Hilary J Bethancourt1,2, Mario Kratz3,4,5, Shirley A A Beresford3,4, M Geoffrey Hayes6,7,8, Christopher W Kuzawa7,9, Paulita L Duazo10, Judith B Borja10,11, Daniel T A Eisenberg12,13. 1. Department of Anthropology, University of Washington, Seattle, WA, USA. hilaryjb@u.washington.edu. 2. Center for Studies in Demography and Ecology, University of Washington, Seattle, WA, USA. hilaryjb@u.washington.edu. 3. Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA. 4. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. 5. Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle, WA, USA. 6. Division of Endocrinology, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. 7. Department of Anthropology, Northwestern University, Evanston, IL, USA. 8. Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. 9. Institute for Policy Research, Northwestern University, Evanston, IL, USA. 10. Office of Population Studies Foundation, University of San Carlos, Cebu City, Philippines. 11. Department of Nutrition and Dietetics, University of San Carlos, Cebu City, Philippines. 12. Department of Anthropology, University of Washington, Seattle, WA, USA. 13. Center for Studies in Demography and Ecology, University of Washington, Seattle, WA, USA.
Abstract
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.
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.
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