Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies.

Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies.
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DOI:
10.1136/bmj.g1610
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发表时间:
2014-03-19
期刊:
BMJ (Clinical research ed.)
影响因子:
--
通讯作者:
Qi L
Qi L
中科院分区:
其他
文献类型:
--
作者:
Qi Q;Chu AY;Kang JH;Huang J;Rose LM;Jensen MK;Liang L;Curhan GC;Pasquale LR;Wiggs JL;De Vivo I;Chan AT;Choi HK;Tamimi RM;Ridker PM;Hunter DJ;Willett WC;Rimm EB;Chasman DI;Hu FB;Qi L

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目的探讨遗传易感性和油炸食品消费与体重指数(BMI)和肥胖之间的交互作用。设计前瞻性队列研究。设置美国的卫生专业人员。参与者来自护士健康研究的9623名女性,来自卫生专业人员随访研究的6379名男性,以及来自女性基因组健康研究的21名 421女性的重复队列。主要结果:随访期间重复测量体重指数。结果在《护士健康研究》和《卫生专业人员随访研究》中,油炸食品摄入量与基于体重指数的32个体重指数相关变异的遗传风险评分之间存在交互作用(P≤0.001交互作用)。在遗传风险得分最高的三分之一的参与者中,每周食用油炸食品四次或更多与每周食用油炸食品少于一次的人之间的BMI差异女性为1.0(SE 0.2),男性为0.7(SE 0.2),而遗传风险得分最低的三分之一的参与者中,相应的差异为0.5(SE 0.2)和0.4(SE 0.2)。基因-饮食相互作用在女性基因组健康研究(P<0.001相互作用)中得到了复制。从不同的角度来看,油炸食品的摄入量越高,肥胖的基因联系就越强。在合并的三个队列中,每10个风险等位基因的体重指数在每周食用油炸食品少于1次、1~3次和4次或更多时的差异分别为1.1(SE0.2)、1.6(SE0.3)和2.2(SE0.6)(P<0.001交互作用);每10个危险等位基因对肥胖的优势比(95%可信区间)分别为1.61(1.4~1.87)、2.12(1.73~2.59)和2.72(2.12~3.48)(交互作用P=0.002)。此外,在中枢神经系统中高度表达或已知作用的基因的变异体与油炸食品的摄入量存在显著的交互作用,其中与脂肪质量和肥胖相关的变异体显示出最强的结果(P<0.001交互作用)。结论提示油炸食品的摄入与肥胖的遗传背景存在交互作用,提示在肥胖遗传易感人群中,减少油炸食品的摄入尤为重要。
Objective To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity. Design Prospective cohort study. Setting Health professionals in the United States. Participants 9623 women from the Nurses’ Health Study, 6379 men from the Health Professionals Follow-up Study, and a replication cohort of 21 421 women from the Women’s Genome Health Study. Main outcome measure Repeated measurement of BMI over follow-up. Results There was an interaction between fried food consumption and a genetic risk score based on 32 BMI-associated variants on BMI in both the Nurses’ Health Study and Health Professionals Follow-up Study (P≤0.001 for interaction). Among participants in the highest third of the genetic risk score, the differences in BMI between individuals who consumed fried foods four or more times a week and those who consumed fried foods less than once a week amounted to 1.0 (SE 0.2) in women and 0.7 (SE 0.2) in men, whereas the corresponding differences were 0.5 (SE 0.2) and 0.4 (SE 0.2) in the lowest third of the genetic risk score. The gene-diet interaction was replicated in the Women’s Genome Health Study (P<0.001 for interaction). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.1 (SE 0.2), 1.6 (SE 0.3), and 2.2 (SE 0.6) for fried food consumption less than once, one to three times, and four or more times a week (P<0.001 for interaction); and the odds ratios (95% confidence intervals) for obesity per 10 risk alleles were 1.61 (1.40 to 1.87), 2.12 (1.73 to 2.59), and 2.72 (2.12 to 3.48) across the three categories of consumption (P=0.002 for interaction). In addition, the variants in or near genes highly expressed or known to act in the central nervous system showed significant interactions with fried food consumption, with the FTO (fat mass and obesity associated) variant showing the strongest result (P<0.001 for interaction). Conclusion Our findings suggest that consumption of fried food could interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity.
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