Tools in the assessment of sarcopenia

• Main Authors: Cooper, C. (Author), Fielding, R. (Author), Visser, M. (Author), van Loon, L.J (Author), Rolland, Y. (Author), Orwoll, E. (Author), Reid, K. (Author), Boonen, S. (Author), Dere, W. (Author), Epstein, S. (Author), Tsouderos, Y. (Author), Sayer, A.A (Author), Rizzoli, R. (Author), Reginster, J.Y (Author), Kanis, J.A (Author)
• Other Authors: Mitlak, B. (Contributor)
• Format: Article
• Language: English
• Published: 2013-09.
• Subjects: Article
• Online Access: Get fulltext; Get fulltext; Get fulltext; Get fulltext

 Objective We aimed to test the fetal overnutrition hypothesis by comparing the associations of maternal and paternal adiposity (sum of skinfolds) with adiposity and cardiovascular risk factors in children. Design Children from a prospective birth cohort had anthropometry, fat percentage (bio-impedance), plasma glucose, insulin and lipid concentrations and blood pressure measured at 9·5 years of age. Detailed anthropometric measurements were recorded for mothers (at 30 ± 2 weeks' gestation) and fathers (5 years following the index pregnancy). Setting Holdsworth Memorial Hospital, Mysore, India. Subjects Children (n 504), born to mothers with normal glucose tolerance during pregnancy. Results Twenty-eight per cent of mothers and 38 % of fathers were overweight/obese (BMI ? 25·0 kg/m2), but only 4 % of the children were overweight/obese (WHO age- and sex-specific BMI ? 18·2 kg/m2). The children's adiposity (BMI, sum of skinfolds, fat percentage and waist circumference), fasting insulin concentration and insulin resistance increased with increasing maternal and paternal sum of skinfolds adjusted for the child's sex, age and socio-economic status. Maternal and paternal effects were similar. The associations with fasting insulin and insulin resistance were attenuated after adjusting for the child's current adiposity. Conclusions In this population, both maternal and paternal adiposity equally predict adiposity and insulin resistance in the children. This suggests that shared family environment and lifestyle, or genetic/epigenetic factors, influence child adiposity. Our findings do not support the hypothesis that there is an intra-uterine overnutrition effect of maternal adiposity in non-diabetic pregnancies, although we cannot rule out such an effect in cases of extreme maternal obesity, which is rare in our population.