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. 2011;6(6):e20816.
doi: 10.1371/journal.pone.0020816. Epub 2011 Jun 29.

Increased genetic variance of BMI with a higher prevalence of obesity

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Increased genetic variance of BMI with a higher prevalence of obesity

Benjamin Rokholm et al. PLoS One. 2011.

Abstract

Background and objectives: There is no doubt that the dramatic worldwide increase in obesity prevalence is due to changes in environmental factors. However, twin studies suggest that genetic differences are responsible for the major part of the variation in body mass index (BMI) and other measures of body fatness within populations. Several recent studies suggest that the genetic effects on adiposity may be stronger when combined with presumed risk factors for obesity. We tested the hypothesis that a higher prevalence of obesity and overweight and a higher BMI mean is associated with a larger genetic variation in BMI.

Methods: The data consisted of self-reported height and weight from two Danish twin surveys in 1994 and 2002. A total of 15,017 monozygotic and dizygotic twin pairs were divided into subgroups by year of birth (from 1931 through 1982) and sex. The genetic and environmental variance components of BMI were calculated for each subgroup using the classical twin design. Likewise, the prevalence of obesity, prevalence of overweight and the mean of the BMI distribution was calculated for each subgroup and tested as explanatory variables in a random effects meta-regression model with the square root of the additive genetic variance (equal to the standard deviation) as the dependent variable.

Results: The size of additive genetic variation was positively and significantly associated with obesity prevalence (p = 0.001) and the mean of the BMI distribution (p = 0.015). The association with prevalence of overweight was positive but not statistically significant (p = 0.177).

Conclusion: The results suggest that the genetic variation in BMI increases as the prevalence of obesity, prevalence of overweight and the BMI mean increases. The findings suggest that the genes related to body fatness are expressed more aggressively under the influence of an obesity-promoting environment.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Flowchart for selection of twins from the 1994 survey.
The flowchart shows how eligible twin pairs were selected from the twin survey conducted in 1994. From the returned questionnaire we excluded twin pairs with incomplete information on one of the twins in a pair, opposite sex twin pairs and twin pairs with extreme BMI values.
Figure 2
Figure 2. Flowchart for selection of twins from the 2002 survey.
The flowchart shows how eligible twin pairs were selected from the twin survey conducted in 2002. From the returned questionnaire we excluded twin pairs with incomplete information on one of the twins in a pair, opposite sex twin pairs and twin pairs with extreme BMI values.
Figure 3
Figure 3. Regression models for the A (additive genetic) and E (unique environmental) component.
The (square root of the) additive genetic variance and unique environmental variation is plotted against each of the proxy variables obesity prevalence, overweight prevalence and the mean of the BMI distribution. Each circle represents a subgroup. The size of the circle is inversely proportionate to the standard error of AGV for each subgroup. The regression line shows the best fit with larger circles given more weight. The blue punctured and red regression line represents the stratified analyses for males and females, respectively.

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