The Etiology of Substance Abuse
There are a variety of reasons why any discussion of the etiology of substance abuse must remain somewhat speculative. In the first place, much of the accumulated data are retrospective in nature, that is, gathered (often long) after drug use has begun. Thus, it is difficult to sort out the potential causes for taking drugs from the possible effects of having consumed them. For example, does low self-esteem produce or result from drug abuse? Or, do both variables derive from poor social skills?
Well-controlled cross-sectional designs such as those cited by Block, Block, and Keys (1988) and Kandel (1980) can increase confidence in our etiological suppositions, as can longitudinal research that examines the relationships between personal-social variables and subsequent drug use (e.g., Baumrind, 1990; Shedler & Block, 1990). However, exemplary longitudinal projects are rare and, in any event, do not fully establish causality; there is no methodological substitute for the inability of researchers to randomly assign individuals to the personal-social variables presumably leading to substance abuse.
Yet another obstacle to the construction of a consensually validated etiological theory stems from the manner in which drugs may be classified. For example, some researchers study only alcoholism; others may study more than one drug but categorize them in idiosyncratic ways. Moreover, researchers differ widely in their definition of terms. Some define "abuse" as a single exploratory puff on a pipe full of marijuana; others restrict the term's meaning to chronic addiction. Only the most confirmed optimist would expect to find stable predictors in the wake of shifting criterion variables. Given related issues such as the differing availabilities of certain drugs and the disparate social sanctions their use may engender (e.g., tobacco vs heroin), useful etiological theory may need to be drug specific.
Because of the foregoing difficulties, our goals in this course module are rather modest. We will begin with a review of general behavioral factors that undergird most etiological frameworks, including classical decision theory. Although decision theory can be invoked to support the use of information-based programming (the most common prevention modality of the past two decades), it has not yet been embellished to include more recently published behavioral correlates which at least theoretically contribute to the initiation and maintenance of drug use. We will examine a number of these correlates in closer detail, including a brief review of purported biological determinants of alcoholism, before concluding with a summary of Marlatt's comprehensive etiological framework.
General Behavioral Factors
The sources of reinforcement for taking drugs were catalogued long ago on a theoretical level by Cahoon and Cosby (1972), Horan (1973), and Miller (1973). For example, both physiological positive reinforcement (euphoria) and social positive reinforcement (enhanced peer status) may occur after drug use. Moreover, modeling is an efficient substitute for trial-and-error learning; we needn't experience social reinforcement directly, but rather can readily learn about whatever payoffs exist from watching the behavior of others.
Positive reinforcement may act alone or in conjunction with negative reinforcement; in other words, one might use drugs because of the "reward" that follows or the "pain" that precedes taking drugs. Negative reinforcement, likewise, may be physiological or social, as in warding off a withdrawal reaction or escaping from a noxious home, school, or vocational life. A vicious cycle can easily develop because continual use of drugs usually produces a worsening of one's physical and social condition, which then may be followed by more and more relief-seeking (drug-taking) behavior.
Many current etiological models of substance abuse ultimately derive from one or more of these elementary behavioral factors. For example, the "peer cluster theory" of Oetting and Beauvais (1987) and Lichtenstein's (1982) "natural history of a smoker's career" pay considerable homage to social reinforcement as a precursor to substance abuse. Similarly, escape from ghetto stressors and/or other untoward life events are prominent features of frameworks developed by Lex (1987), Lisansky-Gomberg (1987), Morales (1984), and Rhodes and Jason (1990).
In more recent years these behavioral factors have been given a "cognitive" overlay. It has been argued, for example, that substance abusers differ from users (e.g., social drinkers) both in their (faulty) beliefs about potential benefits of the drug and in their ability to cope with the stress of everyday life (Abrams & Niaura, 1987; Cooper, Russell, & George, 1988; George & Marlatt, 1983; Wilson, 1987). Etiological models and consequent intervention paradigms have become increasingly cognitive and complex.
Many counseling professionals are familiar with the cognitive-behavioral components of classical decision theory applied to the field of career development (e.g., Katz, 1966); however, they may not be aware that classical decision theory provides the basis for an etiological model of substance abuse essential to the logic of information-based prevention programming.
Classical Decision Theory and Drug Use
The behavioral factors underlying drug use mentioned above fit rather comfortably into a classical-decision-theory framework (cf. Broadhurst, 1976; Horan, 1979; Mausner, 1973). In its simplest form, classical decision theory posits that our choice of a given activity rests on the cornerstone concepts of value and probability.
Subjective values are known as utilities and (like reinforcers) may be positive or negative in nature. Indulging in or abstaining from drugs, for example, will result in a variety of utilities. Depending on the particular peer group, drug abstinence might be met with approval or ridicule. Similarly, the physical effects of drug consumption might be perceived as pleasant or aversive. Utilities can be quantified in such a way as to imply that one alternative may be far more desirable than another. If peer approval is important to us and our peer group abhors the use of drugs, and if we perceive the effects of a particular drug to be unpleasant, our choice is obvious. Our choice is much less obvious if our peer group advocates the use of drugs. In this case, our decision would rest on the magnitudes we attach to peer approval and physical comfort.
The foregoing example presumes that the probabilities of the relevant utilities are certain (i.e., equal to 1.0). In many decisions, however, the probabilities of the various utilities accruing are much less than inevitable. For example, "getting caught" with drugs by parents or police might be perceived as quite horrible. However, in a given situation, the odds of this occurring might be very slight. Classical decision theory thus suggests that in choice situations we select the alternative with the highest subjectively-expected-utility (SEU). In other words we qualify our utilities with an estimation of how likely they are to be realized if we implement a given alternative. In deciding whether or not to smoke marijuana on a given occasion, for example, we would: (a) identify the possible positive and negative utilities; (b) weight them (e.g., on a 1 to 10 scale); (c) multiply each utility score by each probability "guesstimate"; and finally (d) select the alternative with the highest perceived payoff (total SEU value).
Although classical decision theory does not proclaim that everyone purposefully goes through the foregoing mental gymnastics prior to choosing, the mathematical relationships involved are good predictors of which alternative we will eventually select (see Bauman, 1980). Curiously enough, classical decision theory not only accounts for what we in fact do; it also has strong implications for what we ought to do. Whenever the former does not correspond with the latter, factors such as irrational utilities or inaccurate probability information can usually be found lurking in the background.
Unfortunately, classical decision theory has not evolved to accommodate newly emerging etiological data in the substance abuse field. How, for example, do faulty child-rearing practices contribute to the development of irrational utilities and what can be done to remediate such irrationality? Consequently, in the behaviorally-oriented substance-abuse literature, classical decision theory is far less popular than the more ambitious formulations of others (e.g., Marlatt, 1978). Let us now turn to a number of environmental and individual correlates upon which more complex etiological models may be built.
Environmental and Individual Correlates
Environmental correlates refer to the influences of family, peers, and availability. A wide variety of family variables apparently contribute to substance abuse by children and adolescents. These include rather obvious factors such as favorable attitudes or actual use of drugs by parents (Barnes & Welte, 1986; Harford, 1984; Harford & Grant, 1986; Kandel & Adler, 1982; Newcomb & Bentler, 1988a; Newcomb, Chou, Bentler, & Huba, 1988) and more circuitous influences such as the absence of perceived parental support, excessive permissiveness, chaotic living conditions, family disruption through divorce or separation, and inconsistent parenting styles (Block, Block & Keyes, 1988; Kovach & Glickman, 1986). Interestingly, disruption per se may be less important when strong mutual attachments exist between parents and their offspring (Hawkins, Lishner, Catalano, & Howard, 1986). Moreover, Baumrind's (1990) data indicate that the presence of such attachments along with coherent and consistent parenting styles are "protective" against substance abuse. As the adolescent matures, the influence of family variables wanes while that of the peer group becomes primary, peaking between the ages of 18 and 21 (Harford, 1984; Kandel, 1980; Kandel & Adler, 1982).
Peer group variables are consistently predictive of substance use (e.g., Newcomb & Bentler, 1986; Newcomb, et al., 1988), undoubtedly through modeling and social reinforcement processes (Harford & Grant, 1986). Indeed, the power of these processes has been experimentally demonstrated on alcohol consumption (Dericco & Garlington, 1977) and in the formation of expressed drug attitudes (Stone & Shute, 1977). Additionally, there appear to be "drug specific" peer subcultures that engage in, for example, alcohol or marijuana, and eschew the use of other substances (Spieger & Harford, 1987).
Availability is also associated with increased consumption of various substances (Spieger & Harford, 1987). For example, living in college dormitories precipitates more drug use than does living with one's parents, presumably because of decreased opportunity (Bachman, O'Malley, & Johnston, 1984). Moreover, Helzer's (1987) review of large scale epidemiological studies in many countries supports the notion that increased availability of alcohol contributes to alcohol-related problems and morbidity rates.
Individual correlates of substance abuse include gender, personality, and cognitive motivations. The role of gender is relatively straightforward; male adolescents abuse more substances, especially alcohol and marijuana, than females (Barnes & Welte, 1986; Newcomb, et. al., 1988, Newcomb, Fahy, & Skager, 1986); however, this is no longer the case for tobacco (Kandel, 1980). Although males and females self-report similar reasons for using drugs (Johnston & O'Malley, 1986), females appear to be more vulnerable to peer and family influences (Kandel, 1986).
Personality variables related to substance abuse have received considerable attention over the past decade (see Block et al., 1988). Many researchers believe there is no evidence for a unitary "addictive personality" (Kandel, 1980; Kandel, 1986; Nathan & Lansky, 1978; Spieger & Harford, 1987), yet Shedler and Block's (1990) exemplary study of 101 young adults tracked from preschool to 18 years of age would seem to suggest otherwise. They sorted abstainers, experimenters, and abusers into distinct diagnostic categories and concluded that the latter "were maladjusted, showing a distinct personality syndrome marked by interpersonal alienation, poor impulse control, and manifest emotional distress." Moreover, differences between these categories "could be traced to the earliest years of childhood and related to the quality of parenting received" (p. 612.
In any event, there is little consensus in the research community about which personality variables contribute to substance abuse. Some argue that there are very few personality precursors, with the most prominent being unconventionality or nonconformity with adult societal expectations (e.g., Baumrind, 1990); others posit characteristics such as sensation seeking (Hawkins et al., 1986), depressed mood (Kashani, Keller, Solomon, Reid & Mazzzola, 1985), and low self-esteem (Hawkins et al., 1986). Still others believe that personality determinants vary with the type of drug abused and the gender of the abuser; for example, personality correlates suggested for marijuana use include rebelliousness, nontraditional values, de-emphasis on achievement, and self-centeredness, while those for other drugs include distancing and distrustfulness for females, and aggressiveness for males (Block et al, 1988). Baumrind (1990) concludes that any role played by personality characteristics is overshadowed by the family variables discussed earlier.
Cognitive variables such as self-reported motivations or reasons for substance use have important intervention implications given their high correlations with actual substance use and the fact that they may differentiate type of substance used, frequency of use, age of user, and stage of use (initiation vs maintenance). For example, reported motivations for alcohol and marijuana abuse include "getting away from problems," while those for cocaine and amphetamines involve "staying alert and awake." Moreover, "self-medicating" motives increase with consumption frequency and age of the abuser; in contrast, younger adolescents and infrequent users commonly cite social cohesion as a reason for use (see Baumrind, 1990; Hawkins et al., 1986; Johnston & O'Malley, 1986; Kovach & Glickman, 1986; Newcomb & Bentler, 1988; Newcomb et al., 1986, 1988).
Biological Determinants of Alcoholism
Research on the biological determinants of alcoholism flows from the assumption that variability in the use and abuse of alcohol arises from genetic and environmental factors and their interactions (Searles, 1988). Four methods of inquiry are typically used: family history (consanguinity), twin, adoption, and, more recently, high-risk-group studies.
Family, twin, and adoption studies have shown a definite "familial" nature to the development of alcoholism, but the relative influence of genetic and environmental factors has not been established. Some reports suggest genetic "links" (e.g., Blum et al., 1990; Goodwin, Schulsinger, Hermansen, Guze, & Winokur, 1973; Kaij, 1960); others demonstrate little or no such influence (see Murray, Clifford, & Gurling's, 1983, extensive review). The lack of consistency here may well be a function of numerous conceptual and methodological flaws. These include, for example, inaccurate determination of zygosity, inadequate diagnostic criteria, inappropriate samples, and poor operational definitions of environmental factors (e.g., Helzer, 1987; Murray et al., 1983; Searles, 1988). Nevertheless, this line of research does suggest that males have a higher vulnerability for the development of alcoholism than females (e.g., Saunders & Williams, 1983). Prior to a recent report indicating the possible presence of a genetic marker for some forms of alcoholism (Blum et al., 1990), no other study has found any biological marker(s) exclusively responsible for the development of alcoholism (e.g., Reed, 1985; Stabenau, 1985; Swinson, 1983.
High-risk-group research rests on an investigative strategy that identifies non-alcoholic individuals who have a family history of alcohol abuse, matches them with a control group having no such family history, and compares these groups on a variety of responses to alcohol ingestion. Emerging differences would presumably serve as "markers" for genetically controlled mechanisms contributing to alcohol abuse. For example, sons of alcoholics rate themselves as less intoxicated and demonstrate smaller decrements in cognitive performance than sons of non-alcoholics, even when there are no significant differences in time to reach peak blood-alcohol-concentration (BAC) levels (Schuckit, 1981). Moreover, on electro-physiological measures, sons of alcoholics demonstrate less alpha wave activity compared to sons of non-alcoholics, suggesting that ethanol may have different reinforcing effects on individuals at high risk for alcoholism (Schuckit, 1987).
It is often the case that investigators report more variability within the groups than between them on biochemical, neuro-psychological, and electro-physiological responses to alcohol ingestion, and one's subsequent susceptibility to later alcohol-related problems. Nevertheless, high-risk-group research has become increasingly prominent since previous attempts to find a genetic marker solely responsible for predisposing a given population to alcohol abuse have not been especially fruitful (Schuckit, 1987).
The Marlatt Model
Marlatt's evolving biopsychosocial model of the addiction process incorporates many of the above-mentioned etiological correlates in an attempt to account for the initiation, maintenance, and change of substance abuse behavior (e.g., Marlatt, 1978; Marlatt, Baer, Donovan, & Kivlahan, 1988). The initiation stage includes both genetic and social factors which place one at risk for addiction. For example, high levels of acetaldehyde may protect against the development of alcoholism in Asians, whereas peer drug use, poor self-esteem, and/or parental sociopathy may predispose one to becoming an addict. The transition and maintenance stage explains the passage from social to deviant usage patterns. The pharmacological effects of the drug, the person's psychological set, and a complex system of physical and social stimuli that comprise the setting in which the drug is consumed are all involved. Initiation of the change process begins as individuals become increasingly aware of the difficulties that drugs have produced in their lives. These negative consequences underlie self-change attempts and/or the seeking of treatment. The success of the active change process(or treatment) is influenced by characteristics of both the patient and the program and whether the two are appropriately matched. Finally, maintenance of successful change primarily involves relapse prevention efforts imbued with the recognition that single lapses are highly probable. We will move on to the topic of intervention (prevention and treatment) after covering how substance abuse is assessed.