Abstract
OBJECTIVES: Psychosocial stress is postulated to hasten senescence in part by accelerating the shortening of telomere length (TL). One pathway through which this may happen is via increasing inflammation and innate immune system activation-a pathway which recent studies suggest acts more strongly for those who grew up in low microbial environments. Thus, we hypothesized that: (1) Psychosocial stress will be inversely associated with TL, (2) early life microbial environments will predict TL, and (3) microbial environments will moderate the association between psychosocial stress and TL. METHODS: We utilized data from the Cebu Longitudinal Health and Nutrition Survey based in the Philippines (N = 1410). We determined early life microbial environments by season of birth and exposure to animal feces. Psychosocial stress measures included perceived stress in adulthood, lifetime socioeconomic status (SES), and parental instability in childhood. TL was measured in blood from young adults by qPCR. RESULTS: Contrary to predictions, we found that higher SES was associated with shorter TL and no association of TL with the other stress variables. Individuals born in the higher microbial exposure season had shorter TL, but early life microbial environments did not moderate the association between psychosocial stress and TL. CONCLUSIONS: The unexpected inverse association between SES and TL suggests that higher SES, while indexing lower psychosocial stress, may impact TL more strongly through nonstress factors in the Philippines, such as unhealthy behavior. The inverse association between microbial environments and TL is consistent with other evidence connecting early life infections to decreased life expectancies.