Project Summary/Abstract
Early life adversity, including childhood maltreatment and other traumas, is a major risk factor for a host of
health conditions, including psychiatric disorders, obesity, diabetes, and cardiovascular disease. Health
behaviors, such as diet, sleep, and activity, are linked to childhood adversity and can further contribute to risk
for these conditions. These effects compound over time and poor health outcomes are most evident in adults
when biological effects of stress and health behaviors combine with age-related decline to produce frank
disease. There is now evidence that these processes begin early in life and that some of the health outcomes
can be observed in childhood. Converging evidence from animal models and recent human studies indicate
that mitochondria play a key role in coordinating the stress response and in the aging process. Here we
hypothesize that early stress alters mitochondrial DNA and mitochondrial function and that this may be a
mechanism of risk for stress- and age-related disorders. The proposed study leverages data and specimens
available in a longitudinal developmental study of childhood maltreatment that includes rich data on exposures,
biomarkers of aging, and health outcomes. Results of this study are expected to provide insight into the
biological mechanisms of adversity-related risk for accelerated aging and risk for disease, and provide targets
for new treatment and prevention approaches.