Genetic and environmental sources of covariation between early drinking and adult functioning.

Abstract

The vast majority of individuals initiate alcohol consumption for the first time in adolescence. Given the widespread nature of its use and evidence that adolescents may be especially vulnerable to its effects, there is concern about the long-term detrimental impact of adolescent drinking on adult functioning. While some researchers have suggested that genetic processes may confound the relationship, the mechanisms linking drinking and later adjustment remain unclear. The current study utilized a genetically-informed sample and biometric modeling to examine the nature of the familial influences on this association and identify the potential for genetic confounding. The sample was drawn from the Minnesota Twin Family Study, a longitudinal study consisting of 2,764 twins assessed in two cohorts at regular follow-ups from age 17 to age 29 (older cohort) or age 11 to age 29 (younger cohort). A broad range of adult measures was included assessing substance use, antisocial behavior, personality, socioeconomic status, and social functioning. A bivariate Cholesky decomposition was used to examine the common genetic and environmental influences on adolescent drinking and each of the measures of adult adjustment. The results revealed that genetic factors and non-shared environmental influences were generally most important in explaining the relationship between adolescent drinking and later functioning. While the presence of non-shared environmental influences on the association are not inconsistent with a causal impact of adolescent drinking, the findings suggest that many of the adjustment issues associated with adolescent alcohol consumption are best understood as genetically-influenced vulnerabilities.

A Co-Twin Control Study of the Relationship Between Adolescent Drinking and Adult Outcomes

“…At age 29, outcomes were selected based on other prospective studies that incorporated distinct measures of substance use, antisocial behaviors, socioeconomic standing, mental health, and social relationships (e.g., Chatterji, 2006;Dogan et al, 2010;Green et al, 2016;Skogen et al, 2016). The reliability and validity of the selected measures are discussed in more detail in Hicks et al (2010), Foster et al (2014), and Waldron et al (2017), as well as the supplementary material.…”

“…As discussed above, given the possibility that preexisting childhood differences within a twin pair could confound the 1 In Table 1, the descriptive statistics and regression of the adult outcomes on the ACI were originally reported in Waldron et al (2017); they are duplicated here merely for reference. The novel analyses are the regression of the adult outcomes on measures of early alcohol use.…”

“…A handful of recent studies (e.g., Richmond-Rakerd et al, 2016) have incorporated biometric modeling to determine the familial source of the co-variation between adolescent drinking and later functioning. Most recently, Waldron et al (2017) demonstrated that genes were important for explaining the relationship between a measure of adolescent alcohol consumption and adult outcomes, underscoring that genetic confounding is a potential concern that should be addressed in studies of the impact of adolescent alcohol use.…”

“…The current study sought to address limitations of the literature thus far and build on previous work (see Waldron et al, 2017) by implementing the fi rst known longitudinal prospective co-twin control study of adolescent drinking and functioning in later adulthood. Although Waldron et al (2017) used the current sample for biometric analyses of adolescent alcohol consumption and adult functioning, they did not incorporate measures of initiation, preventing comparisons of different adolescent drinking phenotypes.…”

“…The current study sought to address limitations of the literature thus far and build on previous work (see Waldron et al, 2017) by implementing the fi rst known longitudinal prospective co-twin control study of adolescent drinking and functioning in later adulthood. Although Waldron et al (2017) used the current sample for biometric analyses of adolescent alcohol consumption and adult functioning, they did not incorporate measures of initiation, preventing comparisons of different adolescent drinking phenotypes. In addition, where biometric analyses use structural equation modeling to describe latent genetic or environmental influences, co-twin control studies are based on a counterfactual model that explicitly tests whether associations are due to confounding factors or exposure-this conceptual interpretation of the co-twin analyses is important given the need to gauge the causal impact of adolescent drinking.…”