Contributions of maternal and paternal adiposity and smoking to adult offspring adiposity and cardiovascular risk: the midspan family study

Han, T.S., Hart, C.L. , Haig, C. , Logue, J. , Upton, M.N., Watt, G.C.M. and Lean, M.E.J. (2015) Contributions of maternal and paternal adiposity and smoking to adult offspring adiposity and cardiovascular risk: the midspan family study. BMJ Open, 5(11), e007682. (doi:10.1136/bmjopen-2015-007682) (PMID:26525718) (PMCID:PMC4636631)

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Abstract

Objective: Obesity has some genetic basis but requires interaction with environmental factors for phenotypic expression. We examined contributions of gender-specific parental adiposity and smoking to adiposity and related cardiovascular risk in adult offspring. Design: Cross-sectional general population survey. Setting : Scotland. Participants: 1456 of the 1477 first generation families in the Midspan Family Study: 2912 parents (aged 45–64 years surveyed between 1972 and 1976) who had 1025 sons and 1283 daughters, aged 30–59 years surveyed in 1996. Main measures: Offspring body mass index (BMI), waist circumference (WC), cardiometabolic risk (lipids, blood pressure and glucose) and cardiovascular disease as outcome measures, and parental BMI and smoking as determinants. All analyses adjusted for age, socioeconomic status and family clustering and offspring birth weight. Results: Regression coefficients for BMI associations between father–son (0.30) and mother–daughter (0.33) were greater than father–daughter (0.23) or mother–son (0.22). Regression coefficient for the non-genetic, shared-environment or assortative-mating relationship between BMIs of fathers and mothers was 0.19. Heritability estimates for BMI were greatest among women with mothers who had BMI either <25 or ≥30 kg/m2. Compared with offspring without obese parents, offspring with two obese parents had adjusted OR of 10.25 (95% CI 6.56 to 13.93) for having WC ≥102 cm for men, ≥88 cm women, 2.46 (95% CI 1.33 to 4.57) for metabolic syndrome and 3.03 (95% CI 1.55 to 5.91) for angina and/or myocardial infarct (p<0.001). Neither parental adiposity nor smoking history determined adjusted offspring individual cardiometabolic risk factors, diabetes or stroke. Maternal, but not paternal, smoking had significant effects on WC in sons (OR=1.50; 95% CI 1.13 to 2.01) and daughters (OR=1.42; 95% CI 1.10 to 1.84) and metabolic syndrome OR=1.68; 95% CI 1.17 to 2.40) in sons. Conclusions: There are modest genetic/epigenetic influences on the environmental factors behind adverse adiposity. Maternal smoking appears a specific hazard on obesity and metabolic syndrome. A possible epigenetic mechanism linking maternal smoking to obesity and metabolic syndrome in offspring is proposed. Individuals with family histories of obesity should be targeted from an early age to prevent obesity and complications.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Upton, Dr Mark and Lean, Professor Michael and Hart, Dr Carole and Watt, Professor Graham and Haig, Dr Caroline and Logue, Dr Jennifer
Authors: Han, T.S., Hart, C.L., Haig, C., Logue, J., Upton, M.N., Watt, G.C.M., and Lean, M.E.J.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
College of Medical Veterinary and Life Sciences > Institute of Health and Wellbeing > General Practice and Primary Care
College of Medical Veterinary and Life Sciences > Institute of Health and Wellbeing > Public Health
College of Medical Veterinary and Life Sciences > Institute of Health and Wellbeing > Robertson Centre
College of Medical Veterinary and Life Sciences > School of Medicine, Dentistry & Nursing
Journal Name:BMJ Open
Publisher:BMJ Publishing Group
ISSN:2044-6055
ISSN (Online):2044-6055
Copyright Holders:Copyright © 2015 Han TS, et al.
First Published:First published in BMJ Open 5(11):e007682
Publisher Policy:Reproduced under a Creative Commons License

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