Egg consumption and risk of coronary artery disease, potential amplification by high genetic susceptibility: a
Xue Xia1, Fangchao Liu2, Keyong Huang3
1Department of Epidemiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; Key Laboratory of Cardiovascular Epidemiology, Chinese Academy of Medical Sciences, Beijing, China; Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Background:
Remarkable heterogeneity has been observed among population-based studies on egg consumption and risk of coronary artery disease (CAD). Whether genetic susceptibility serves as a potential explanation for this inconsistency remains unknown.
Objectives:
We performed a prospective cohort study to investigate the association of egg consumption with incident CAD at different genetic susceptibilities.
Methods:
We included 34,111 participants without CAD at baseline from the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China. Egg consumption was assessed with food frequency questionnaires. Genetic susceptibility was quantified by a predefined polygenic risk score (PRS) with 540 genetic variants. The hazard ratio (HR) and 95% confidence interval (95% CI) of incident CAD associated with egg consumption and PRS were estimated using the Cox proportional hazards models.
Results:
Over a median 11.7 y of follow-up, 1,128 incident cases of CAD were recorded. Both higher egg consumption and increased PRS were related to higher risk of CAD. When stratified by genetic risk, each increment of 3 eggs/wk was associated with a 5% higher risk of CAD for participants at low to intermediate genetic risk (HR: 1.05; 95% CI: 1.01, 1.09), whereas risk increased to HR 1.10 (95% CI: 1.05, 1.16) for those at high genetic risk; a significant synergistic interaction was also indicated at both multiplicative (Pinteraction = 0.007) and additive (relative excess risk: 0.73; 95% CI: 0.24, 1.22) scales. When the joint effect was examined, in comparison with those at low to intermediate genetic risk and consuming <1 egg/wk, the HR (95% CI) was 2.95 (2.41, 3.62) for participants with high genetic risk and consumption of ≥10 eggs/wk, and the corresponding standardized 10-y CAD rates increased from 1.37% to 4.24%.
Conclusions:
Genetic predisposition may synergistically interact with egg consumption in relation to increased CAD risk. PRS-stratified recommendations on egg consumption may help formulate personalized nutrition policies.
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