Hilary J. Bethancourt, Mario Kratz, Shirley A. A. Beresford, M. Geoffrey Hayes, Christopher W. Kuzawa, Paulita L. Duazo, Judith B. Borja, Daniel T. A. Eisenberg
Purpose: Telomeres, DNA–protein structures that cap and protect chromosomes, are thought to shorten more rapidly when exposed to chronic inflammation and oxidative stress. Diet and nutritional status may be a source of inflammation and oxidative stress. However, relationships between telomere length (TL) and diet or adiposity have primarily been studied cross-sectionally among older, overweight/obese populations and yielded inconsistent results. Little is known about the relationship between diet or body composition and TL among younger, low- to normal-weight populations. It also remains unclear how cumulative exposure to a specific diet or body composition during the years of growth and development, when telomere attrition is most rapid, may be related to TL in adulthood. Methods: In a sample of 1459 young adult Filipinos, we assessed the relationship between blood TL at ages 20.8–22.5 and measures of BMI z-score, waist circumference, and diet collected between the ages of 8.5 and 22.5. TL was measured using monochrome multiplex quantitative PCR, and diet was measured using multiple 24-h recalls. Results: We found no associations between blood TL and any of the measures of adiposity or between blood TL and the seven dietary factors examined: processed meats, fried/grilled meats and fish, non-fried fish, coconut oil, fruits and vegetables, bread and bread products, and sugar-sweetened beverages. Conclusions: Considering the inconsistencies in the literature and our null results, small differences in body composition and consumption of any single pro- or anti-inflammatory dietary component may not by themselves have a meaningful impact on telomere integrity, or the impact may differ across distinct ecological circumstances. © 2015, Springer-Verlag Berlin Heidelberg.
Department of Anthropology, University of Washington, Seattle, WA, United States; Center for Studies in Demography and Ecology, University of Washington, Seattle, WA, United States; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, United States; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, United States; Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle, WA, United States; Division of Endocrinology, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, United States; Department of Anthropology, Northwestern University, Evanston, IL, United States; Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, United States; Institute for Policy Research, Northwestern University, Evanston, IL, United States; Office of Population Studies Foundation, University of San Carlos, Cebu City, Philippines; Department of Nutrition and Dietetics, University of San Carlos, Cebu City, Philippines
