Childhood adversity heightens the impact of later-life caregiving stress on telomere length and inflammation.

摘要

OBJECTIVE: To address the question of whether childhood abuse and other adversities have lasting, detectable consequences for inflammation and cell aging late in life, and whether the effects are large enough to be discernible beyond that of a major chronic stressor, dementia family caregiving. Previous research on the physical health consequences of childhood abuse and other adversities has been based on data from young or middle-aged adults. METHOD: In this community sample of 132 healthy older adults (mean age = 69.70 years; standard deviation = 10.14), including 58 dementia family caregivers and 74 non-caregivers, blood samples were analyzed for interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and telomere length, a measure of cell aging. Depressive symptoms were assessed by the Center for Epidemiological Studies Depression Scale. RESULTS: After controlling for age, caregiving status, gender, body mass index, exercise, and sleep, the presence of multiple childhood adversities was related to both heightened IL-6 (0.37 +/- 0.03 log10 pg/mL versus 0.44 +/- 0.03 log10 pg/mL) and shorter telomeres (6.51 +/- 0.17 Kb versus 5.87 +/- 0.20 Kb), compared with the absence of adversity; the telomere difference could translate into a 7- to 15-year difference in life span. Abuse was associated with heightened IL-6 and TNF-alpha levels; for TNF-alpha, this relationship was magnified in caregivers compared with controls. Moreover, abuse and caregiving status were associated significantly and independently with higher levels of depressive symptoms. CONCLUSIONS: Adverse childhood events are related to continued vulnerability among older adults, enhancing the impact of chronic stressors. Childhood adversities cast a very long shadow.