LAUSR

Background Telomeres have been reported to be shorter in individuals exposed to psychosocial stress and in those with depression. Since negative environmental stress is a risk factor for depression, the present study tested whether stressors in childhood (CA) and recent adulthood (NLE) predicted telomere attrition directly and/or indirectly through individuals’ depressive status 3-6 years before TL measurement; and then if social interaction and coping strategies in adulthood influenced the relationship between depressive status and TL. Methods Participants were 337 individuals with a recent depression diagnosis and 574 screened controls that derived from a longitudinal population-based cohort study conducted in Stockholm, Sweden. Relative TL was determined using qPCR. Relationships between key variables stressors, depressive status, social interaction, coping strategies and TL were explored by path analysis in males and females, adjusting for age. Results The key variables were correlated in expected directions. In females, depressive status and age had direct negative effects on TL (p Discussion Our study consolidates previous findings that TL is shorter in depression. In other words, exposure to environmental stress is associated with higher risk of depression, which in turn associates with shorter TL. While in females there was no statistically significant pathway through social interaction or coping strategy, in males, depressive status was associated with TL through AVSI, AVAT and the coping strategy worry. In addition, in males CA had a significant indirect effect on TL through AVSI, AVAT and depressive status. This sex difference in pathways might be explained by the sex differences in social-cognitive styles, coping or reaction to stress and relationship provisions. Good social relationships play a positive role in reducing the impact of stress and in turn enhance well-being and health habits, whereas weak social interactions and corresponding improper coping relate with the dysregulation of stress- responsive biological systems e.g. the HPA axis and inflammation. Previous studies have linked the dysfunction of these biological systems to accelerated telomere erosion.