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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Public Health, University of Helsinki, Helsinki, Finland (KS, TL, LB, KHP, and JK); the Institute of Preventive Medicine, Copenhagen Capital Region, Centre for Health and Society, Copenhagen, Denmark (ALH, BLH, and TIAS); the Obesity Research Unit, Department of Psychiatry, Helsinki University Hospital, Helsinki, Finland (KHP and AR); the Institute of Regional Health Services Research and the Danish Twin Registry, University of Southern Denmark, Odense, Denmark (KS and KOK); the Department of Mental Health, National Institute for Health and Welfare, Helsinki, Finland (JK); and the Institute for Molecular Medicine FIMM, Helsinki, Finland (JK).
2 The GEMINAKAR project was supported by grants from the Danish Medical Research Council, the Danish Diabetes Association, the NOVO Foundation, the Danish Heart Foundation, and Apotekerfonden. The FinnTwin12 study was supported by the National Institute on Alcohol Abuse and Alcoholism (grant and AA-12502), the European Union Fifth Framework Program (QLG2-CT-2002-01254), the Academy of Finland (grants 100499 and 201461), the Academy of Finland Centre of Excellence in Complex Disease Genetics, Helsinki University Central Hospital grants, and grants from Yrjö Jahnsson Foundation, Jalmari & Rauha Ahokas Foundation, Juho Vainio Foundation, and Finnish Cultural Foundation. The present study was supported by DIOGENES (Diet, Obesity and Genes), which was supported by the European Community (contract no. FP6-513946), http://www.diogenes-eu.org/. 3 Address correspondence to K Silventoinen, Department of Public Health, University of Helsinki, PO Box 41, Mannerheimintie 172 FIN-00014, University of Helsinki, Helsinki, Finland. E-mail: karri.silventoinen{at}helsinki.fi.
Background: The development of obesity is still a poorly understood process that is dependent on both genetic and environmental factors.
Objective: The objective was to examine how physical activity and the proportion of energy as protein in the diet modify the genetic variation of body mass index (BMI), waist circumference, and percentage body fat.
Design: Twins from Denmark (756 complete pairs) and Finland (278 complete pairs) aged 18–67 and 21–24 y, respectively, participated. The proportion of energy as protein in the diet was estimated by using food-frequency questionnaires. The participants reported the frequency and intensity of their leisure time physical activity. Waist circumference and BMI were measured. Percentage body fat was assessed in Denmark by using a bioelectrical impedance method. The data were analyzed by using gene-environment interaction models for twin data with the Mx statistical package (Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA).
Results: High physical activity was associated with lower mean values, and a high proportion of protein in the diet was associated with higher mean BMI, waist circumference, and percentage body fat and a reduction in genetic and environmental variances. Genetic modification by physical activity was statistically significant for BMI (–0.18; 95% CI: –0.31, –0.05) and waist circumference (–0.14; 95% CI: –0.22, –0.05) in the merged data. A high proportion of protein in the diet reduced genetic and environmental variances in BMI and waist circumference in Danish men but not in women or in Finnish men.
Conclusions: Our results suggest that, in physically active individuals, the genetic variation in weight is reduced, which possibly suggests that physical activity is able to modify the action of the genes responsible for predisposition to obesity, whereas the protein content of the diet has no appreciable effect.
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