Chronic stress exposure and daily stress appraisals relate to biological aging marker p16INK4a.

ABSTRACT: Previous research has linked exposure to adverse social conditions with DNA damage and accelerated telomere shortening, raising the possibility that chronic stress may impact biological aging pathways, ultimately increasing risk for age-related diseases. Less clear, however, is whether these stress-related effects extend to additional hallmarks of biological aging, including cellular senescence, a stable state of cell cycle arrest. The present study aimed to investigate associations between psychosocial stress and two markers of cellular aging-leukocyte telomere length (LTL) and cellular senescence signal p16INK4a. Seventy-three adults (Mage?=?43.0, SD?=?7.2; 55% female) with children between 8-13 years of age completed interview-based and questionnaire measures of their exposures to and experiences of stress, as well as daily reports of stress appraisals over an 8-week diary period. Blood samples were used to assess markers of cellular aging: LTL and gene expression of senescent cell signal p16INK4a (CDKN2A). Random effects models covarying for age, sex, ethnicity/race, and BMI revealed that participants with greater chronic stress exposure over the previous 6 months (b?=?0.011, p?=? .04), perceived stress (b = 0.020, p?

SUBMITTER: Rentscher KE 

PROVIDER: S-EPMC6420375 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature