K Komulainen1, L Pulkki-Råback1,2, M Jokela1, L-P Lyytikäinen3, N Pitkänen4, T Laitinen4, M Hintsanen5,1, M Elovainio1,6, T Hintsa1, A Jula6, M Juonala7,8,9, K Pahkala4,10, J Viikari7,8, T Lehtimäki3, O Raitakari4,11, L Keltikangas-Järvinen1. 1. Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland. 2. Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland. 3. The Department of Clinical Chemistry, Fimlab Laboratories, Pirkanmaa Hospital District, School of Medicine, University of Tampere, Tampere, Finland. 4. Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland. 5. Unit of Psychology, University of Oulu, Oulu, Finland. 6. National Institute for Health and Welfare, Finland. 7. Department of Medicine, University of Turku, Turku, Finland. 8. Division of Medicine, Turku University Hospital, Turku, Finland. 9. Murdoch Childrens Research Institute, Parkville, VIC, Australia. 10. Paavo Nurmi Centre, Sports & Exercise Medicine Unit, Department of Health and Physical Activity, University of Turku, Turku, Finland. 11. Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland.
Abstract
OBJECTIVES: The life-course development of body mass index (BMI) may be driven by interactions between genes and obesity-inducing social environments. We examined whether lower parental or own education accentuates the genetic risk for higher BMI over the life course, and whether diet and physical activity account for the educational differences in genetic associations with BMI. SUBJECTS/ METHODS: The study comprised 2441 participants (1319 women, 3-18 years at baseline) from the prospective, population-based Cardiovascular Risk in Young Finns Study. BMI (kg/m2) trajectories were calculated from 18 to 49 years, using data from six time points spanning 31 years. A polygenic risk score for BMI was calculated as a weighted sum of risk alleles in 97 single-nucleotide polymorphisms. Education was assessed via self-reports, measured prospectively from participants in adulthood and from parents when participants were children. Diet and physical activity were self-reported in adulthood. RESULTS: Mean BMI increased from 22.6 to 26.6 kg/m2 during the follow-up. In growth curve analyses, the genetic risk score was associated with faster BMI increase over time (b=0.02, (95% CI, 0.01-0.02, P<0.001)). The association between the genetic risk score and BMI was more pronounced among those with lower educational level in adulthood (b=-0.12 (95% CI, -0.23-0.01); P=0.036)). No interaction effect was observed between the genetic risk score and parental education (b=0.05 (95% CI, -0.09-0.18; P=0.51)). Diet and physical activity explained little of the interaction effect between the genetic risk score and adulthood education. CONCLUSIONS: In this prospective study, the association of a risk score of 97 genetic variants with BMI was stronger among those with low compared with high education. This suggests lower education in adulthood accentuates the risk of higher BMI in people at genetic risk.
OBJECTIVES: The life-course development of body mass index (BMI) may be driven by interactions between genes and obesity-inducing social environments. We examined whether lower parental or own education accentuates the genetic risk for higher BMI over the life course, and whether diet and physical activity account for the educational differences in genetic associations with BMI. SUBJECTS/ METHODS: The study comprised 2441 participants (1319 women, 3-18 years at baseline) from the prospective, population-based Cardiovascular Risk in Young Finns Study. BMI (kg/m2) trajectories were calculated from 18 to 49 years, using data from six time points spanning 31 years. A polygenic risk score for BMI was calculated as a weighted sum of risk alleles in 97 single-nucleotide polymorphisms. Education was assessed via self-reports, measured prospectively from participants in adulthood and from parents when participants were children. Diet and physical activity were self-reported in adulthood. RESULTS: Mean BMI increased from 22.6 to 26.6 kg/m2 during the follow-up. In growth curve analyses, the genetic risk score was associated with faster BMI increase over time (b=0.02, (95% CI, 0.01-0.02, P<0.001)). The association between the genetic risk score and BMI was more pronounced among those with lower educational level in adulthood (b=-0.12 (95% CI, -0.23-0.01); P=0.036)). No interaction effect was observed between the genetic risk score and parental education (b=0.05 (95% CI, -0.09-0.18; P=0.51)). Diet and physical activity explained little of the interaction effect between the genetic risk score and adulthood education. CONCLUSIONS: In this prospective study, the association of a risk score of 97 genetic variants with BMI was stronger among those with low compared with high education. This suggests lower education in adulthood accentuates the risk of higher BMI in people at genetic risk.
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