theories

The cognitive-behavioral theories offer a variety of motivations for taking drugs. One such explanation states that humans take drugs to experience variety (Weil & Rosen, 1993). The need for variety is demonstrated in cross-cultural expressions such as singing, dancing, running, and joking. Drug use is associated with a variety of activities—for example, religious services, self-exploration, altering moods, escaping boredom or despair, enhancing social interaction, enhancing sensory experience or pleasure, and stimulating creativity and performance. A study on inner-city youths revealed that youths are motivated to take drugs out of a desire for variety, citing curiosity, celebration, getting high, and rebelling as reasons for drug use. (In the study, the youths celebrate or explore drugs by using alcohol at home, whereas they choose to use illegal marijuana away from the home [Esbensen & Huizinga, 1990].) Assuming that people enjoy variety, it follows that they repeat actions that bring pleasure (positive reinforcement).

The desire to experience pleasure is another cognitive explanation for drug use and abuse. Some animals seek alcohol and even work for it (by pushing a lever) to repeat a pleasant experience. Alcohol and other drugs are chemical surrogates of natural reinforcers such as eating, drinking, and reproductive behavior. Social drinkers and alcoholics both report using alcohol to relax, even though tests of actual tension-reducing effects of alcohol have yielded quite different results; scientific observations of persons using alcohol actually show them to become more depressed, anxious, and nervous (NIAAA, 1996). The dependent behavior is maintained by the degree of reinforcement the alcohol provides, and this, in turn, depends on the actor’s perception of his or her need hierarchy and “the likelihood that this course of action will meet the most important needs better than other available options” (Krivanek, 1989, p. 96). Since alcohol and drugs are more powerful and persistent than natural reinforcers to which the human brain is accustomed, they set the stage for addiction.

With time, the brain adapts to the presence of the drug or alcohol. The removal of the substance from the host reveals certain abnormalities experienced by the brain. The host experiences unpleasant withdrawal symptoms, such as anxiety, agitation, tremors, increased blood pressure, and in severe cases, seizures. Naturally, one wants to avoid painful stimuli; by consuming the substance anew, an individual can avoid the unpleasant symptoms of withdrawal. Repetitive action motivated by the avoidance of unpleasant stimuli is called negative reinforcement. (In an alcoholic, the need to avoid withdrawal symptoms generally occurs from 6 to 48 hours after the last drink.) Another source of negative reinforcement may lie in the avoidance of unpleasant things other than withdrawal. There is a high correlation between traumatic events and subsequent substance abuse (Janoff-Bulman, 1992). The traumatized individual may take drugs to avoid unpleasant memories or heightened physiological states such as startle responses.

Learning Theory

Closely related to cognitive-behavioral theories is learning, or reinforcement, theory. Learning theory assumes that alcohol or drug use results in a decrease in psychological states such as anxiety, stress, and tension, thus positively reinforcing the user. This learned response continues until physical dependence develops, at which time the aversion of withdrawal symptoms becomes a prime motivation for drug use (Tarter & Schneider, 1976).

There is a considerable amount of evidence to support that part of learning theory related to alcohol use and physiological aversion. Abrupt cessation of drinking will lead to unpleasant symptoms of withdrawal (A & DRCC, 1995). For the alcoholic, withdrawal can lead to trembling, shaking, hallucinations, and tonic-clonic seizures, formerly known as grand mal seizures. Similarly, for the heroin addict, abrupt withdrawal may lead to symptoms much like a case of severe flu. In each case, the addict quickly learns that these symptoms may be avoided by resuming use of the drug.

An interesting view of becoming a heroin addict is provided by Krivanek (1989). Dependencies that involve drug use follow the same basic principles of learning theory, as all other dependencies. Krivanek views drug dependence as a psychological phenomenon that can vary in intensity from a mild involvement to an addiction that seriously restricts the user’s other behaviors. Pattison, Sobell, and Sobell (1977) view alcoholism as a continuum. That is, “An individual’s use of alcohol can be considered as a point on a continuum from nonuse, to nonproblem drinking, to various degrees of deleterious drinking” (p. 191).

Learning theory is helpful in treatment planning because it addresses the adaptive consequences of drinking. (For a more extensive discussion of adaptation and addiction, see Peele [1998].) Also, behavioral treatments have incorporated learning theory into a treatment framework based on the premise that what has been learned can be unlearned (Bandura, 1969). It follows that intervening early is important, since there will be fewer behaviors to unlearn. Learning theory is also quite adaptable to the systems view, which is followed throughout this book.

Psychodynamic Theories

Psychodynamic theories are more difficult to substantiate than most other psychological theories because they deal with hard to operationalize concepts and with events that may have occurred many years before the onset of addiction. Although Dr. Sigmund Freud never devoted a single paper to the subject of alcoholism, his disciples were not the least bit reluctant to apply psychoanalytic theories to alcohol addiction. The earliest explanations linked alcoholism with the “primal addiction” of masturbation (Bonaparte, Freud, & Kris, 1954). Later, most explanations linked alcoholism to ego deficiencies, suggesting that alcohol is used to attain a sense of security. This theory assumes that during childhood, inadequate parenting, along with the child’s individual constitution, caused the child to form weak attachments to significant others, resulting in a need to compensate for or dull the insecurity. This is accomplished in the consumption of alcoholic beverages (Chordokoff, 1964). Alcohol abuse has also been explained by psychoanalytic theorists as an expression of hostility and of homosexuality. Still others view alcoholics as self-destructive, narcissistic, or orally fixated (Schuckit, 1986). Psychoanalytic theory has even blamed the development of alcoholism on the failure of mothers to provide milk (Menninger, 1963).

A major problem with psychoanalytic theories is that experiences such as early childhood deprivation are not specific to alcoholism or addiction to other drugs. In fact, they are commonly reported by non-addicted adults with a variety of other psychological problems. Perhaps the most serious shortcoming is in the psychodynamic theories’ implications for the treatment of alcoholism or drug addiction. Many counselors warn that a nondirective approach that focuses solely on the patients’ development of insight into their problems neglects the addictive power of alcohol or other drugs (Cunynghame, 1983).

Nevertheless, there is a feeling among some scholars (Collins, Blaine, & Leonard, 1999) that psychodynamic approaches should not be dismissed because they serve “to guide a substantial portion of clinical practice” (p. 162). Even though the empirical support of psychodynamic theory is scanty, it has shown a remarkable resiliency and the ability to capture the imagination of practitioners.

Personality Theories

Personality theories, which frequently overlap the psychodynamic theories, assume that certain personality traits predispose an individual to drug use. An individual with a so-called alcoholic personality is often described as dependent, immature, and impulsive (Schuckit, 1986). Other personality theorists have described alcoholics as highly emotional, immature in interpersonal relationships, having low frustration tolerance, being unable to express anger adequately, and confused in their sex-role orientation (Catanzaro, 1967). After reviewing these personality theories, Keller (1972) summarized them in Keller’s law: The investigation of any trait in alcoholics will show that they have either more or less of it. However, the many scales that have been developed in an attempt to identify alcoholic personalities have failed to distinguish consistently the personality traits of alcoholics from those of non-alcoholics. One of the subscales of the Minnesota Multiphasic Personality Inventory (MMPI) does differentiate alcoholics from the general population, but it may actually detect only the results of years of alcohol abuse, not underlying personality problems (MacAndrew, 1979).

There is some evidence that individuals with an antisocial personality (as defined in the DSM-IV, APA, 1994) have a higher incidence of alcoholism than the general population. There is no evidence that this personality disorder caused the alcoholism, but these individuals were more disposed to develop alcohol problems because of their antisocial personality. Apart from this relatively rare occurrence of the antisocial personality, alcoholics have not been found to exhibit a specific cluster of personality traits (Sherfey, 1955). Vaillant (1994) argues persuasively that personality (as well as psychological) factors are, at most, of minimal consequence as a cause of alcoholism. There have been similar attempts to link a constellation of certain personality traits to drug addiction as well as alcoholism (Gossop & Eysenck, 1980). A consensus seems to have evolved that personality traits are not of much importance in explaining drug dependence. In fact, most of those who work in this field agree that an individual can become dependent irrespective of personality attributes (Raistrick & Davidson, 1985). One book lists 94 personality characteristics that have been attributed to drug addicts by various theorists (Einstein, 1983). These include many characteristics that are polar opposites of one another—for example: poor self-image and grandiose self-image, ego inflation and ego contraction, self-centered and externalization, pleasure-seekers and pleasure-avoiders, and several dozen other contradictory pairs.

A report to the National Academy of Sciences (“Addictive Personality,” 1983) concludes that there is no single set of psychological characteristics that embraces all addictions. However, there are, according to the report, “significant personality factors that can contribute to addiction.” These factors number 4 (not 94) and are as follows:

Impulsive behavior, difficulty in delaying gratification, an antisocial personality, and a disposition toward sensation seeking.

A high value on nonconformity combined with a weak commitment to the goals for achievement valued by the society.

A sense of social alienation and a general tolerance for deviance.

A sense of heightened stress. (This may help explain why adolescence and other stressful transition periods are often associated with severe drug and alcohol problems.) (pp. 11, 15).

Research on personality theories of addiction seems to have waned during the 1990s, and there are few recent empirical studies that focus on this explanation for addiction.

Biological Theories

Biophysiological and genetic theories assume that addicts are constitutionally predisposed to develop a dependence on alcohol or drugs. These theories support a medical model of addiction. Their advocates apply disease terminology and generally place responsibility for the treatment of addicts in the hands of physicians, nurses, and other medical personnel. In reality, the medical model is generally practiced only during the detoxification phase.

Generally speaking, biological theories branch into one of two explanations: neurobiological and genetic. There has been such an explosion of knowledge in recent years in the neurobiology of addiction that we have devoted a separate chapter to it (see Chapter 3). But at this point, we will briefly review the research on genetics.

Genetic Theories

Recent studies supported by the National Institute on Drug Abuse (NIDA, 2008 ) found that a variant in the gene for a nicotinic receptor subunit doubled the risk for nicotine addiction among smokers. This is the first evidence of a genetic variation influencing both the likelihood of nicotine addiction and an individual’s risk for the severe health consequences of tobacco use. National Institute on Alcohol Abuse and Alcoholism (NIAAA) has funded the Collaborative Studies on Genetics of Alcoholism (COGA) since 1989, but specific genetic factors have never been established as a definite cause of alcoholism, although the statistical associations between genetic factors and alcohol abuse are very strong (NIAAA, 2009). A great volume of research has been amassed in this area over the last several decades, and much of the evidence points toward alcoholism as an inherited trait. It has been observed that (1) adopted children more closely resemble their biological parents than their adoptive parents in their use of alcohol (Goodwin, Hill, Powell, & Viamontes, 1973), (2) alcoholism occurs more frequently in some families than in others (Cotton, 1979), and (3) concurrent alcoholism rates are higher in monozygotic twin pairs (53.5 percent) than in dizygotic pairs (28.3 percent) (Kaij, 1960). Children of alcoholics are three to seven times more likely to be at risk of alcoholism (Koopmans & Boomsina, 1995). Having an alcoholic parent (but not necessarily both parents) can increase the risk of becoming an alcoholic. Yet even in the presence of elevated risks, only 33 percent sons and 15 percent daughters of alcoholics demonstrate evidence of the disorder.

Some genetic theorists speculate that an inherited metabolic defect may interact with environmental elements and eventually lead to alcoholism. This genetotrophic theory posits an impaired production of enzymes within the body (Williams, 1959). Others hypothesize that inherited genetic traits result in a deficiency of vitamins (usually of the vitamin B complex), which leads to a craving for alcohol as well as cellular or metabolic changes (Tarter & Schneider, 1976).

It is important to remember that, despite the impressive statistical relationships in these studies implying a genetic link, no specific genetic marker that predisposes a person toward alcoholism has ever been isolated. The first biological marker established for alcoholism was thought to be color blindness, but a few years later, it was demonstrated that color blindness was actually a result of severe alcohol abuse (Valera, Rivera, Mardones, & Cruz-Coke, 1969). Several other genetic discoveries have met a similar fate. A workshop on genetic and biological markers in drug and alcohol abuse suggests promising areas for genetic research, such as polymorphisms in gene products and DNA polymorphisms (Nichols, 1986). A more recent study reports that the so-called dopamine D2 receptor gene, which affects the capacity of cells to absorb dopamine, was present in 77 percent of the brains of alcoholics and only 28 percent of non-alcoholics (Blum et al., 1990).

In 1990, the front page of an edition of The New York Times hailed the discovery of a gene claimed to be directly linked to alcoholism. Two years later, this so-called alcoholism gene, formally known as the dopamine D2 receptor gene, had become the focus of a bitter controversy. Blum and Noble insisted that their finding had been amply documented by subsequent research, and they took steps to market a test for genetic susceptibility to alcoholism. Blum suggested that job applicants, children, and perhaps even fetuses could be tested.

In Blum and Noble’s experiments, the D2 gene was shown to have at least two variants, or alleles, called A1 and A2. They found the A1 allele in the genetic material of 69 percent of the alcoholics studied, compared to only 20 percent of the controls. Blum and Noble theorized that A1 carriers may use alcohol or other drugs excessively to compensate for a reduced ability to absorb pleasure-inducing dopamine.

A study of 862 men and 913 women who had been adopted early in life by nonrelatives identified two types of alcoholism (Boham, Cloninger, von Knorring, & Sigvardsson, 1984). Type I, or milieu-limited, alcoholism is found in both sexes and is associated with alcoholism in either biological parent, but an environmental factor—low occupational status of the adoptive father—also had to be present as a condition for alcoholism to occur in the offspring. Type II, known as male-limited alcoholism, is more severe but accounts for fewer cases. It is found only in men, and it does not appear to be affected by environmental factors.

Vaillant (1983), however, points out the potential biases in the preceding study. He says that the study failed to control for the environmental effect of parental alcoholism. He continues by pointing out that antisocial personality disorder must be distinguished from alcohol dependence and that developmental effects of abusing individuals must be controlled. Furthermore, for his studies, Vaillant excludes individuals with other major psychiatric disorders that could, by themselves, directly contribute to alcohol dependence. Such cases (direct and uncomplicated cases) are estimated to represent 60 to 70 percent of the alcohol-dependent population (Schuckit, 1986).

The notion of Type I and Type II alcoholics hangs, in part, on the age of the onset of alcoholism. Vaillant (1983) found in a study of alcohol-abusing men in inner cities and in college that age of onset and degree of antisocial symptomatology correlated with disturbed family environments but was independent of positive or negative heredity for alcoholism. In other words, this negated the hypothesis that heredity predicts the age of onset. “Alcoholic abuse began 11 years earlier for the socially disadvantaged men with a heredity negative for alcoholism than for the college men with two or more alcoholic relatives.” In other words, early-onset alcohol abusers in inner cities had no more alcoholic relatives than did late-onset alcohol abusers in college. Furthermore, inner-city men were 10 times as likely as the college men to come from multi-problem families, to exhibit traits of sociopathy, to have delinquent parents, and to have spent time in jail.

These findings lead one to ask: “How do biological factors interact with environment to contribute to heavy enough drinking over long enough periods of time to produce physical and psychological dependence?” (Schuckit, 1986). Vaillant (1983) suggests that rather than there being two kinds of alcoholism, there may be (1) genetic loading (predicting whether one develops alcoholism) and (2) an unstable childhood environment (predicting when one loses control of alcohol). (Late onset is less associated with dependence, substance-related problems, hyperactivity, and dysfunctional families in one’s youth.)

Genetic research on addiction shows promise, but it is an incredibly complex activity. Even the most sanguine recent studies still use phrases such as “the gene that may influence alcoholism and addiction” (Science Daily, 2007). The Human Genome Project (HGP), supported by the National Institutes of Health and the U.S. Department of Energy, has been an important impetus in the search for genes related to alcohol behavior (NIAAA, 2000). The research was completed in 2003, but analysis of the data may take several additional years (HGP, 2008).

Sociocultural Theories

There is little high-quality research regarding the macrovariables that seek to explain addiction (Esbensen & Huizinga, 1990). Yet, as we mentioned earlier, almost every known culture has discovered the use of beverage alcohol. “All societies establish a quota of deviance necessary for boundary setting”; rules around alcohol and drug use are a part of boundary setting. The ways in which different societies encourage, permit, or regulate the use of alcohol varies considerably, however.

For the most part, sociocultural theories have been generated by observations of differences or similarities between cultural groups or subgroups. Sociocultural theorists are prone to attribute differences in drinking practices, problem drinking, and alcoholism to environmental factors. For example, socially disorganized communities often fail to realize the common values of their residents and to maintain effective social controls. Therefore, inner-city drug use is more rampant than in the suburbs.

We know that differential rates of alcohol use between genders vary greatly between nations (Bloomfield, Gmel, & Wilsnack, 2006). Unless greater biological differences occur between women, from country to country, or between men, from country to country (a remote possibility), it seems logical that culture is a strong influence on alcohol use.

According to Goode (1972), the social context of drug use strongly influences, perhaps even determines, “four central aspects of drug reality” (p. 3): drug definitions, drug effects, drug-related behavior, and the drug experience. The sociocultural perspective stands in direct opposition to what is called the chemicalistic fallacy—the view that drug A causes behavior X.

Because no object or event has meaning in the abstract, all these central aspects must be interpreted in light of social phenomena surrounding drug use. For example, morphine and heroin are not very different pharmacologically and biochemically. Yet heroin is regarded as a dangerous drug with no therapeutic value, whereas morphine is defined primarily as a medicine. Definitions are shaped by the social milieu surrounding the use of each substance.

People using morphine as an illegal street drug experience a “rush” or a “high” generally unknown to patients using the same drug in a hospital setting. Psychedelic drugs, such as peyote, which are taken for religious purposes (as in some Native American churches), do not typically result in religious or mystical experiences when taken simply to get high. Drugs, according to Goode (1972), only potentiate certain kinds of experiences; they do not produce them. It is important to distinguish between drug effects and the drug experience. Many changes may take place in the body when a chemical is ingested, not all of which are noted and classified by the user. A drug may have a more or less automatic effect of dilating the pupils, causing ataxia or amblyopia, and so on, but the experience is subject to the cognitive system of the user’s mind. A person must be attuned to certain drug effects to interpret them, categorize them, and place them within appropriate experiential and conceptual realms (Goode, 1972). One’s propensity to use drugs, the way one behaves when one uses drugs, and one’s definitions of abuse and addiction are all influenced by one’s sociocultural system. Why else would someone define heroin and LSD as dangerous drugs, yet almost never perceive social drinkers and smokers as drug users?

Supracultural Theories

The pioneering work of Bales (1946) provides some general hypotheses regarding the relationships among culture, social organization, and the use of alcohol. He proposed that a culture that produces guilt, suppressed aggression, and sexual tension and that condones the use of alcohol to relieve those tensions is likely to have a high rate of alcoholism. Bales also believed that collective attitudes toward alcohol use dramatically influence rates of alcoholism. He classified these attitudes as favoring (1) abstinence, (2) ritual use connected with religious practices, (3) convivial drinking in a social setting, and (4) utilitarian drinking (drinking for personal, self-interested reasons). The utilitarian attitude, especially in a culture that induces much inner tension, is the most likely to lead to problem drinking, whereas the other three mitigate against alcohol problems.

Also important in Bales’s (1946) theory is the degree to which a society offers alternatives to alcohol use for the release of tension and for providing a substitute means of satisfaction. A social system with a strong emphasis on upward economic or social mobility will excessively frustrate an individual who has no available means of achieving success. In such a system, high rates of alcohol use would be expected (Tarter & Schneider, 1976).

Unfortunately, few alternatives to alcohol or drugs seem to exist in most modern societies. In traditional societies, such as the hill tribes of Malaysia, a shaman may assist tribesmen in achieving a trancelike state in which endorphin levels are altered (Laderman, 1987). Also at the supracultural level, Bacon (1974) theorizes that alcoholism is likely to be a problem in a society that combines a lack of indulgence of children with demanding attitudes toward achievement and negative attitudes regarding dependent behavior in adults. Another important factor in sociocultural theories is the degree of societal consensus regarding alcohol use. In cultures in which there is little agreement regarding drinking limits and customs, a higher rate of alcoholism is expected (Trice, 1966). Cultural ambivalence regarding alcohol use results in weak social controls and allows the drinker to avoid being labeled as a deviant.

Culture-Specific Theories

According to Room, in “wet” drinking cultures, alcohol is used almost daily, with few restrictions on availability. Conversely, although legal and social restrictions govern drinking in “dry” cultures, binge drinking and even violent drunken behavior may be seen as acceptable (2001). Levin (1989) describes two examples of cultural contrast in attitudes toward drinking: the contrast between French and Italian drinking practices and the contrast between Irish and Jewish drinking practices.

There are many similarities between the French and Italian cultures; both are heavily Catholic and both produce and consume large quantities of alcohol. The French, however, drink wine and spirits, both with meals and without, and both with and away from the family. The French do not strongly disapprove of drunkenness, and they consider it bad manners to refuse a drink. On the other hand, the Italians drink mostly with meals and mostly with family, and they usually drink wine. They strongly disapprove of drunkenness, and they do not pressure people into drinking. As one might expect, France has one of the highest rates of alcoholism in the world, whereas Italy’s rate is only one-fifth as great. (In 1952, Italy had the second-highest rate of wine consumption in the world, consuming only half of the amount of wine consumed in France [Kinney & Leaton, 1987].) The strong sanctions against drunkenness and social control imposed by learning to drink low-proof alcoholic beverages in moderation seems to have something to do with the lower rate of Italian alcoholism.

In a fashion, studies of Irish and Jewish drinking practices draw some sharp contrasts. The Irish have high proportions of both abstainers and problem drinkers, whereas Jews have low proportions of both (Levin, 1989). The Irish drink largely outside the home in pubs; Jews drink largely in the home with the family and on ceremonial occasions. The Irish excuse drunkenness as “a good man’s fault”; Jews condemn it as something culturally alien. Bales found Irish drinking to be largely convivial on the surface, but purely utilitarian drinking was a frequent and tolerated pattern. Jewish drinking, on the other hand, was mostly ceremonial. Again, it is no surprise that the Irish alcoholism rate is one of the highest in the world, and the Jewish rate is one of the lowest (Bales, 1946).

Subcultural Theories

There have been many investigations of sociological and environmental causes of alcoholism at the subcultural level. Within the same culture, a great diversity in alcoholism rates has been related to age, sex, ethnicity, socioeconomic class, religion, and family background (Bloomfield, Gmel & Wilsnack, 2006; Tarter & Schneider, 1976). One of the landmark studies of social variables at this level was conducted more than three decades ago by Calahan (1970). He specified that social environment determines to a large extent whether an individual will drink and that sociopsychological variables also determine the level of drinking. In becoming a problem drinker, variables such as age, sex, ethnicity, and social position influence the probability that a person will learn to drink as a dominant response. Labeling the person as a heavy drinker then reinforces the probability of that response.

Of course, these processes do not occur in isolation from other factors, such as the process of physical addiction. Goode (1984), Laurie (1971), Imlah (1971), and many others have examined the sociocultural context of drug addiction and found there to be many similarities to alcoholism. A major difference is in the outcast nature of certain illicit drug users such as heroin addicts. Users of illegal drugs such as heroin may be more socially isolated than alcoholics because of their addiction. Also, certain types of drug addiction seem to thrive within specific subcultures. Heroin addiction is a persistent problem among jazz musicians. Inner-city youths frequently “huff” spray paint or sniff glue. With three feet of hose and an empty can, Native American youths on certain reservations can easily get high on gasoline fumes.

The impact of gender on drug use presents an interesting perspective on sociocultural theories. Either a culture-specific or subcultural model can be used in explaining the differences between male and female drug-related behaviors in the United States. Historically, female drinking has been less accepted than male drinking in the United States, and being intoxicated is clearly more disapproved of for women than for men (Gomberg, 1986). Similar gender differences exist throughout the world (Bloomfield, Gmel, & Wilsnack, 2006). These double standards may account for the much lower rate of problem drinking noted among women. Social pressure and social stigma may result in less problem drinking by women as a subgroup of the larger U.S. culture.

Some aspects of this phenomenon may be culture specific, however. The fact that men seem to drink more and have more problems because of alcohol in some cultures and not in others fits into a supracultural model of drug use. The degree of female problem drinking appears to be related to cultural norms regarding the overall status of women within different societies. Bear in mind that the vast majority of the research on alcohol and drug abuse has been conducted on men only. Only recently have gender-related issues in this area begun to be systematically examined.

Alternative Explanations

Fingarette (1985) sees alcoholism as “neither sin nor disease.” Instead, he views it as a lifestyle. According to Fingarette, proponents of the disease model describe alcoholism as a disease characterized by loss of control over drinking. Recovery is possible only if one voluntarily seeks and enters treatment and voluntarily abstains from drinking. Only then can one be cured. Cured from what? From a disease that makes voluntary abstention impossible and makes drinking uncontrollable! This, says Fingarette (1985), is an amazing contradiction.

His alternative explanation views the “persistent heavy drinking of the alcoholic as a central activity” of the individual’s way of life. Each person develops his or her unique way of life, which consists of a number of central activities. Some will adopt parenting as a central activity, while others will place sex, physical thrills, or their careers at the center. Why do some people choose drinking as a central feature? Fingarette (1985) says that there is no general answer but that the explanation lies not only in motives but also in a person’s cultural background, life circumstances, special life crises, and physical abnormalities. No single item will be the reason.

Fingarette (1985) believes that it is no harder for the alcoholic to choose to stop drinking than it is for others to abandon activities central to their ways of life. “We should see the alcoholic, not as a sick and defective human being, but as a human being whose way of life is self-destructive. The difficulty we face is stubborn human nature, not disease” (p. 63).

In a similar fashion, Peele (1988) has examined the evidence on addiction and concluded that “we have disarmed ourselves in combating the precipitous growth of addictions by discounting the role of values in creating and preventing addiction and by systematically overlooking the immorality of addictive misbehavior” (p. 224). This is not a revival of the addiction as sin model but an argument that addicts and alcoholics do differ from other people in the ways in which they prioritize their values.

As noted at the outset of this chapter, William S. Burroughs (1977) attempted to answer the question, “why does a person become a drug addict?” in his book Junky. “The answer is that he usually does not intend to become an addict. You don’t wake up one morning and decide to be a drug addict . . . You become a narcotics addict because you do not have strong motivations in any other direction” (p. xv). Schaler (2000) has a similar view of addiction. He denies that there is any such thing as addiction, in the sense of a “deliberate and conscious course of action which the person literally cannot stop doing” (p. xv). He views addiction as a metaphorical disease, not a physical disease.

Stages of Alcoholism

One of the first attempts to describe the development of alcoholism is found in Jellinek’s (1952) study of 2,000 male members of Alcoholics Anonymous. He characterized alcoholism as an insidious disease that progresses through well-defined phases, each with symptoms that develop in the majority of persons in an additive, orderly fashion. In Jellinek’s (1960) model, the drinker progresses through four distinct stages: (1) prealcoholic symptomatic phase; (2) prodromal phase; (3) crucial phase; and (4) chronic phase (see Figure 2.1).

In the prealcoholic symptomatic phase, drinking is associated with rewarding relief from tension or stress, something almost all drinkers engage in occasionally. The person who is more predisposed toward alcoholism (due to chromosomes, culture, or other factors) will tend to increase the frequency of relief drinking over a period of time. At the same time, the drinker develops a physical tolerance to alcohol, so that increasingly larger amounts are needed to bring the same degree of relief from stress or tension.

The onset of blackouts marks the beginning of the prodromal phase. These are periods of amnesia not associated with the loss of consciousness. The drinker may seem to be acting normally, but later have no recall of those events that occurred while in a blackout. This phase is also characterized by an increase in the need for alcohol (and attempts to hide the need for alcohol), surreptitious drinking, and increasing guilt.

The primary hallmark of the crucial phase is loss of control over drinking, as evidenced by the inability to abstain from drinking or the inability to stop once started. During this stage, the drinker often will begin the day’s drinking in the morning, will experience behavior problems in relation to employment and social life, and will frequently seek to avoid family and friends.

The final stage, or chronic phase, finds the drinker intoxicated for several days at a time. Drinking becomes obsessive, and both serious physical and emotional problems are evident. According to Jellinek’s (1960) original model, this is where the alcoholic hits bottom. Although this work was a pioneering effort in the field of alcoholism research, we must remember that Jellinek’s samples were (1) all AA members, (2) all in the latter stages of alcoholism, and (3) all males.

This traditional view of alcohol addiction was supported by many other prominent scholars, however. Mann (1968) described alcoholism as a “progressive disease, which, if left untreated, grows more virulent year by year” (p. 3). Others seem to have conveniently ignored available scientific evidence in making assertions such as “the true alcoholic is no more able to metabolize ethanol than a diabetic can handle sugar” (Madsen, 1974, p. 94). Others conclude that alcoholism is the result of an allergy and that “one does not become an alcoholic: One is born an alcoholic” (Kessel, 1962, p. 128).

Vaillant (1995) was involved in one of the most comprehensive studies of alcoholism. Two samples were observed over a 45-year period, and a third group was observed for 8 years. Among the sample of 110 core-city alcohol abusers, Vaillant identified four patterns: (1) progressive alcoholism; (2) return to asymptomatic drinking; (3) stable abstinence; and (4) atypical, non-progressive alcoholism. Although this study generally supports the developmental or progressive nature of Jellinek’s (1960) model, it is important to note that Vaillant’s study observed both reversibility and non-progressive alcoholism among a substantial proportion of subjects. Over the period of the study, 18 of the 110 subjects returned to social or asymptomatic drinking. (Jellinek himself identified several patterns of problematic drinking as not fitting into a disease model.)

The traditional concept of the nature and progress of addiction to alcohol was also challenged by Pattison, Sobell, and Sobell (1977). Perhaps the major difference in their view of alcohol dependence (a more precise, less value-laden term than addiction), is found in the following two assertions:

The development of alcohol problems follows variable patterns over time and does not necessarily proceed inexorably to severe final stages.

Recovery from alcohol dependence bears no necessary relation to abstinence, although such a concurrence is frequently the case. (pp. 4–5)

FIGURE 2.1

The Natural History of Alcoholism According to Jellinek’s Model Based on Male Members of AA.

Source: From Alcoholism: Development, Consequences, and Interventions, 3/e by N.J. Estes and M.E. Heinemann. Copyright © 1986 Elsevier Ltd.

Thus, a controversy was launched that continues today. Not only did Pattison, Sobell, and Sobell not believe in the disease model, but they also felt that alcohol dependence could be reversed. They pointed to some evidence that certain alcoholics had been able to return to social drinking. They also felt that the unproven assumptions that formed the basis for the traditional concept of alcoholism as a disease had been an impediment to proper treatment.

The Course of Cocaine Addiction

Other models of drug abuse/addiction reduce the number of stages to three: early, middle, and late. Washton’s (1989) model of cocaine addiction describes it as a chronic disease that grows progressively worse if it is not treated. (Chronic indicates that cocaine addiction is never a single-acute episode but is marked by a permanent condition, with a continued vulnerability to recurring symptoms.)

According to Washton (1989), cocaine addiction is progressive and predictable in its course. “The disease of cocaine addiction is chronic, never reverses, and grows progressively more severe if left untreated” (p. 55). In the early stage of addiction, the user’s brain chemistry is altered, withdrawal from normal activities is usually observed, and mood swings occur with increasing frequency. The middle stage of addiction is characterized by loss of control over cocaine use, impaired school or work performance, and denial of the problem. (“I’m not an addict; I just use the stuff a lot!”) One can see that this is roughly comparable to the crucial phase in Jellinek’s (1960) model of alcoholism. The late stage of addiction brings serious behavioral and emotional problems to the user, and it can terminate in severe depression, cocaine psychosis, and death.

A Multicausal Model

Which of these etiological models or explanations of drug abuse is correct? All are probably helpful, at least in a heuristic sense, but no single model or theory adequately explains the phenomenon of dependency or addiction. A significant advance in the study of chemical dependency is the realization that it is probably not a unitary disorder (West, 2006). Pattison and Kaufman (1982) made a strong case for a multivariate model of alcoholism more than two decades ago. Even though there may be similar behavioral topography in all addicted individuals, the etiology and motivation for drug use may differ widely. Available evidence points strongly to the possibility that addiction may be manifest through different mechanisms. Therefore, a model such as the one in Figure 2.2 may be helpful in understanding this phenomenon.

For some individuals, a genetic predisposition or physiological dysfunction is a necessary condition for drug use, drug abuse, and subsequent addiction. On the other hand, some people with disturbances in their personal development or interpersonal orientation but with no known genetic predisposition or biochemical aberration may become addicted to a drug. This debate over which model is really best is valuable only in the sense that it leads one to see the utility in an interdisciplinary, multicausal model.

This model is similar to the public health model, promoted in recent years by health care and other human service professionals. The model conceptualizes the problem of chemical dependency in terms of an interaction among three factors: the agent, the host, and the environment. In most public health areas, the agent is an organism (e.g., a virus), but in this case, it is ethanol. The second factor is the host—the chemically dependent person, including the person’s genetic composition, cognitive structure, expectations about drug experiences, and personality. The last factor consists of the social, cultural, political, and economic variables that affect the use of alcohol or drugs and the resulting consequences. The public health approach involves the examination of the complex interaction of the multitude of variables affecting the agent, the host, and the environment (Hester & Sheehy, 1990).

FIGURE 2.2

A Model of Drug Addiction.

Source: From Alcoholism and Drug Addiction by D. Raistrick and R. Davidson. Copyright © 1985 Elsevier Ltd.