Interactions
Interactions
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DOI：
10.1136/bmj.e865
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发表时间：
2012-02
期刊：
影响因子：
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通讯作者：
Larry Minear;Thomas G. Weiss
中科院分区：
文献类型：
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作者：
Larry Minear;Thomas G. Weiss
背景：以前的研究表明，现代肥胖环境加重了肥胖的遗传风险。然而，这些研究已被证明是有争议的，如果有的话，哪些环境措施会加重对高体重指数（BMI）的遗传易感性。研究方法：我们使用了来自英国生物银行研究的多达12万名成年人来测试这一假设，即高风险的致胖环境和行为会加重肥胖的遗传易感性。我们使用BMI作为结果，使用69种肥胖遗传风险评分（GRS）和12种致胖环境指标作为暴露。这些措施包括汤森剥夺指数（TDI）作为衡量社会经济地位，看电视，“西化”的饮食和体育活动。我们进行了几个阴性对照试验，包括随机选择不同平均BMI的组，使用模拟环境，并包括防晒使用作为环境。结果如下：我们发现基因与环境的相互作用与TDI（Pinteraction ¼ 3（cid：2）10 - 10），自我报告的电视观看（Pinteraction ¼ 7（cid：2）10 - 5）和自我报告的身体活动（Pinteraction ¼ 5（cid：2）10 - 6）。在50%生活在相对贫困环境中的人群中，携带10个额外的BMI提高等位基因与身高1.73米的人体重增加约3.8公斤有关。相比之下，在50%生活在最少贫困的人群中，携带10个额外的BMI提高等位基因与大约2.9公斤的额外体重相关。与阴性对照（包括防晒使用）的相互作用较弱，但存在，表明可能存在残留混淆。结论：我们的发现表明，致胖环境加重了遗传易感成年人肥胖的风险。在我们测试的因素中，相对的社会剥夺最能反映致胖环境的各个方面。特别是在减少油炸食品，碳酸饮料消费和饮食中的遗传倾向肥胖。
Background: Previous studies have suggested that modern obesogenic environments accentuate the genetic risk of obesity. However, these studies have proven controversial as to which, if any, measures of the environment accentuate genetic susceptibility to high body mass index (BMI). Methods: We used up to 120 000 adults from the UK Biobank study to test the hypothesis that high-risk obesogenic environments and behaviours accentuate genetic susceptibility to obesity. We used BMI as the outcome and a 69-variant genetic risk score (GRS) for obesity and 12 measures of the obesogenic environment as exposures. These measures included Townsend deprivation index (TDI) as a measure of socio-economic position, TV watching, a ‘Westernized’ diet and physical activity. We performed several negative control tests, including randomly selecting groups of different average BMIs, using a simulated environment and including sun-protection use as an environment. Results: We found gene–environment interactions with TDI (Pinteraction ¼ 3 (cid:2) 10 –10 ), self-reported TV watching (Pinteraction ¼ 7 (cid:2) 10 –5 ) and self-reported physical activity (Pinteraction ¼ 5 (cid:2) 10 –6 ). Within the group of 50% living in the most relatively deprived situations, carrying 10 additional BMI-raising alleles was associated with approximately 3.8 kg extra weight in someone 1.73m tall. In contrast, within the group of 50% living in the least deprivation, carrying 10 additional BMI-raising alleles was associated with approximately 2.9 kg extra weight. The interactions were weaker, but present, with the negative controls, including sun-protection use, indicating that residual confounding is likely. Conclusions: Our findings suggest that the obesogenic environment accentuates the risk of obesity in genetically susceptible adults. Of the factors we tested, relative social deprivation best captures the aspects of the obesogenic environment responsible. specific-ally at fried-food reduction, fizzy-drink consumption and diet in those genetically predisposed to obesity.