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fat_genetics

Page history last edited by loniemc@... 11 years, 8 months ago

Sources tying fat to genetics

 

Stunkard, Albert, TI Sorensen, C Hanis, TW Teasdale, R Chakraborty, WJ Schull, and F Schulsinger. “An Adoption Study of Human Obesity.” New England Journal of Medicine. 314 (Jan 23, 1986): 193-198.

 

Weight researcher Albert Stunkard has concluded through studying twins and adopted children that genetics are much more likely to determine body size

 

 

 

Stunkard, Albert, JR Harris, NL Pedersen, and GE McClearn. “Body Mass Index of Twins Who Have Been Reared Apart.” New England Journal of Medicine 322.21 (24 May 1990): 1483-1487.

 

Weight researcher Albert Stunkard has concluded through studying twins and adopted children that genetics are much more likely to determine body size

 

 

Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment1,2,3

 

Jane Wardle, Susan Carnell, Claire MA Haworth and Robert Plomin

 

1 From the Department of Epidemiology and Public Health, Health Behaviour Research Centre, University College London, London, United Kingdom (JW and SC), and the Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom (CMAH and RP)

 

Background: Body mass index (BMI) has been shown to be highly heritable, but most studies were carried out in cohorts born before the onset of the "obesity epidemic."

 

Objective: We aimed to quantify genetic and environmental influences on BMI and central adiposity in children growing up during a time of dramatic rises in pediatric obesity.

 

Design: We carried out twin analyses of BMI and waist circumference (WC) in a UK sample of 5092 twin pairs aged 8–11 y. Quantitative genetic model-fitting was used for the univariate analyses, and bivariate quantitative genetic model-fitting was used for the analysis of covariance between BMI and WC.

 

Results: Quantitative genetic model-fitting confirmed substantial heritability for BMI and WC (77% for both). Bivariate genetic analyses showed that, although the genetic influence on WC was largely common to BMI (60%), there was also a significant independent genetic effect (40%). For both BMI and WC, there was a very modest shared-environment effect, and the remaining environmental variance was unshared.

 

Conclusions: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. Most of the genetic effect on abdominal adiposity is common to BMI, but 40% is attributable to independent genetic influences. Environmental effects are small and are divided approximately equally between shared and nonshared effects. Targeting the family may be vital for obesity prevention in the earliest years, but longer-term weight control will require a combination of individual engagement and society-wide efforts to modify the environment, especially for children at high genetic risk.

 

 

 

 

 

 

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