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 various genetic susceptibilities. They found that genetic predisposition synergistically interacts with an increased risk of CAD related to 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 big reason for death and disability worldwide, is reported to be related to genetic aspects identified as single nucleotide polymorphisms (SNPs), which could be quantified to assist predict the chance of CAD in a person. Moreover, modifiable lifestyle-related aspects comparable to eating regimen are also known to be related to the chance of CAD. Nevertheless, limited evidence is on the market on the potential influence of dietary aspects on the chance of CAD amongst people from different genetic backgrounds.
While eggs are a wealthy and reasonably priced 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 1 whole egg per day, this advice doesn’t consider the genetic variability amongst populations. Moreover, previous population-based studies provide conflicting evidence on the association between egg consumption and the chance of CAD. Subsequently, the current study aimed to research the potential influence of genetic susceptibility on the association of egg consumption with the chance of incident CAD. From a public health perspective, it further aimed to discover the population of people most benefited by a reduced consumption of eggs.
Concerning the study
As a component of the “prediction for atherosclerotic heart problems risk in China” (China-PAR) project, the current study included 34,111 individuals with eligible genotype data and without CAD on the baseline. The exclusion criteria included missing data on egg consumption and a history of chronic diseases comparable to 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 judge the egg consumption of participants on the baseline in addition to within the follow-up visits. On 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 evaluate the genetic susceptibility, the researchers derived a combined predefined polygenic risk rating (PRS) based on 540 SNPs for CAD and related traits. Participants’ blood samples were used for genotyping, and the person PRS for every individual was calculated. Further, other covariates were assessed using questionnaires, including sociodemographic characteristics in addition to traditional risk aspects comparable to 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 usage of a cohort-stratified Cox proportional hazards regression model to find out the hazard ratio (HR) for incident CAD related to PRS and egg consumption.
Results and discussion
The prevalence of hypertension and diabetes, in addition to the chance of incident CAD, was found to extend with increased egg consumption. In a median follow-up of 11.7 years, 1,128 cases of CAD were reported among the many participants. The cumulative incidence of CAD was found to be highest within the participants consuming ≥ 10 eggs/week (HR = 1.42). Further, the chance of incident CAD was found to have a linear relationship with PRS. Predictably, the individuals with the upper genetic risk (standard deviation of PRS) showed a significantly higher incidence of CAD as in comparison with those with the lower genetic risk.
Further, it was found that the chance of CAD increased with an increased consumption of eggs in individuals of low genetic risk (HR = 1.05) in addition to high genetic risk (HR = 1.10). Nevertheless, 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 primary time, this study identified a big synergistic interplay between egg consumption and genetic aspects, indicating that the connection between egg consumption and CAD risk will not be homogeneous between individuals with various genetic backgrounds. The long-term follow-up of participants, the big sample size, and the stringent quality control are among the study’s strengths. Nevertheless, the study doesn’t consider the whole cholesterol and energy intake of participants. Further research is required to grasp the biological mechanisms underlying the interactions observed on this study.
Conclusion
Overall, this massive, prospective study provides evidence that the chance of incident CAD is elevated in individuals with higher egg consumption and genetic predisposition. The findings of this study could be potentially applied to develop personalized dietary recommendations for people at a greater genetic risk of CAD, thereby aiding the prevention of the disease and improving public health outcomes.