期刊
PLOS GENETICS
卷 18, 期 6, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.1010162
关键词
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资金
- MRC Human Genetics Unit quinquennial programme grant QTL in Health and Disease [MC_UU_00007/10]
- Estonian Research Council [IUT20-60, PRG1291, PUT1665, PRG1197]
- European Union through the European Regional Development Fund [20142020.4.01.15-0012 GENTRANSMED, 2014-2020.4.2.2]
- Estonian Research Roadmap grant [2014-2020.4.01.16-0125]
- European Research Roadmap grant [2014-2020.4.01.16-0125]
- Medical Research Council [MR/N003284/1, MCPC_13048, MC-UU_12015/1, MC_UU_00006/1]
- Medical Research Council
- Wellcome Trust [074548]
- UK Medical Research Council Epidemiology Unit core grant [MC_UU_00006/2, MC_UU_00006/3]
- UK Medical Research Council [MC_UU_00011/4]
- Swiss National Science Foundation [31003A_169929]
- American Diabetes Association [7-21-JDFM005]
- National Institutes of Health [P30 DK040561]
- Swiss National Science Foundation (SNF) [31003A_169929] Funding Source: Swiss National Science Foundation (SNF)
Diet is a crucial factor in human health, and using Mendelian randomization, this study provides evidence of causal associations between specific eating patterns and obesity, blood lipid status, and several other risk factors and health outcomes.
Diet is considered as one of the most important modifiable factors influencing human health, but efforts to identify foods or dietary patterns associated with health outcomes often suffer from biases, confounding, and reverse causation. Applying Mendelian randomization in this context may provide evidence to strengthen causality in nutrition research. To this end, we first identified 283 genetic markers associated with dietary intake in 445,779 UK Biobank participants. We then converted these associations into direct genetic effects on food exposures by adjusting them for effects mediated via other traits. The SNPs which did not show evidence of mediation were then used for MR, assessing the association between genetically predicted food choices and other risk factors, health outcomes. We show that using all associated SNPs without omitting those which show evidence of mediation, leads to biases in downstream analyses (genetic correlations, causal inference), similar to those present in observational studies. However, MR analyses using SNPs which have only a direct effect on the exposure on food exposures provided unequivocal evidence of causal associations between specific eating patterns and obesity, blood lipid status, and several other risk factors and health outcomes. Author summaryFood and drink consumption is one of the most important factors influencing human health and wellbeing. The role of diet in human physiology and disease has been widely studied, but challenges in accurately assessing long term diet result in contradicting findings. Mendelian randomization is a statistical technique that uses genetic variants associated with modifiable exposures to estimate the causal effect of an exposure to a health outcome and could be extremely useful in the context of diet-health relationships. In our study, we initially identified genetic variants associated to 29 measures of food and drink consumption. We then show that genetic variants associated with food and drink consumption are subject to reverse causation and confounding. We have thus developed a statistical genetics method to identify genetic variants directly associated with food and drink consumption. By using these genetic variants (and their corresponding direct effects) in Mendelian randomization analyses we provided consistent evidence of causal associations of food and drink consumption with obesity, blood lipid status, and several other risk factors and health outcomes.
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