Background: Breakfast skipping has been linked to poor cardiometabolic health in observational studies, but the causality remains unknown. Herein, we used Mendelian randomization (MR) approach to elucidate the potential causal effects of breakfast skipping on cardiometabolic traits.
Methods: Genetic association estimates for breakfast skipping, cardiometabolic diseases, and cardiometabolic risk factors were extracted from the UK Biobank and several large genome-wide association studies. Two-sample MR analyses were performed primarily using the inverse variance weighted method, followed by sensitivity analysis to test the reliability of results.
Results: MR results indicated no causal relationship between breakfast shipping with coronary heart disease (odds ratio [OR]: 1.079, 95 % confidence interval [CI]: 0.817-1.426; p = 0.591), stroke (OR: 0.877, 95 % CI: 0.680-1.131; p = 0.311), and type 2 diabetes mellitus (OR: 1.114, 95 % CI: 0.631-1.970; p = 0.709). However, genetically predicted breakfast skipping was significantly associated with increased body mass index (β: 0.250, standard error [SE]: 0.079; p = 0.001), waist-to-hip ratio (β: 0.177, SE: 0.076; p = 0.019), and low-density lipoprotein cholesterol (β: 0.260, SE: 0.115; p = 0.024). We found no evidence of association of genetic liability to breakfast skipping with blood pressure, glycemic traits, and other blood lipids. Sensitivity analysis supported the above results.
Conclusion: Our study suggested that breakfast skipping is causally linked to weight gain and higher serum low-density lipoprotein cholesterol, which may mediate the increased risk of cardiometabolic diseases reported in epidemiological studies.
Keywords: Breakfast skipping; Cardiometabolic health; Causality; Mendelian randomization.
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