Bethancourt Hilary J, Kratz Mario, Beresford Shirley A A, Hayes M Geoffrey, Kuzawa Christopher W, Duazo Paulita L, Borja Judith B, Eisenberg Daniel T A
Department of Anthropology, University of Washington, Seattle, WA, USA.
Center for Studies in Demography and Ecology, University of Washington, Seattle, WA, USA.
Eur J Nutr. 2017 Feb;56(1):295-308. doi: 10.1007/s00394-015-1080-1. Epub 2015 Oct 26.
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.
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.
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.
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.
端粒是覆盖并保护染色体的DNA-蛋白质结构,人们认为当暴露于慢性炎症和氧化应激时,端粒会更快缩短。饮食和营养状况可能是炎症和氧化应激的一个来源。然而,端粒长度(TL)与饮食或肥胖之间的关系主要是在老年超重/肥胖人群中进行横断面研究的,结果并不一致。对于年轻的低体重至正常体重人群,饮食或身体成分与TL之间的关系知之甚少。在生长发育阶段,端粒损耗最为迅速,在此期间对特定饮食或身体成分的累积暴露与成年期TL之间的关系也仍不清楚。
在1459名年轻的菲律宾成年人样本中,我们评估了20.8 - 22.5岁时的血液TL与8.5至22.5岁期间收集的BMI z评分、腰围和饮食测量值之间的关系。使用单色多重定量PCR测量TL,使用多次24小时饮食回忆法测量饮食。
我们发现血液TL与任何肥胖指标之间均无关联,血液TL与所检测的七种饮食因素之间也无关联,这七种饮食因素分别是加工肉类、油炸/烤肉和鱼类、非油炸鱼类、椰子油、水果和蔬菜、面包及面包制品,以及含糖饮料。
考虑到文献中的不一致性以及我们的阴性结果,身体成分的微小差异以及任何单一促炎或抗炎饮食成分的摄入本身可能不会对端粒完整性产生有意义的影响,或者这种影响在不同的生态环境中可能会有所不同。