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Article Excerpt
CHILDREN OF ALCOHOLICS (COAs) are at an increased risk for developing alcoholism themselves (McGue, 1997; Merikangas and Avenevoli, 2000; Sher, 1997). This association can be explained by both genetic and environmental factors. Twin studies have shown that approximately 40%-60% of the variance in alcoholism is due to genetic factors (Heath, 1995b; Kendler et al., 1992; True et al., 1999b). Of the substantial nongenetic variance that remains, the extant twin and adoption literature has provided more support for nonshared environmental effects than shared (within family) environmental effects (Kendler et al., 1992; Newlin et al., 2000; Prescott and Kendler, 1999; True et al., 1999b).
Several explanations have been offered to account for the lack of evidence for family environmental effects. First, most twin studies of alcoholism have been conducted with older samples, in which genetic influences might be stronger than with adolescent and young adult samples (Heath et al., 1997; Knopik et al., 2004; Rose et al., 2001). Second, reliance on longer-term retrospective reports to capture early family environmental influences may not be able to provide reliable measures of these effects. Third, the classical twin study has an inherent weakness, in that variance due to a gene by shared environment interaction is included in the estimate of additive genetic variance unless explicitly defined and modeled (Eaves et al., 1977; Jacob et al., 2001a; Jacob and Johnson, 1999). Thus, it may be necessary to use more complex analytic procedures with the classical twin design in order to identify gene by environment (G x E) interaction effects (e.g., Boomsma et al., 2002; Heath et al., 1989; Neale and Cardon, 1992; Rose et al., 2001) and to use a21ternative, genetically informative designs that are better suited for identifying family environmental effects and their interactions with genetic influences (Rietveld et al., 2003).
Family influences comprise both family genetic and family environmental (also referred to as "shared environmental" or "between family") effects; the latter are in contrast with environmental influences that are not shared by all siblings in a family and tend to make siblings different rather than similar to one another. Various family environmental effects might influence the eventual development of alcohol-related problems. Alcohol-specific effects include parent modeling of alcohol consumption and/or the development of alcohol expectancies that serve to encourage consumption; examples of alcohol-nonspecific effects are inadequate parenting, child abuse, and socioeconomic adversity. In addition, there are the complex interactions between alcohol-specific and alcohol-nonspecific effects. The hypothesis that alcohol-specific effects play a role in the etiology of alcohol-use disorders (AUDs) is dependent on the presence of parental alcohol consumption during the child's development (Andrews et al., 1993; Ellis et al., 1997).
Based on the above considerations, it might be hypothesized that early exposure to parental AUDs either combines additively with family genetic influences in predicting offspring alcohol outcomes and/or interacts with family genetic influences in accounting for offspring alcohol outcomes. Review of the relevant literature, however, reveals very few efforts to test this hypothesis (e.g., Orford and Velleman, 1990), and, to our knowledge, there have been no studies of this issue in which the study design allows for separation of genetic risk for AUD by virtue of having a biological parent with an AUD and early exposure to pathogenic parental alcohol behavior.
The "children-of-twins" (COT) design (sometimes referred to as a "pseudo-adoption" design; Jacob et al., 2001b) is a genetically informative design that is ideal for examining the issues of genetic, environmental, and gene-by-environment interaction effects in the transmission of alcohol abuse and dependence. In a recently published study making use of twins from the Vietnam Era Twin Registry (VETR; Eisen et al., 1987), their offspring, and the mothers of the offspring, Jacob et al. (2003) reported that absence of an alcoholic family environmental risk (i.e., the rearing father was unaffected) in the presence of high genetic risk (offspring of unaffected twins whose monozygotic co-twin had a history of alcohol dependence) reduced the impact of the genetic diathesis. This finding suggests that family environment may indeed be a risk factor for alcoholism.
The objective of the current study was to examine the role of exposure to paternal alcoholism during the child's formative years (to age 12) in the development of offspring AUD during adolescence and young adulthood using a design allowing for the separation of genetic and nongenetic influences. We hypothesized that family effects are alcohol-specific (e.g., modeling of alcohol use/abuse, the learning of alcohol expectancies, etc.) such that the existence of paternal genetic risk (i.e., history of paternal alcoholism) without exposure to paternal alcoholism during the child's formative years should serve to reduce the child's subsequent risk for AUD.
Method
Subjects
Data for the present study were obtained from our longitudinal twin-family study of alcoholism, which was begun in 1999. The sample consisted of members of the Vietnam Era Twin (VET) Registry, their offspring, and the mothers of the offspring, all of whom participated in a structured diagnostic interview. A complete description of the VET Registry's construction (Eisen et al., 1987; Henderson et al., 1990) and method of determining zygosity have been reported elsewhere (Eisen et al., 1989). Details of the offspring sample have also been previously reported (Jacob et al., 2003; Sartor et al., 2003; Scherrer et al., 2004).
Male twin pairs were eligible for study participation if one or both members of a pair were identified as having a lifetime diagnosis of Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-III-R; American Psychiatric Association, 1987), alcohol dependence (AD), which was derived from a 1992 telephone administration of the Diagnostic Interview Schedule (Harvard Drug Study [HDS]; Tsuang et al., 1996). The cohort also included a random sample of twin pairs in which neither co-twin had AD. At least one member of each twin pair...
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