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. 2011;6(11):e27135.
doi: 10.1371/journal.pone.0027135. Epub 2011 Nov 7.

Increasing genetic variance of body mass index during the Swedish obesity epidemic

Benjamin Rokholm  1 , Karri Silventoinen, Per Tynelius, Michael Gamborg, Thorkild I A Sørensen, Finn Rasmussen
Affiliations

Increasing genetic variance of body mass index during the Swedish obesity epidemic

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 and family studies suggest that genetic differences are responsible for the major part of the variation in adiposity within populations. Recent studies show that the genetic effects on body mass index (BMI) may be stronger when combined with presumed risk factors for obesity. We tested the hypothesis that the genetic variance of BMI has increased during the obesity epidemic.

Methods: The data comprised height and weight measurements of 1,474,065 Swedish conscripts at age 18-19 y born between 1951 and 1983. The data were linked to the Swedish Multi-Generation Register and the Swedish Twin Register from which 264,796 full-brother pairs, 1,736 monozygotic (MZ) and 1,961 dizygotic (DZ) twin pairs were identified. The twin pairs were analysed to identify the most parsimonious model for the genetic and environmental contribution to BMI variance. The full-brother pairs were subsequently divided into subgroups by year of birth to investigate trends in the genetic variance of BMI.

Results: The twin analysis showed that BMI variation could be explained by additive genetic and environmental factors not shared by co-twins. On the basis of the analyses of the full-siblings, the additive genetic variance of BMI increased from 4.3 [95% CI 4.04-4.53] to 7.9 [95% CI 7.28-8.54] within the study period, as did the unique environmental variance, which increased from 1.4 [95% CI 1.32-1.48] to 2.0 [95% CI 1.89-2.22]. The BMI heritability increased from 75% to 78.8%.

Conclusion: The results confirm the hypothesis that the additive genetic variance of BMI has increased strongly during the obesity epidemic. This suggests that the obesogenic environment has enhanced the influence of adiposity related genes.

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Conflict of interest statement

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

Figures

Figure 1
Figure 1. The prevalence of obesity in the full sample of conscripts by year of birth with 95% CI.
Figure 2
Figure 2. The additive genetic variance (95% confidence intervals) and unique environmental variance of BMI plotted against year of birth.
Figure 3
Figure 3. The prevalence of obesity plotted against the additive genetic and the unique environmental variance of BMI for each birth cohort.
The regression lines are shown for the genetic and environmental variance vs. prevalence of obesity.
See this image and copyright information in PMC

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