Inverse association between adiposity and telomere length: The fels longitudinal study

Abstract

Objectives To assess the relationship between telomere length and adiposity, using dual-energy X-ray absorptiometry (DXA) and magnetic resonance imaging (MRI), in addition to conventional anthropometric proxies including body mass index (BMI) and cardiovascular disease risk factors. Methods A cross-sectional sample of 309 non-Hispanic white participants in the Fels Longitudinal Study aged 8 to 80 yr (52% female) was included. Average telomere length was measured by quantitative PCR. Results Telomere length was negatively correlated with age (r = −0.32, P < 0.0001) and had numerous significant correlations with established cardiovascular disease risk factors including waist circumference (r = −0.33), apolipoprotein B (r = −0.26), systolic blood pressure (r = −0.28), and fasting serum glucose (r = −0.15); all P < 0.0025. In back-ward selection linear regression models of telomere length, adiposity measures were consistently retained in the best models; BMI, waist circumference, hip circumference, total body fat, and visceral adipose tissue volume were all inversely associated with telomere length at the nominal P < 0.05 level or lower, independent of age, sex, systolic blood pressure, and fasting serum lipid, lipoprotein, and glucose concentrations. The negative association of BMI with telomere length was stronger among younger than older participants (P for interaction, 0.03). Conclusions Individuals with higher total and abdominal adiposity have lower telomere length, a marker of cellular senescence, suggesting obesity may hasten the aging process. Longitudinal studies are required to establish the causal association of early life adiposity with biological aging.

Leukocyte telomere length and its relation to food and nutrient intake in an elderly population

“…Literature on the association of adiposity and LTL is based on cross-sectional studies and the findings are conflicting as some of the studies, including ours, found no association between BMI or other measures of adiposity and LTL, 4,5,22,[47][48][49] whereas some have reported significant inverse associations. 7,8,16,19,50 A recent cross-sectional study assessing total body and abdominal obesity in subjects aged 8-80 years noticed that the negative association between BMI and LTL is stronger among young subjects compared with the old. 7 Previous studies noticed LTL to be positively associated with physical activity 17 and socioeconomic status 19 and negatively associated with smoking.…”

“…7,8,16,19,50 A recent cross-sectional study assessing total body and abdominal obesity in subjects aged 8-80 years noticed that the negative association between BMI and LTL is stronger among young subjects compared with the old. 7 Previous studies noticed LTL to be positively associated with physical activity 17 and socioeconomic status 19 and negatively associated with smoking. 16 However, we did not confirm these results in our study, adjusting for physical activity, education and smoking.…”

“…4,5 Accelerated telomere shortening is associated with aging and aging-related diseases, such as hypertension, coronary heart disease and heart failure. [5][6][7] Shorter LTL has also been associated with higher body mass index (BMI), 7,8 insulin resistance and type 2 diabetes, 9,10 as well as with some forms of cancer. 11,12 Genetic, epigenetic and environmental factors influence LTL.…”

Obesity accelerates epigenetic aging of human liver

“…Leukocyte telomere length, which is a widely used biomarker of aging, has been found to be negatively correlated with body mass index (BMI) (3)(4)(5)(6)(7). Although the observed correlation between BMI and telomere length is relatively weak (r = 0.12) (4), it is remarkable that these studies demonstrated that BMI is associated with an age acceleration effect in blood.…”

Childhood obesity: a life-long health risk

“…Similarly, an important aspect of obesity-associated vascular injury obtained from preclinical and clinical studies, is that many of the vascular changes found in obesity are highly similar to those seen with aging [37] , which not only represents a physiological process but in itself represents a strong and independent risk factor for future cardiovascular events [37] . As with aging [37] , experimental or human obesity shows an attenuation of endothelium-dependent vasodilation [38,39] , a decrease in NO bioactivity [38,39] in conjunction with NO synthase uncoupling [37] , an increase in prostanoid-mediated endothelium-dependent contractions [40][41][42] , telomere shortening [43][44][45][46] , increased vascular stiffness [47] , and increased arterial intima-media thickness [26,48] . Obesity also increases tissue levels of endothelin-1 [38,49,50] , a strong vasoconstrictor peptide and atherogenic growth factor and proinflammatory stimulus [51] .…”