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现代人的生活方式或是造成肥胖流行的罪魁祸首

来源:生物谷 2016-07-08 08:55

图片来源:medicalxpress.com

2016年7月6日 讯 /生物谷BIOON/ --一项刊登在the Journal of the American Medical Association上的一篇研究报告中,来自美国研究者的最新研究显示,肥胖病流行的罪魁祸首或许是如今的生活环境而不是基因。来自加利福尼亚大学的研究者Maria Glymour表示,20世纪晚些时候出生的美国人很有可能会发胖很多,而这或许并不较高的肥胖遗传风险所致。

具有较高肥胖遗传风险的人们似乎会更多受到现代社会发展的影响,从而促进其变得肥胖,比如廉价高热量食物、步行机会降低等。有些人尤其会对环境状况变得敏感从而促进机体肥胖。研究者认为,自从肥胖流行开始,甚至低肥胖风险的个体都会变得肥胖,这或许就表明,环境会影响到每个人,但高肥胖风险的个体总会被较多地影响着。

这项研究中,研究者对1900年至1958年间出生的8800名成年个体的数据进行了研究分析,他们根据每一位参与者是否携带了和肥胖相关的29种遗传突变来计算其肥胖遗传风险分值,随后将危险评分同每位参与者的实际体重指数(BMI)进行对比。研究者发现,随着时间延续,肥胖相关基因的存在并不会在人群中增加,而随着现代社会生活环境的改变,这些基因对BMI的影响却会在随后的几十年里增加。

Glymour表示,对于肥胖流行最根本的解释或许依赖于环境的改变,尽管本文研究并没有证明这两者之间存在某种因果关系。如今现代社会环境中有很多中因素都会同个体机体的遗传性相互作用来使得个体肥胖风险增加。其中一种可能性就是遗传因子会影响饥饿,或许携带某种遗传突变会使得个体持续饥饿,同时这些个体也很容易获得热量较高的食物。而另外一种解释就是现代社会的很多便利性会使得个体经常久坐,从而导致肥胖流行的发生。

体重增加实际上是两方面的等式,即我们摄入卡路里的量vs机体燃烧卡路里的量,人们往往会花费大量金钱在快餐上,而且很少参加体育活动;最后研究者表示,肥胖基因的流行或许并不会改变人群的肥胖流行,而造成人群肥胖流行的的罪魁祸首却是人们所生活的环境。(生物谷Bioon.com)

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Association of a Genetic Risk Score With Body Mass Index Across Different Birth Cohorts

Stefan Walter, PhD1; Iván Mejía-Guevara, PhD2; Karol Estrada, PhD3; Sze Y. Liu, PhD2; M. Maria Glymour, ScD1

 

Importance Many genetic variants are associated with body mass index (BMI). Associations may have changed with the 20th century obesity epidemic and may differ for black vs white individuals. Objective Using birth cohort as an indicator for exposure to obesogenic environment, to evaluate whether genetic predisposition to higher BMI has a larger magnitude of association among adults from more recent birth cohorts, who were exposed to the obesity epidemic at younger ages. Design, Setting, and Participants Observational study of 8788 adults in the US national Health and Retirement Study who were aged 50 years and older, born between 1900 and 1958, with as many as 12 BMI assessments from 1992 to 2014. Exposures A multilocus genetic risk score for BMI (GRS-BMI), calculated as the weighted sum of alleles of 29 single nucleotide polymorphisms associated with BMI, with weights equal to the published per-allele effects. The GRS-BMI represents how much each person’s BMI is expected to differ, based on genetic background (with respect to these 29 loci), from the BMI of a sample member with median genetic risk. The median-centered GRS-BMI ranged from −1.68 to 2.01. Main Outcomes and Measures BMI based on self-reported height and weight. Results GRS-BMI was significantly associated with BMI among white participants (n = 7482; mean age at first assessment, 59 years; 3373 [45%] were men; P <.001) and among black participants (n = 1306; mean age at first assessment, 57 years; 505 [39%] were men; P <.001) but accounted for 0.99% of variation in BMI among white participants and 1.37% among black participants. In multilevel models accounting for age, the magnitude of associations of GRS-BMI with BMI were larger for more recent birth cohorts. For example, among white participants, each unit higher GRS-BMI was associated with a difference in BMI of 1.37 (95% CI, 0.93 to 1.80) if born after 1943, and 0.17 (95% CI, −0.55 to 0.89) if born before 1924 (P = .006). For black participants, each unit higher GRS-BMI was associated with a difference in BMI of 3.70 (95% CI, 2.42 to 4.97) if born after 1943, and 1.44 (95% CI, −1.40 to 4.29) if born before 1924. Conclusions and Relevance For participants born between 1900 and 1958, the magnitude of association between BMI and a genetic risk score for BMI was larger among persons born in later cohorts. This suggests that associations of known genetic variants with BMI may be modified by obesogenic environments.

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