Extending the vulnerability-stress model of mental disorders: three-dimensional NPSR1 × environment × coping interaction study in anxiety.

摘要: Background The general understanding of the ‘vulnerability–stress model’ mental disorders neglects modifying impact resilience-increasing factors such as coping ability. Aims Probing a conceptual framework integrating both adverse events and in an extended ‘vulnerability–stress–coping disorders, effects functional neuropeptide S receptor gene (NPSR1) variation (G), early adversity (E) (C) on anxiety were addressed three-dimensional G × E C model. Method In two independent samples healthy probands (discovery: n = 1403; replication: 630), interaction NPSR1 rs324981, childhood trauma (Childhood Trauma Questionnaire, CTQ) self-efficacy measure ability (General Self-Efficacy Scale, GSE) trait (State-Trait Anxiety Inventory) was investigated via hierarchical multiple regression analyses. Results samples, differed function genotype, CTQ GSE score β 0.129, P 3.938 10−8; 0.102, 0.020). A allele carriers, relationship between moderated by self-efficacy: higher resulted low scores, lower levels. turn, TT homozygotes displayed increased unaffected self-efficacy. Conclusions Functional are suggested prime moderators vulnerability–stress model anxiety, further modified protective effect This approach – introducing additional dimension shaping risk constellation, thus suggesting might inform targeted preventive or therapeutic interventions strengthening to promote resilient functioning.