PURPOSE: Emerging work suggests that both environmental and genetic factors contribute to risk of depression in adolescents, and that these factors may differ between genders. We assessed whether features of the social environment (SE), measured at varying levels, and genetic factors jointly contribute to the risk of depression in adolescent males and females. METHODS: Using data from a national survey of U.S. adolescents, we applied cross-sectional, multilevel mixed models to assess the contribution of: (i) 5-HTTLPR genotype and respondent-level building conditions to depressive symptom score (DSS); and (ii) 5-HTTLPR genotype and neighborhood-level building conditions to DSS. Models testing potential gene-SE interactions were also conducted. All models were stratified by gender and adjusted for age, race/ethnicity, family structure, parental education, and social support. RESULTS: Among females, adjusted analyses indicated that sl genotype carriers enjoyed a marginally significant (p = .07) protective effect against higher DSS in models assessing respondent-level building conditions. In contrast, among males, adjusted analyses predicted significantly higher DSS for residents of neighborhoods with relatively poor building conditions (p < .01). No significant gene-SE interactions were detected for either gender. CONCLUSIONS: These results suggest that adverse, macro-level SE factors increase risk of depression to a greater extent in adolescent males than in females. Intervention strategies designed to improve mental health in adolescent populations should consider a growing body of work suggesting that the contextual factors conferring increased risk of depression differ among males and females.
PURPOSE: Emerging work suggests that both environmental and genetic factors contribute to risk of depression in adolescents, and that these factors may differ between genders. We assessed whether features of the social environment (SE), measured at varying levels, and genetic factors jointly contribute to the risk of depression in adolescent males and females. METHODS: Using data from a national survey of U.S. adolescents, we applied cross-sectional, multilevel mixed models to assess the contribution of: (i) 5-HTTLPR genotype and respondent-level building conditions to depressive symptom score (DSS); and (ii) 5-HTTLPR genotype and neighborhood-level building conditions to DSS. Models testing potential gene-SE interactions were also conducted. All models were stratified by gender and adjusted for age, race/ethnicity, family structure, parental education, and social support. RESULTS: Among females, adjusted analyses indicated that sl genotype carriers enjoyed a marginally significant (p = .07) protective effect against higher DSS in models assessing respondent-level building conditions. In contrast, among males, adjusted analyses predicted significantly higher DSS for residents of neighborhoods with relatively poor building conditions (p < .01). No significant gene-SE interactions were detected for either gender. CONCLUSIONS: These results suggest that adverse, macro-level SE factors increase risk of depression to a greater extent in adolescent males than in females. Intervention strategies designed to improve mental health in adolescent populations should consider a growing body of work suggesting that the contextual factors conferring increased risk of depression differ among males and females.
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