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Use of genetic markers and gene-diet interactions for interrogating population-level causal influences of diet on health

机译：利用遗传标记和基因-饮食相互作用来询问饮食对健康的人口水平因果影响

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Differences in diet appear to contribute substantially to the burden of disease in populations, and therefore changes in diet could lead to major improvements in public health. This is predicated on the reliable identification of causal effects of nutrition on health, and unfortunately nutritional epidemiology has deficiencies in terms of identifying these. This is reflected in the many cases where observational studies have suggested that a nutritional factor is protective against disease, and randomized controlled trials have failed to verify this. The use of genetic variants as proxy measures of nutritional exposure—an application of the Mendelian randomization principle—can contribute to strengthening causal inference in this field. Genetic variants are not subject to bias due to reverse causation (disease processes influencing exposure, rather than vice versa) or recall bias, and if obvious precautions are applied are not influenced by confounding or attenuation by errors. This is illustrated in the case of epidemiological studies of alcohol intake and various health outcomes, through the use of genetic variants related to alcohol metabolism (in ALDH2 and ADH1B). Examples from other areas of nutritional epidemiology and of the informative nature of gene–environment interactions interpreted within the Mendelian randomization framework are presented, and the potential limitations of the approach addressed.
机译：饮食差异似乎在很大程度上加剧了人口的疾病负担，因此饮食的变化可能导致公共卫生的重大改善。这是基于对营养对健康的因果关系的可靠识别，不幸的是，营养流行病学在识别这些方面存在不足。这在很多情况下都得到了反映，观察研究表明营养因素可以预防疾病，而随机对照试验未能对此进行验证。使用遗传变异作为营养暴露的替代指标（孟德尔随机原则的应用）可以有助于加强该领域的因果推断。遗传变异不会因反向因果关系（疾病过程影响暴露，而不是相反）而产生偏见或召回偏见，并且如果采取了明显的预防措施，则不会因混淆或错误导致的衰减而受到影响。通过使用与酒精代谢有关的遗传变异（在ALDH2和ADH1B中），对酒精摄入和各种健康结果进行的流行病学研究证明了这一点。提供了营养流行病学其他领域的实例以及孟德尔随机化框架内解释的基因与环境相互作用的信息性质的示例，并探讨了该方法的潜在局限性。

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