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. 2008 Jun;65(6):674-82.
doi: 10.1001/archpsyc.65.6.674.

Genetic and environmental influences on alcohol, caffeine, cannabis, and nicotine use from early adolescence to middle adulthood

Affiliations

Genetic and environmental influences on alcohol, caffeine, cannabis, and nicotine use from early adolescence to middle adulthood

Kenneth S Kendler et al. Arch Gen Psychiatry. 2008 Jun.

Abstract

Context: While both environmental and genetic factors are important in the etiology of psychoactive substance use (PSU), we know little of how these influences differ through development.

Objective: To clarify the changing role of genes and environment in PSU from early adolescence through middle adulthood.

Design: Retrospective assessment by life history calendar, with univariate and bivariate structural modeling.

Setting: General community.

Participants: A total of 1796 members of male-male pairs from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders.

Main outcome measures: Levels of use of alcohol, caffeine, cannabis, and nicotine recorded for every year of the respondent's life.

Results: For nicotine, alcohol, and cannabis, familial environmental factors were critical in influencing use in early adolescence and gradually declined in importance through young adulthood. Genetic factors, by contrast, had little or no influence on PSU in early adolescence and gradually increased in their effect with increasing age. The sources of individual differences in caffeine use changed much more modestly over time. Substantial correlations were seen among levels of cannabis, nicotine, and alcohol use and specifically between caffeine and nicotine. In adolescence, those correlations were strongly influenced by shared effects from the familial environment. However, as individuals aged, more and more of the correlation in PSU resulted from genetic factors that influenced use of both substances.

Conclusions: These results support an etiologic model for individual differences in PSU in which initiation and early patterns of use are strongly influenced by social and familial environmental factors while later levels of use are strongly influenced by genetic factors. The substantial correlations seen in levels of PSU across substances are largely the result of social environmental factors in adolescence, with genetic factors becoming progressively more important through early and middle adulthood.

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Figures

Figure 1
Figure 1
The frequency of any use of caffeine, alcohol, nicotine, and cannabis by year from ages 9 to 41 years.
Figure 2
Figure 2
Test-retest reliability for level of nicotine, alcohol, caffeine, and cannabis use for ages 11 to 35 years (n=142) as assessed by polychoric correlations. Error bars indicate ±1 SE.
Figure 3
Figure 3
Polychoric correlations±1 SE in monozygotic (MZ) twins and dizygotic (DZ) twins for the average daily number of caffeine-containing drinks for ages 9 to 35 years (A), the average daily number of cigarettes for ages 13 to 35 years (B), the average number of alcoholic drinks consumed per month for ages 14 to 35 years (C), and the average number of units of cannabis consumed per month for ages 14 to 35 years (D).
Figure 4
Figure 4
Parameter estimates ± 1 SE for the contributions to variation in liability to psychoactive drug use of additive genetic effects (a2), familial environmental factors (c2), and the individual-specific environment (e2) by year for the average daily number of caffeine-containing drinks for ages 9 to 35 years (A), the average daily number of cigarettes for ages 13 to 35 years (B), the average number of alcoholic drinks consumed per month for ages 14 to 40 years (C), and the average number of units of cannabis consumed per month for ages 14 to 35 years (D). The actual parameter estimates are depicted by the black lines, and the colored regions represent the possible range of estimates ± 1 SE.
Figure 5
Figure 5
The polychoric correlation in individual twins between different forms of psychoactive drug use from ages 10 to 35 years.
Figure 6
Figure 6
Parameter estimates ± 1 SE for the contributions to covariation in liability to pairs of psychoactive drug use of additive genetic effects (a2), familial environmental factors (c2), and the individual-specific environment (e2) by year for ages 14 to 35 years for alcohol-cannabis (A), nicotine-cannabis (B), nicotine-alcohol (C), and nicotine-caffeine (D). The actual parameter estimates are depicted by the black lines, and the colored regions represent the possible range of estimates ± 1 SE.

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