In a prospective cohort study published in The American Journal of Clinical Nutrition, researchers in China investigated the association between egg consumption and coronary artery disease (CAD) at varying genetic susceptibilities. They found that genetic predisposition synergistically interacts with an increased risk of CAD associated with egg consumption.
Study: Egg consumption and risk of coronary artery disease, potential amplification by high genetic susceptibility: a prospective cohort study. Image Credit: MasAnyanka / Shutterstock
Background
CAD, a significant cause of death and disability worldwide, is reported to be associated with genetic factors identified as single nucleotide polymorphisms (SNPs), which can be quantified to help predict the risk of CAD in an individual. Additionally, modifiable lifestyle-related factors such as diet are also known to be associated with the risk of CAD. However, limited evidence is available on the potential influence of dietary factors on the risk of CAD among people from different genetic backgrounds.
While eggs are a rich and affordable source of dietary protein, lecithin, and unsaturated fatty acids, they contain high levels of cholesterol. Although the American Heart Association recommends the consumption of up to one whole egg per day, this recommendation does not consider the genetic variability among populations. Additionally, previous population-based studies provide conflicting evidence on the association between egg consumption and the risk of CAD. Therefore, the present study aimed to investigate the potential influence of genetic susceptibility on the association of egg consumption with the risk of incident CAD. From a public health perspective, it further aimed to identify the population of individuals most benefited by a reduced consumption of eggs.
About the study
As a part of the "prediction for atherosclerotic cardiovascular disease risk in China" (China-PAR) project, the present study included 34,111 individuals with eligible genotype data and without CAD at the baseline. The exclusion criteria included missing data on egg consumption and a history of chronic diseases such as cancer, end-stage renal diseases, or cardiovascular diseases.
The mean age of participants was 52.3 years, and 41.8% were males. Food frequency questionnaires were used to evaluate the egg consumption of participants at the baseline as well as in the follow-up visits. At the baseline, the participants consumed eggs at frequencies of <1 egg/week (15.61%), 1–<3 eggs/week (23.68%), 3–<6 eggs/week (24.5%), 6–<10 eggs/week (17.81%), and ≥10 eggs/week (18.39%).
To assess the genetic susceptibility, the researchers derived a combined predefined polygenic risk score (PRS) based on 540 SNPs for CAD and related traits. Participants' blood samples were used for genotyping, and the individual PRS for each individual was calculated. Further, other covariates were assessed using questionnaires, including sociodemographic characteristics as well as traditional risk factors such as family history of CAD, smoking, alcohol consumption, intake of high-cholesterol foods, body mass index, hypertension, diabetes, hypercholesterolemia, and physical activity. The statistical analyses included the use of a cohort-stratified Cox proportional hazards regression model to determine the hazard ratio (HR) for incident CAD associated with PRS and egg consumption.
Results and discussion
The prevalence of hypertension and diabetes, as well as the risk of incident CAD, was found to increase with increased egg consumption. In a median follow-up of 11.7 years, 1,128 cases of CAD were reported among the participants. The cumulative incidence of CAD was found to be highest in the participants consuming ≥ 10 eggs/week (HR = 1.42). Further, the risk of incident CAD was found to have a linear relationship with PRS. Predictably, the individuals with the higher genetic risk (standard deviation of PRS) showed a significantly higher incidence of CAD as compared to those with the lower genetic risk.
Further, it was found that the risk of CAD increased with an increased consumption of eggs in individuals of low genetic risk (HR = 1.05) as well as high genetic risk (HR = 1.10). However, the effect of increased egg consumption on CAD risk was more substantial in those with a high genetic risk. Overall, the researchers observed an increasing trend in incident CAD, as estimated using HRs and 10-year cumulative rates, in individuals with higher egg consumption and genetic susceptibility.
For the first time, this study identified a significant synergistic interplay between egg consumption and genetic factors, indicating that the relationship between egg consumption and CAD risk may not be homogeneous between people with varying genetic backgrounds. The long-term follow-up of participants, the large sample size, and the stringent quality control are some of the study's strengths. However, the study does not consider the total cholesterol and energy intake of participants. Further research is required to understand the biological mechanisms underlying the interactions observed in this study.
Conclusion
Overall, this large, prospective study provides evidence that the risk of incident CAD is elevated in individuals with higher egg consumption and genetic predisposition. The findings of this study can be potentially applied to develop personalized dietary recommendations for individuals at a greater genetic risk of CAD, thereby aiding the prevention of the disease and improving public health outcomes.
Genetics studies have a diversity problem that researchers struggle to fix