Research Paper Volume 8, Issue 11 pp 2689—2701
Investigating the associations between adiposity, life course overweight trajectories, and telomere length
- 1 Medical Research Council Unit for Lifelong Health and Ageing at UCL, University College London, London WC1B 5JU, UK
- 2 Division of Haematology/Oncology, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55292, Indonesia
- 3 PILAR Research and Education, Cambridge CB1 2JD, UK
- 4 Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA
- 5 Driver Group, L.L.C., San Francisco, CA 94158, USA
Received: June 25, 2016 Accepted: August 29, 2016 Published: September 18, 2016
https://doi.org/10.18632/aging.101036How to Cite
Abstract
Obesity may accelerate ageing through chronic inflammation. To further examine this association, we assessed current adiposity, adiposity at early adulthood and life course overweight trajectories in relation to leukocyte telomere length (LTL). We included a total of 7,008 nationally representative U.S. residents and collected information on objectively measured body mass index (BMI), waist circumference and percent body fat. BMI at age 25 and overweight trajectories were assessed using self-reported history. Leukocyte telomere length (LTL) relative to a standard DNA reference (T/S ratio) was quantified by polymerase chain reaction (PCR). Linear regression models were used to examine the difference in LTL across adiposity measures at examination, BMI at age 25, and overweight trajectories. A 0.2% decrease in telomere length (95% CI: -0.3 to -0.07%) was observed for every kg/m2 increase in BMI, whereas a unit increase in waist circumference (cm) and percent body fat contributed to a 0.09% and 0.01% decrease in LTL, respectively. Higher BMI and being obese at age 25 contributed to lower LTL at older ages. Associations between weight loss through life course and LTL were observed, which further marked the importance of life course adiposity dynamics as a determinant of ageing.