Deconstructing the role of the exposome in youth suicidal ideation: Trauma, neighborhood environment, developmental and gender effects

剖析暴露组在青少年自杀意念中的作用:创伤、邻里环境、发育和性别的影响

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Abstract

Environment (E) is pivotal in explaining variability in brain and behavior development, including suicidal ideation (SI) and behavior. It is therefore critical to systematically study relationships among environmental exposures (i.e., exposome) and suicidal phenotypes. Here, we evaluated the role of individual-level adversity and neighborhood environment and their interaction (E x E) in association with youth SI. Sample included youth (N = 7,054, ages 11-21) from the Philadelphia Neurodevelopmental Cohort, which investigated clinical phenotypes in a diverse US community population. We examined cross-sectional associations of environmental exposures with lifetime history of SI (n = 671), focusing on interactions between individual-level exposures to assaultive trauma (n = 917) and neighborhood-level socioeconomic status (SES) quantified using geocoded Census data. Models included potential confounds and overall psychopathology. Results showed that assaultive trauma was strongly associated with SI (OR = 3.3, 95%CI 2.7-4, p < .001), while low SES was not (p = .395). Both assault and low SES showed stronger association with SI in females, and in early adolescence (all E X gender/age interactions, p < .05). In traumatized youths, lower SES was associated with less SI, with no SES effects on SI in non-traumatized youths (Assault X SES interaction, Wald = 8.19, p = .004). Associations remained significant controlling for overall psychopathology. No single SES variable emerged above others to explain the moderating effect of SES. These findings may suggest a stress inoculation effect in low SES, where youths from higher SES are more impacted by the deleterious trauma-SI association. Determining which environmental factors contribute to resilience may inform population specific suicide prevention interventions. The cross-sectional study design limits causal inferences.

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