Faculty Collaboration Database

Chronic stress exposure and daily stress appraisals relate to biological aging marker p16^INK4a. Psychoneuroendocrinology 2019 Apr;102:139-148

Date

12/18/2018

Pubmed ID

30557761

Pubmed Central ID

PMC6420375

DOI

10.1016/j.psyneuen.2018.12.006

Scopus ID

2-s2.0-85058417542 (requires institutional sign-in at Scopus site)   36 Citations

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 p16^INK4a. Seventy-three adults (M_age = 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 p16^INK4a (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 <  .001), and accumulated daily stress appraisals over the 8-week period (b = 0.013, p =  .02) showed increased p16^INK4a. No significant associations with LTL were found. These findings extend previous work on the impact of stress on biological aging by linking chronic stress exposure and daily stressful experiences to an accumulation of senescent cells. Findings also support the hypothesis that chronic stress is associated with accelerated aging by inducing cellular senescence, a common correlate of age-related diseases.

Author List

Rentscher KE, Carroll JE, Repetti RL, Cole SW, Reynolds BM, Robles TF

Author

Kelly E. Rentscher PhD Assistant Professor in the Psychiatry and Behavioral Medicine department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adult
Aging
Biomarkers
Cellular Senescence
Cyclin-Dependent Kinase Inhibitor p16
Female
Genes, p16
Humans
Leukocytes
Male
Middle Aged
Signal Transduction
Stress, Psychological
Telomere
Telomere Shortening