油炸食品可放大遗传性肥胖风险

《英国医学杂志》(BMJ) (doi: 10.1136/bmj.g1610)3月19日发表的一项大型队列研究显示，吃油炸食品与遗传风险之间存在显著相互作用，经常吃油炸食品可加剧肥胖的遗传易感性。

在这项研究中，哈佛公共卫生学院的Qibin Qi医生及其同事分析了以下3个不同的研究人群中的油炸食物食用情况：2个人群分别为9,263人和6,379人的美国男性队列，另1个人群为21,421人的美国女性队列，所有人均具有欧洲血统。研究者通过问卷获取油炸食品的摄入信息，并与遗传肥胖风险评分和体重指数(BMI)进行比较。在2个较小的队列中，在肥胖遗传风险最高三分位数受试者中观察到的大量摄入油炸食物与BMI的关联，是在最低三分位数受试者中观察到的关联的近2倍，表明油炸食物的摄入与BMI之间的关联程度因遗传易感性而异。

在这2个队列中，在遗传风险最高的女性和男性中，每周吃≥4次油炸食物的受试者与每周吃＜1次油炸食物的受试者的BMI差异分别为1.0和0.7。在风险最低三分位数女性和男性中，这一差异分别为0.5和0.4。在第3个全部为女性的队列中，也观察到基因-饮食相互作用(P＜0.001)。

通过32种已知的BMI相关变异体在各例受试者中的负荷情况测定遗传风险。在总共37,063 例受试者中，每周吃油炸食物＜1次、1~3次和≥4次的受试者的BMI/10个风险等位基因差异分别为1.1、1.6和2.2 (P＜0.001)。这3个油炸食物摄入类别的肥胖/10个风险等位基因的比值比分别为1.61、2.12和2.72(P=0.002)。

既往研究发现，FTO(脂肪量和肥胖相关)基因的变异体与BMI和食欲相关，而当前研究发现，FTO变异体与油炸食物摄入之间的相互作用最强烈。研究者无法解释所观察到的基因与油炸食物之间的相互作用，但表示研究结果在校正包括其他膳食和生活方式因素(如摄入含糖饮料、体力活动和看电视)在内的混杂因素后未出现显著不同。

上述研究结果首次表明，肥胖遗传易感性较高的个体更易出现过食油炸食物对肥胖的不良影响，并且表明过食油炸食物可放大肥胖的遗传效应。

研究者表示，该研究的局限性包括：观察性设计、使用单个种族类别和全女性重复队列，以及可能存在不明混杂因素。

该研究获美国国立卫生研究院资助，基因分型方面获默克公司支持。其中1个队列的研究从安进公司获得基因分型方面的支持。研究者均声明没有与该研究相关的经济利益冲突。

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By: JENNIE SMITH, Cardiology News Digital Network

Frequent consumption of fried foods may exacerbate a genetic predisposition to obesity, according to results from a large cohort study that found a significant interaction between fried food consumption and genetic risk.

The study, published March 19 in BMJ (doi: 10.1136/bmj.g1610), looked at fried food consumption in three separate study populations: two cohorts of 9,263 and 6,379 U.S. men, and a cohort of 21,421 U.S. women, all of European ancestry.
 
The researchers, led by Qibin Qi, Ph.D., of the Harvard School of Public Health in Boston, compared subjects’ intake of fried foods, as assessed by questionnaires, with genetic obesity risk scores and body mass index. In the two smaller cohorts, the association between high fried food consumption and BMI was nearly double among those in the top tertile of genetic risk for obesity compared with those in the lowest tertile, suggesting that the degree of association between fried food consumption and BMI varied among people with different genetic predispositions.

In those two cohorts, the differences in BMI among those who consumed fried foods four or more times a week and those who consumed them less than once week were 1.0 in women and 0.7 in men who had the highest genetic risk profile. Among subjects in the lowest tertile of risk, the differences were 0.5 among women and 0.4 among men. The gene-diet interaction was replicated in the third, all-female cohort (P less than .001).

Genetic risk was measured by each individual’s load of 32 known BMI-associated variants. In the combined three cohorts, totalling 37,063 subjects, the differences in BMI per 10 risk alleles were 1.1, 1.6, and 2.2, respectively, for fried food consumption less than once, one to three times, and four or more times a week (P less than .001). The odds ratios for obesity per 10 risk alleles were 1.61, 2.12, and 2.72 across the three categories of fried food consumption (P = .002).

A variant of the FTO (fat mass and obesity–associated) gene, shown in previous studies to be linked to BMI and to appetite, was seen as having the strongest interaction with fried food consumption in this study.

Dr. Qi and colleagues could not explain the observed interaction between genes and fried food in particular, but noted that their results did not differ significantly after adjustment for confounders that included other dietary and lifestyle factors such as sweetened beverage intake, physical activity, and television watching.

The results, Dr. Qi and colleagues wrote, suggest for the first time that "individuals with a greater genetic predisposition to adiposity might be more susceptible to the adverse influence of overconsumption of fried food on adiposity," and that "overconsumption of fried foods might magnify genetic effects on adiposity."

The researchers noted as limitations of their study its observational design, its use of a single ethnic category and an all-female replication cohort, and the possibility of confounding by unknown factors.

The study was funded by the National Institutes of Health, with support from Merck for genotyping. One of the cohort studies used in this analysis had received genotyping support from Amgen. None of its authors disclosed conflicts of interest related to their research.