BACKGROUND: In adults, about 40% of the variance in risk of Major Depressive Disorder (MDD) is due to genetic factors, but little data exist on the heritability of youth MDD. The goal of this study was the genetic analysis of MDD in an epidemiologically and genetically representative sample of adolescent female twins. METHODS: A sample of 3416 female adolescent twins systematically ascertained from birth records was assessed using a structured telephone interview that included a comprehensive DSM-IV-based section for the diagnostic assessment of MDD. Mean subject age at time of assessment was 15.5 and participation rate exceeded 85%. Genetic modeling was conducted taking into consideration the problem of censoring, i.e., that younger adolescents were not through their period of risk for adolescent onset of MDD. RESULTS: Lifetime self-reported MDD prevalence ranged from 1% under age 12 to 17.4% at age 19 and older. The genetic variance in risk of MDD was 40.4% (95% confidence interval (CI): 23.9-55.1), with the remaining variance explained by non-shared environmental effects 59.6% (95%CI: 44.9-76.1). Shared environmental effects were not significant. A significant recall bias was observed with older respondents on average reporting later onsets for their first episode of MDD. CONCLUSIONS: The genetic and environmental contributions to risk of MDD in this representative sample of female adolescent twins are remarkably analogous to findings from adult samples. These results are congruent with a conceptualization of adolescent MDD and adult MDD as having very similar etiologic determinants.
BACKGROUND: In adults, about 40% of the variance in risk of Major Depressive Disorder (MDD) is due to genetic factors, but little data exist on the heritability of youth MDD. The goal of this study was the genetic analysis of MDD in an epidemiologically and genetically representative sample of adolescent female twins. METHODS: A sample of 3416 female adolescent twins systematically ascertained from birth records was assessed using a structured telephone interview that included a comprehensive DSM-IV-based section for the diagnostic assessment of MDD. Mean subject age at time of assessment was 15.5 and participation rate exceeded 85%. Genetic modeling was conducted taking into consideration the problem of censoring, i.e., that younger adolescents were not through their period of risk for adolescent onset of MDD. RESULTS: Lifetime self-reported MDD prevalence ranged from 1% under age 12 to 17.4% at age 19 and older. The genetic variance in risk of MDD was 40.4% (95% confidence interval (CI): 23.9-55.1), with the remaining variance explained by non-shared environmental effects 59.6% (95%CI: 44.9-76.1). Shared environmental effects were not significant. A significant recall bias was observed with older respondents on average reporting later onsets for their first episode of MDD. CONCLUSIONS: The genetic and environmental contributions to risk of MDD in this representative sample of female adolescent twins are remarkably analogous to findings from adult samples. These results are congruent with a conceptualization of adolescent MDD and adult MDD as having very similar etiologic determinants.
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