Telomere trajectories from early adolescence to adulthood following early institutionalization: Protective effects of foster care in the Bucharest Early Intervention Project

BACKGROUND: Early institutional rearing is associated with adverse biological and health outcomes in later life, including accelerated cellular aging as measured by telomere length. However, the extent to which foster care intervention can mitigate these risks, and whether telomere dynamics predict cardiometabolic health in young adulthood remains unclear. OBJECTIVE: The present study aimed to estimate the association between early institutional care, randomization to foster care (intent-to-treat), and longitudinal changes in telomere length from ages 12-22 years among participants of the Bucharest Early Intervention Project (BEIP), and to determine whether the rate of telomere shortening predicts cardiometabolic health in early adulthood. METHODS: The study included 156 BEIP participants who had been randomly assigned to either foster care or care-as-usual, with an additional comparison group of never-institutionalized peers. Buccal DNA was collected, and telomere length (T/S ratio) was measured at two to five timepoints between the ages 12 and 22. Cardiometabolic health at age 22 was assessed using metabolic z-scores and criteria for metabolic syndrome. RESULTS: Participants assigned to foster care exhibited a significantly slower decline in telomere length over the 10-year period compared to those in care-as-usual. Ever-institutionalized and never-institutionalized groups had similar overall patterns of telomere decline. Sex-specific analyses indicated that among the foster care group, males had shorter telomere length at age 12 than females, but rates of telomere shortening were similar between sexes over time. The rate of telomere attrition between ages 12 and 22 was not associated with cardiometabolic outcomes at age 22. CONCLUSION: Foster care intervention during early childhood may protect against telomere shortening among previously institutionalized children, highlighting its role in buffering the long-term impact of early adversity on cellular aging. However, variation in telomere shortening during adolescence and young adulthood did not predict cardiometabolic risk at age 22.