Maternal adiposity and infancy growth predict later telomere length: a longitudinal cohort study.
Maternal overweight and obesity during pregnancy, and childhood growth patterns are risk factors influencing long-term health outcomes among the offspring. Furthermore, poor health condition has been associated with shorter leukocyte telomere length in adult subjects. We aimed to assess whether maternal adiposity during pregnancy and growth trajectory during infancy predict leukocyte telomere length (LTL) in later life.



We studied a cohort of 1082 subjects belonging to the Helsinki Birth Cohort Study, born between 1934 and 1944. They underwent two clinical visits 10 years apart (2001-2004 and 2011-2013), during which LTL and anthropometrics were assessed. Birth records included birth weight, length, maternal body mass index (BMI) at the end of pregnancy. Serial measurements of height and weight from birth to 11 years were available.



Higher maternal BMI was associated with shorter LTL in elderly women (r=-0.102, P=0.024) but not in men. Also, in women but not in men shorter LTL and greater telomere shortening over a 10-year interval were predicted by higher weight at 12 months of age (P=0.008 and P=0.029, respectively), and higher weight gain during the first 12 months of life (P=0.008 and P=0.006, respectively), particularly between 6 and 9 months of age (P=0.002 for both LTL and LTL shortening rate). A correlation between younger age at adiposity rebound and shorter LTL at 60 years (P=0.022) was also found.



High maternal adiposity during pregnancy is associated with shorter LTL in elderly female offspring, but not in men. Moreover, higher weight and weight gain during the first year of life and younger age at adiposity rebound predict shorter LTL in older age in women, suggesting that rapid growth during the perinatal period accelerates cellular aging in late adulthood.
Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy.
M A
MA
Guzzardi
Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy.
P
P
Iozzo
National Institute for Health and Welfare, Chronic Disease Prevention Unit, Helsinki, Finland.|Folkhälsan Research Center, Helsinki, Finland.
M K
MK
Salonen
National Institute for Health and Welfare, Chronic Disease Prevention Unit, Helsinki, Finland.|Children's Hospital, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.|PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
E
E
Kajantie
National Institute for Health and Welfare, Chronic Disease Prevention Unit, Helsinki, Finland.|Folkhälsan Research Center, Helsinki, Finland.|Unit of General Practice, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
J G
JG
Eriksson
D050154:Adiposity / Q000235:genetics*; D000367:Age Factors; D000368:Aged; D000375:Aging; D015992:Body Mass Index; D005260:Female; D005387:Finland / Q000453:epidemiology; D006801:Humans; D007223:Infant; D007962:Leukocytes / Q000378:metabolism*; D008137:Longitudinal Studies; D008297:Male; D009765:Obesity / Q000453:epidemiology* / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D012307:Risk Factors; D016615:Telomere / Q000235:genetics*; D059506:Telomere Shortening; D013997:Time Factors; D015430:Weight Gain / Q000235:genetics*