Stress exposure during childhood and adulthood is linked to increased risk for lifetime disease and shortened telomere length. Shortened telomere length may be involved in the relationship between lifetime stress exposure and an increased risk for disease. The authors conducted a longitudinal study to examine telomere length reduction over time and how it may be related to the total count, duration (acute or chronic), timing (childhood or adulthood), and perceived severity of stressors. A large count of severe, chronic, childhood lifetime stressors significantly predicted shortened telomere length over time.
Many retrospective studies have demonstrated lifetime stressors increasing the risk for future development of psychiatric and physical disorders. Moreover, they have demonstrated how childhood stressors, and trauma in particular, predict shorter telomere length. However, no studies have examined how cumulative stressors change telomere length, especially how the number, duration, timing, and perceived severity of stressors factor in.
Telomeres are the protective caps at the ends of chromosomes that shorten from cell division/replication. Shortened telomeres are linked to increased risk of psychopathology (i.e., depression) and cardiovascular disease.
Participants included 91 mothers of children diagnosed with Autism Spectrum Disorder and 92 mothers of neurotypical children. At baseline, participants provided a blood sample for leukocyte telomere length (LTL) assessment and completed a clinical interview; they were then followed up 24 months after baseline. The Stress and Adversity Inventory for Adults (Adult STRAIN) was used at baseline to assess past stressors. The Current Stressors Checklist (CSC) was used to assess for new stressors at 24 months. A third of the participants took a 4-session mindfulness treatment 6 months prior to the 24-month follow-up.
At baseline, caregivers (of autistic children) had significantly higher counts and severity of chronic and adulthood stressors over their lifetime. The number and severity of acute stressors did not differ between the groups. A greater count and severity of chronic childhood (particularly age 0-12 years) predicted shorter baseline leukocyte telomere length (LTL) as well as greater LTL attrition over time.
A greater count and severity of lifetime chronic stressors were linked to lower baseline LTL and LTL attrition. Moreover, chronic stressors during childhood were particularly significant predictors of LTL attrition and baseline length. In contrast, cumulative stress exposure during adulthood (including chronic) did not predict LTL shortening. Childhood adversity may play a larger role than adulthood adversity in telomere length, but more research is warranted.
Childhood is a sensitive developmental stage, so chronic adversity can have negative biopsychosocial effects (i.e., increased threat appraisals) that persist into adulthood and change telomere dynamics (i.e., alter repair mechanisms).