Engs, Ruth C. [Ed.], "Controversies in the Addition's Field. CHAPTER 5: Howard L. Blane, Ph. D. Environmental Basis for Alcoholic Disorders: Future Prospects

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Environmental Basis for Alcoholic Disorders: Future Prospects*

Howard 1: Blane, Ph. D.

After making a broad case for the historical importance of studying environment in the etiology of alcoholism and related problems, this chapter describes developments in alcohol research during the 1980s as a prelude to focusing upon the environmental aspects of family history of alcoholism as a risk factor for alcoholic disorders. Environmental bases for alcoholic disorders may be sought in sociocultural, social interactional, and psychological factors and models. An emphasis on environment hardly precludes the contribution of biological factors, including genetic and congenital aspects. Indeed, modem alcohol research (that is, since the 1940s) is perhaps unique in that it traditionally viewed alcohol problems as multiply-determined, the product of the interactions between biololgical, psychological, social, and cultural factors, though it was rare that this paradigm guided research. More typically scientists pursued topics within the scientific conventions and agendas of their owndisciplines, with little consideration of contributions, corroborations, contradictions, or interactions from or with other levels of inquiry. In the past decade, however, there is considerable evidence that this situation is changing and an increasing amount of research involves interdisciplinary protocols. Nonetheless, the case for the influence of environmental factors in and of themselves is strong and compelling, founded on research findings accumulated over the years and derived from differing methods, approaches, and social-behavioral disciplines. This vast body of research and theory is touched upon briefly in order to treat more fully recent developments in family history research that are now energizing etiological research.

Sociocultural factors may be seen as establishing the conditions that shape the incidence and prevalence of alcoholic disorders as well as the social boundaries or definitions within which such disorders are expressed. The production, distribution, and cost of alcoholic beverages and

*Preparation of this chapter was supported in part by a grant (AA 06114) from the National Institute on Alcohol Abuse and Alcoholism.


the sanction structure which accompanies them—in a word, availability —comprise of thes conditions. They are the product of complex and incompletely understood processes involving cultural and social values and beliefs and the interplay of political, economic, and religious institutions. A commonly cited example is the near complete absence of drinking and alcoholism in Muslim societies. The total or almost total nonavailability of alcohol in these societies derives from religious proscriptions against alcohol permeating all political, legal, and social structures, thereby creating the extreme of a true abstinence society. Deviations from the near-universal norm are treated harshly without extenuation, but with popular approval. This example illustrates the power sociocultural forces can exert in the determination of behavior regarding the use, or nonuse, of alcoholic beverages.

The forms that drinking and alcoholic disorders assume among individuals are highly varied across and within societies; these variations can be reliably traced to cultural beliefs and values. The classic treatment of such variations and their nonbiological explanation is MacAndrew's and Edgerton's Drunken Comportment( 1969). The wide differences in alcoholism rates among societies where alcohol is readily available are most parsimoniously explained within a socialization of cultural values framework. For instance, the oft-quoted and repeatedly substantiated resistance of Jews to alcoholism, despite the fact that drinking is not prohibited and most of them drink, has been variously attributed to sanctions against drunkenness and excess, the need to maintain vigilance against external incursions, and the value placed upon experiences that enhance and expand rather than dull and narrow mental function. In the case of the Jews, the strength of the forces involved are apparently so great that they have withstood prolonged contact with and extensive assimilation into cultural and societal contexts that include heavy drinking and proneness to alcoholic disorders. This is not always the case: Italian-Americans and Irish-Americans, for example, each show different ways of accommodating to the shift from Europe to the United States (Blane, 1977). The former appear to have adopted a unique pattern that blends both traditional Italian and American drinking norms with a consequent reduction of the high cirrhosis rates characteristic in Italy. Irish-Americans, on the other hand, perhaps as the consequence of fewer socioeconomic constraints in the States, show much higher rates of cirrhosis and other indicators of severe alcoholism than in Ireland. Culture-based arguments and research have been advanced to explain alcohol problem rates in other societies such as the wine-drinking cultures of the Mediterranean, Scandinavia, and other European countries.

At psychological and social levels of analysis, the independent contribution of nonbiological variables


to almost every aspect of the human response to alcohol has been demonstrated; the findings are robust and many have been replicated. Areas relevant to alcoholic disorders include the importance of socialization influences on problem drinking in adolescence and early adulthood (e.g., Barnes, 1990; Huba and gentler, 1982; Donovan, R. Jessor, and L. Lessor, 1983); early dispositional and social influences on subsequent development of alcoholism (e.g., Fillmore,1975; Jones, 1968; 1971; Kammeier, Hoffmann, and Loper, 1973; W. McCord and J. McCord, 1960); and learning influences on the phenomena of tolerance and withdrawal (e.g., Siegel, 1979; Solomon, 1977; Vogel-Sprott and Sdao-Jarvie, 1989).

Against this backdrop of significant contributions to environmental interpretations of alcoholic disorders, the decade of the 1980s witnessed en upsurge in the vitality and maturity of alcohol research. The qualitative advance was undoubtedly the product of ten years of prior investment in alcohol-related research by the Federal government. Substantively, it was related to the excitement engendered in the early 1980s by new scientific developments represented in the rethinking or initiation of a profusion of psychosocial models and associated research (Blanc and Leonard, 1987),the tremendous interest in the genetics of alcoholism (e.g., Cloninger, 1987; Schuckit, 1985), and a variety of methodological improvements and refinements. These latter included the increased availability of statistical tools that permit the testing of complex models; greater concern with antecedent-consequent relationships and a corresponding emphasis on planned longitudinal designs, thereby raising confidence in causal attributions; heightened attention to issues of population definition and sampling in order to enhance generalizability; and more emphasis on multimethod measurement and convergent/divergent findings to strengthen the stability of interpretations and to identify potentially important discrepancies.

From an environmental perspective one of the most fascinating and promising lines of inquiry with regard to the etiology of alcoholic disorders is represented by the tremendous outpouring of research on children of alcoholics (COA). Much of the impetus for this efflorescence has been the results of twin and adoption studies that showed higher concordance for alcoholism among monozygotic than dizygotic twins and a high incidence of alcoholism among offspring of alcoholics adopted into nonalcoholic families during infancy (for a critical review of this research, see Searles, 1988). These studies indicated a genetic basis for alcoholism. A concomitant determinant of the outpouring of research on COAs comes from the results of clinical research which has repeatedly shown the high incidence of alcoholic relatives in the histories of alcoholics in treatment.


A third but as yet subsidiary influence has been the highly popular, partly entrepreneurial movement within the provider community around child, adolescent, and adult COAs. This movement includes a national network of author-lecturers, workshops, regional and national meetings, and among adult COAs in particular an associated demand for services, especially group therapy. Research on COAs and family transmission of alcoholism has concentrated upon personality, temperamental, neuropsychological, and behavioral aspects and upon family processes facilitating or inhibiting transmission of outcomes.

Even though recent years have witnessed a tremendous growth in the quantity of research on COAs, it must be acknowledged that this area of investigation is just beginning to develop the conceptual-empirical basis for endeavors that may lead to major advances in our understanding of etiology. In summarizing a recent review of research on COAs, Kindle Searles (1990) conclude: "...COA research...is in its infancy..., many contradictory findings have been reported within each of the disciplinary domains,...relatively few theoretical approaches have been articulated formally with propositions tested to any degree of certainty, and...little evidence exists to suggest the kinds of preventions and interventions that are most likely to be helpful to COAs." (p.217). Part of the problem is that much COA research to date has compared late adolescent or young adult subjects with a family history of alcoholism (usually a parent, but a variety of schemes involving primary or secondary relatives have been used) to those without a family history on variables of convenience (e.g., drinking variables, personality and temperament measures, neuropsychological performance). The underlying assumption is that parental alcoholism (regardless of type, severity, length, course, etc.) will exert an effect (typically, an implicitly direct effect) on a behavior or domain of interest even though the nature of exposure to alcoholic family environment is unknown, cannot be inferred, and is undoubtedly highly variable across subjects. It is not surprising that "many contradictory findings have been reported."

This line of inquiry is nonetheless compelling because it serves to focus etiologic research, bringing to the fore the notion of risk and outcome within the context of human development. As the research has evolved, it has become evident that both risk and outcome are more complex than early studies and their rationales would suggest. Family history of alcoholic disorder may be best construed as a convenient and empirically useful starting point, an index of risks baying to do with family processes and structure that affect child development. Outcomes have, as noted, been almost exclusively studied in adolescent and young adult samples; these distal outcomes implicitly assume some unifomm and linear relation


ships between events in infancy, childhood, and early adolescence. Developmentalists would be quick to point out that such inferences, unless deeply embedded in theory and empirical evidence, are dubious at best. At this early stage of zeroing-in on the investigation of risk and outcome, then, there are not only needs for greater precision in our handling of the definition and measurement of risk and outcome, but a major need to conceptualize what occurs between risk and outcome. A more profitable route will be the emergence of concern with suboutcomes phenomenally unrelated to alcohol use that are more proximal to causal processes and which can be ultimately linked to alcoholic outcomes. Such an approach would be guided by conceptualizations of the developmental linkages between relevant suboutcomes and processes. This is to say, that before family history can confidently be linked to alcoholic disorders, the elucidation of mechanisms, processes, and behaviors that occur at various stages of development and the developmental connections among them is necessary.

One way of thinking about these issues is to assume that parental alcoholism creates disruption in family structure, function, and process, and that disruption affects the child negatively. The first proposition has substantial support in the alcohol literature (e.g., Jackson, 1954; Jacob and Leonard, 1988; Steinglass, Bennett, Wolin, and Reiss, 1987), although it is not clear whether disruptive effects are specific to parental alcoholism as contrasted to other parental psychopathology or other parental conditions that may disrupt the family. The case for the effects of disruption on the child is, of course, far less clear. If such effects do occur, they could assume a direct influence on the child (e.g., alcoholic father's aggression toward child) or an indirect influence through their effects on other family members (e.g., nonalcoholic mother assumes spouse's functions as well as her own, consequently neglecting child). The modes of influence can occur in at least three ways:

The general implications of these considerations for methods include the adoption of developmental designs that articulate life stages beginning at birth, attention to underlying constructs that change phenomenally with growth (a case in point involves the relationships between activity levels, hyperactivity, attention deficit disorder, conduct disorder, and antisocial behavior or sociopathy), and the associated issue of employing measures appropriate to developmental level.


Of course the factors such a finer-grained approach must consider will depend upon the requirements of each investigation, but there are several factors that are important for any study falling within this line of inquiry. Key among these are

Specification of the nature of parental alcoholic disorder is particularly important: severity of alcoholism; aspects of family function that have been affected: whether drinking is steady or binge, occurs at home or outside the home; which parent is alcoholic; if the mother is the alcoholic, possible fetal alcohol effects on the child must be considered. Unfortunately, it is rare that these variations have been systematically taken into account. The effects of drinking on parental function (i.e., the question of disruption) requires specification: role function disruption; assumption of additional functions by the nonaffected spouse; parental conflict about drinking; behavioralinteractional differences between drinking and sober states as such differences relate to consistency or inconsistency of family climate or as they relate to the integrative influences of drinking noted by some observers; specifity of effects.

Knowledge concerning the developmental stage of the child when parental alcoholism is active is critical if we are to understand its impact on COA outcomes. Each developmental phase identifies areas of salient child function and growth, areas that may be adversely affected by disruption, and which in turn may affect later developmental stages. It is likely that the earlier the disruption, the more severe the effects; similarly, the longer the child is exposed to disruptive influences, the more severe the outcome. While the general thrust of COA research has been on alcoholic outcomes, it is equally important to identify nonspecific outcomes and the processes engendering them. Candidates include antisocial personality, depression, and poor social skills. The developmental precursors to both specific and nonspecific outcomes will vary according to developmental state of exposure. This issue has received virtually no attention in COA research. (For more detailed discussion of these issues, see Kindle and Searles (1990), pages 227-229).

One source of the contradictory findings common in COA research relates to the nature of the samples that have been studied. Samples have for the most part been recruited from one of the three sources: children of alcoholics in treatment; adult COAs attending treatment; and adolescent and adult COAs drawn from populations of convenience or from defined population samples often recruited for other purposes. Generalizability is a problem for an but the general population samples. Further complications include measurement techniques for identifying parental alcoholism


that range widely in quality and the relevance and/or quality of measurement of key variables, especially those for general population samples. (See Tarter, Laird, and Moss, (1990), pages 75-76 for a more detailed discussion of sampling issues). Tentatively, it appears that COAs identified on the basis of their parents being in treatment are at higher risk for alcoholic and other negative consequences than those identified in general population samples. If this is the case it becomes important that both types of samples be studied, with the explicit caveat that the samples represent different populations. The question of sampling for very young COAs is a vexing but critical one in terms of the foregoing discussion. Perhaps general population samples can be recruited by screening attendees of prenatal clinics (a likely bias is underrepresentation of lower socioeconomic status subjects) or obstetric delivery services. Young children (say, five years old or younger) of alcoholics in treatment could be recruited from alcoholism treatment units, with due attention to social class differences. Centering etiological alcoholism research early in life is rare indeed; except for some studies of fetal alcohol effect, our only example is Zucker's pioneering theoretical efforts (Zucker and Noll, 1982) and the research that has proceeded from them (Zucker, 1987).

In any event, environmentally-oriented research on the familial transmission of alcoholism, variously referred to as COA research or highrisk research, seems to have reached the endpoint of its initial groundbreaking stage. On the one hand, there appears to be some disarray in terms of a plethora of contradictory findings, lack of conceptual focus with an accompanying overflow of a theoretical descriptive studies, and weak methodologies. On the other, there are several syntheses of the work accomplished thus far that go a long way toward putting family transmission research on a much more solid and sophisticated foundation (e.g., Russell, 1990; Jacob, Seilhamer, and Rushe, 1989). These syntheses indicate the wealth of research opportunities that exist, propose methods and conceptualizations to realize these opportunities, and clarify issues in ways that further accentuate a focus on risk and outcome within a developmental framework.

This chapter suggests a family environment perspective based on the notion that disrupted alcoholic family function affects the child negatively not only with regard to alcohol use but in other psychological and social functions as well. It also suggests that a focus on interactional, modeling, and bidirectional influences in infancy and early childhood is a necessary step in deciphering the "environmental code" that underlies the etiology of alcoholic disorders.



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