Institute of Preventive Medicine, Copenhagen University Hospital, Centre for Health and Society, Copenhagen, Denmark.
PLoS One. 2011;6(6):e20816. doi: 10.1371/journal.pone.0020816. Epub 2011 Jun 29.
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.
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.
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).
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.
毫无疑问，肥胖症患病率在全球范围内的急剧上升归因于环境因素的变化。然而，双胞胎研究表明，遗传差异是导致人群中体重指数（BMI）和其他身体脂肪测量值变化的主要原因。最近的几项研究表明，当与肥胖的假定危险因素结合时，肥胖相关的遗传效应可能更强。我们检验了这样一个假设，即肥胖和超重的更高患病率以及更高的 BMI 平均值与 BMI 遗传变异的更大程度相关。
数据来自 1994 年和 2002 年丹麦进行的两项双胞胎调查中自我报告的身高和体重。总共对 15017 对单卵和双卵双胞胎进行了分组，按出生年份（1931 年至 1982 年）和性别进行分组。使用经典的双胞胎设计，为每个子组计算 BMI 的遗传和环境方差分量。同样，为每个子组计算肥胖症的患病率、超重的患病率和 BMI 分布的平均值，并将其作为随机效应元回归模型的解释变量进行检验，其中因变量为加性遗传方差的平方根（等于标准差）。
加性遗传变异的大小与肥胖症的患病率（p=0.001）和 BMI 分布的平均值（p=0.015）呈正相关且显著相关。与超重患病率的相关性为正相关，但无统计学意义（p=0.177）。
结果表明，BMI 的遗传变异随着肥胖症的患病率、超重的患病率和 BMI 平均值的增加而增加。这一发现表明，与身体脂肪相关的基因在促进肥胖的环境影响下更为激进地表达。
