Stress, Obesity, and Telomere Length in Latino Infants and Toddlers
Location(s): United States
Description
I will analyze telomere length in infants at birth and 2 years of age to evaluate the relationships between development of obesity, exposure to stress, and risk for accelerated telomere attrition. The results of this study will complement my investigations, designed to evaluate the relationship between exposure to prenatal and postnatal depression, levels of adipocyte and gut hormones, and risk for development of obesity at 2 years of age. Shortened telomere length has been found to be associated with chronic diseases in adults, including obesity and chronic stress, but few studies have been conducted in young children. The importance of focusing on telomere shortening in early childhood cannot be underestimated, as telomere attrition happens at a much faster pace during the early years of childhood than in later childhood and adulthood. The University of California, San Francisco (UCSF) is the ideal research environment to conduct this work. The PI will collaborate with Dr. Elizabeth Blackburn, Professor of Biology and Physiology's lab, which will perform analysis of samples for telomere length, and with Elissa Epel, Associate Professor of Psychiatry, who is internationally recognized for studies on the relationship on stress and metabolic pathways to telomere shortening. My basic hypotheses are that infants exposed to excessive maternal weight gain and to maternal depressive symptoms in utero and to postnatal maternal depression and excessive infant weight gain will have the shortest telomeres at age 2 and the greatest decline in telomere length in the first 2 years of life. Those exposed in utero will have the shortest telomeres at birth. The aims are: 1) To evaluate pregnancy exposures, specifically excessive maternal weight gain in pregnancy and depressive symptoms in utero and offspring telomere length trajectories (changes from birth to 2 years); 2) To evaluate early life exposures to postnatal depressive symptoms, rapid infant weight gain in the first 6 months, obesity up to age 2, and telomere length trajectories; and 3) To examine risk factor profiles for a rapid decline in telomere length from birth to age 2. The results from these preliminary studies will form the basis for a R01 application to begin to explore metabolic and genetic programming resulting from pre- and postnatal factors leading to overweight in young children. This project will add analysis of telomere length, the tips of the chromosome in DNA which are a marker of biological aging, to an on-going study involving examining risk factors for obesity in Latino infants. Telomere length will be measured at birth and again at 2 years of age.