Decline in genetic influence on the co-occurrence of alcohol, marijuana, and nicotine dependence symptoms from age 14 to 29.

OBJECTIVE: Cross-sectional studies have demonstrated high rates of comorbidity among substance use disorders. However, few studies have examined the developmental course of incident comorbidity and how it changes from adolescence to adulthood. The authors examine patterns of comorbidity among substance use disorders to gain insight into the effect of shared versus specific etiological influences on measures of substance abuse and dependence.
METHOD: The authors evaluated the pattern of correlations among nicotine, alcohol, and marijuana abuse and dependence symptom counts as well as their underlying genetic and environmental influences in a community-representative twin sample (N=3,762). Symptoms were assessed at ages 11, 14, 17, 20, 24, and 29 years. A single common factor was used to model the correlations among symptom counts at each age. The authors examined age-related changes in the influence of this general factor by testing for differences in the mean factor loading across time.
RESULTS: Mean levels of abuse or dependence symptoms increased throughout adolescence, peaked around age 20, and declined from age 24 to age 29. The influence of the general factor was highest at ages 14 and 17, but decreased from age 17 to age 24. Genetic influences of the general factor declined considerably with age alongside an increase in nonshared environmental influences.
CONCLUSIONS: Adolescent substance abuse or dependence is largely a function of shared etiology. As young people age, their symptoms are increasingly influenced by substance-specific etiological factors. Heritability analyses revealed that the generalized risk is primarily influenced by genetic factors in adolescence, but nonshared environmental influences increase in importance as substance dependence becomes more specialized in adulthood.