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.
| Original language | English (US) |
|---|---|
| Article number | e23145 |
| Journal | American Journal of Human Biology |
| Volume | 30 |
| Issue number | 5 |
| DOIs | |
| State | Published - Sep 1 2018 |
Funding
New analyses funded in part by National Institute of Child Health and Human Development training, Grant/Award Number: T32 HD007543; Center for Studies in Demography & Ecology; qPCR laboratory analyses were funded by NSF (Doctoral Dissertation Improvement, Grant/Award Number: BCS-0962282; Wenner-Gren Foundation; data and sample collection funded by NIH, Grant/Award Numbers: TW05596, DK078150, RR20649, ES10126, DK056350 information New analyses funded in part by National Institute of Child Health and Human Development training, Grant/Award Number: T32 HD007543; Center for Studies in Demography & Ecology; qPCR laboratory analyses were funded by NSF (Doctoral Dissertation Improvement, Grant/Award Number: BCS?0962282; Wenner-Gren Foundation; data and sample collection funded by NIH, Grant/Award Numbers: TW05596, DK078150, RR20649, ES10126, DK056350 We thank Karen Mohlke for sharing aliquots of extracted DNA and genetic information. Eleanor Brindle, Thom McDade, Zaneta Thayer, Ben Trumble, Ben Campbell, Tiffany Pan, Hilary Bethancourt, Dan Grunspan, Rebecca Ortega, Peter Rej, and Amy Klegarth provided valuable feedback on earlier iterations of this work. We thank the many researchers at the Office of Population Studies, University of San Carlos, Cebu, the Philippines, for their central role in study design and data collection, and the Filipino participants, who provided their time and samples for this study.
ASJC Scopus subject areas
- Anthropology
- Genetics
- Ecology, Evolution, Behavior and Systematics
- Anatomy
