TY - JOUR
T1 - Body mass index is negatively associated with telomere length
T2 - A collaborative cross-sectional meta-analysis of 87 observational studies
AU - TELOMAAS group
AU - Gielen, Marij
AU - Hageman, Geja J.
AU - Antoniou, Evangelia E.
AU - Nordfjall, Katarina
AU - Mangino, Massimo
AU - Balasubramanyam, Muthuswamy
AU - De Meyer, Tim
AU - Hendricks, Audrey E.
AU - Giltay, Erik J.
AU - Hunt, Steven C.
AU - Nettleton, Jennifer A.
AU - Salpea, Klelia D.
AU - Diaz, Vanessa A.
AU - Farzaneh-Far, Ramin
AU - Atzmon, Gil
AU - Harris, Sarah E.
AU - Hou, Lifang
AU - Gilley, David
AU - Hovatta, Iiris
AU - Kark, Jeremy D.
AU - Nassar, Hisham
AU - Kurz, David J.
AU - Mather, Karen A.
AU - Willeit, Peter
AU - Zheng, Yun Ling
AU - Pavanello, Sofia
AU - Demerath, Ellen W.
AU - Rode, Line
AU - Bunout, Daniel
AU - Steptoe, Andrew
AU - Boardman, Lisa
AU - Marti, Amelia
AU - Needham, Belinda
AU - Zheng, Wei
AU - Ramsey-Goldman, Rosalind
AU - Pellatt, Andrew J.
AU - Kaprio, Jaakko
AU - Hofmann, Jonathan N.
AU - Gieger, Christian
AU - Paolisso, Giuseppe
AU - Hjelmborg, Jacob B.H.
AU - Mirabello, Lisa
AU - Seeman, Teresa
AU - Wong, Jason
AU - Van Der Harst, Pim
AU - Broer, Linda
AU - Kronenberg, Florian
AU - Kollerits, Barbara
AU - Strandberg, Timo
AU - Eisenberg, Dan T.A.
N1 - Publisher Copyright:
© 2018 American Society for Nutrition.
PY - 2018/9/1
Y1 - 2018/9/1
N2 - Background: Even before the onset of age-related diseases, obesity might be a contributing factor to the cumulative burden of oxidative stress and chronic inflammation throughout the life course. Obesity may therefore contribute to accelerated shortening of telomeres. Consequently, obese persons are more likely to have shorter telomeres, but the association between body mass index (BMI) and leukocyte telomere length (TL) might differ across the life span and between ethnicities and sexes. Objective: A collaborative cross-sectionalmeta-analysis of observational studies was conducted to investigate the associations between BMI and TL across the life span. Design: Eighty-seven distinct study samples were included in the meta-analysis capturing data from 146,114 individuals. Studyspecific age- and sex-adjusted regression coefficients were combined by using a random-effects model in which absolute [base pairs (bp)] and relative telomere to single-copy gene ratio (T/S ratio) TLs were regressed against BMI. Stratified analysis was performed by 3 age categories ("young": 18-60 y; "middle": 61-75 y; and "old": >75 y), sex, and ethnicity. Results: Each unit increase in BMI corresponded to a-3.99 bp (95% CI: -5.17, -2.81 bp) difference in TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -7.67 bp (95% CI:-10.03,-5.31 bp) difference. Each unit increase in BMI corresponded to a -1.58 × 10-3 unit T/S ratio (0.16% decrease; 95% CI: -2.14 × 10-3, -1.01 × 10-3) difference in ageand sex-adjusted relative TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -2.58 × 10-3 unit T/S ratio (0.26% decrease; 95% CI: -3.92 × 10-3, -1.25 × 10-3). The associations were predominantly for the white pooled population. No sex differences were observed. Conclusions: A higher BMI is associated with shorter telomeres, especially in younger individuals. The presently observed difference is not negligible. Meta-analyses of longitudinal studies evaluating change in body weight alongside change in TL arewarranted.
AB - Background: Even before the onset of age-related diseases, obesity might be a contributing factor to the cumulative burden of oxidative stress and chronic inflammation throughout the life course. Obesity may therefore contribute to accelerated shortening of telomeres. Consequently, obese persons are more likely to have shorter telomeres, but the association between body mass index (BMI) and leukocyte telomere length (TL) might differ across the life span and between ethnicities and sexes. Objective: A collaborative cross-sectionalmeta-analysis of observational studies was conducted to investigate the associations between BMI and TL across the life span. Design: Eighty-seven distinct study samples were included in the meta-analysis capturing data from 146,114 individuals. Studyspecific age- and sex-adjusted regression coefficients were combined by using a random-effects model in which absolute [base pairs (bp)] and relative telomere to single-copy gene ratio (T/S ratio) TLs were regressed against BMI. Stratified analysis was performed by 3 age categories ("young": 18-60 y; "middle": 61-75 y; and "old": >75 y), sex, and ethnicity. Results: Each unit increase in BMI corresponded to a-3.99 bp (95% CI: -5.17, -2.81 bp) difference in TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -7.67 bp (95% CI:-10.03,-5.31 bp) difference. Each unit increase in BMI corresponded to a -1.58 × 10-3 unit T/S ratio (0.16% decrease; 95% CI: -2.14 × 10-3, -1.01 × 10-3) difference in ageand sex-adjusted relative TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -2.58 × 10-3 unit T/S ratio (0.26% decrease; 95% CI: -3.92 × 10-3, -1.25 × 10-3). The associations were predominantly for the white pooled population. No sex differences were observed. Conclusions: A higher BMI is associated with shorter telomeres, especially in younger individuals. The presently observed difference is not negligible. Meta-analyses of longitudinal studies evaluating change in body weight alongside change in TL arewarranted.
KW - BMI
KW - Low-grade inflammation
KW - Meta-analysis
KW - Obesity
KW - Observational studies
KW - Telomere length
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U2 - 10.1093/ajcn/nqy107
DO - 10.1093/ajcn/nqy107
M3 - Article
C2 - 30535086
AN - SCOPUS:85054190686
SN - 0002-9165
VL - 108
SP - 453
EP - 475
JO - American Journal of Clinical Nutrition
JF - American Journal of Clinical Nutrition
IS - 3
ER -