While the consumption of chicken as a source of protein has become popularized in recent decades, eggs have been unfairly vilified, in part because of misconceptions regarding their cholesterol content. For decades, the American public was told that eggs, as a source of cholesterol and saturated fats, promote heart disease. 

However, in recent years, studies have clearly shown that eggs — particularly egg yolks — are one of the healthiest foods you can eat, and even though egg yolks are relatively high in cholesterol, numerous studies have confirmed eggs have virtually nothing to do with raising your cholesterol, having only a minimal impact on plasma lipoprotein levels.¹ As previously reported by NPR:²

“[E]ating cholesterol can raise levels of it in the blood, but, as a growing body of research has shown, not by that much. Consuming sugar, trans fats or excessive saturated fat (from unhealthy sources) can be more harmful to cholesterol levels than dietary cholesterol itself. 

Most of the cholesterol in our bodies we make ourselves in the liver, and total body levels are heavily influenced by genetics, gender and age. As more and more research suggests that some degree of cholesterol consumption is harmless, if not healthy, the egg’s reputation is gradually returning.” 

In 2015, dietary cholesterol (and egg restriction) was finally eliminated from the U.S. dietary guidelines, and the controversy appeared to have settled. Now, a new study is again urging people to avoid eggs, linking egg consumption and dietary cholesterol to an increased risk of cardiovascular disease and death.

New Study, Old Arguments

The study^3,4,5 in question, published in the journal JAMA on March 19, 2019, analyzed data from 29,615 American adults pooled from six prospective cohort studies with a median follow-up of 17.5 years, and claims to have found a dose-dependent relationship between egg consumption and cardiovascular disease (CVD) and all-cause mortality. 

The researchers calculated two risk ratios: an adjusted hazard ratio (HR) and an adjusted absolute risk difference (ARD). According to this study:

• Each 300 milligrams (mg) of dietary cholesterol consumed per day (equating to approximately one and a half eggs) had a: 

◦ HR of 17 percent and an ARD of 3.24 percent for CVD 

◦ HR of 18 percent and an ARD of 4.43 percent for all-cause mortality

• Even each additional half an egg consumed per day was associated with higher risk of incident CVD and all-cause mortality 

• Eating three to four eggs per week was associated with a: 

◦ HR of 6 percent and an ARD of 1.11 percent for CVD 

◦ HR of 8 percent and an ARD of 1.93 percent for all-cause mortality

According to lead researcher Wenze Zhong, Ph.D.,⁶ a postdoctoral fellow at the Feinberg School of Medicine at Northwestern University in the Department of Preventive Medicine, the results suggest there’s no safe amount of egg consumption, and the team believes the results should be taken into consideration when the U.S. dietary guidelines are updated. 

“Any level of egg consumption is associated with increased risk of cardiovascular disease and mortality, because we found a dose-response association. Greater consumption means higher risk,” he told Runner’s World.⁷

What’s Wrong With This Egg Study?

A number of health and nutritional experts have already weighed in on the study, pointing out its multiple flaws. As noted by Runner’s World:⁸

“’For one, the amount of risk, or hazard, that’s reported here is trivial —and the way in which they calculated it doesn’t exactly lend itself to an easy determination of someone’s true risk,’ [Stuart] Phillips [Ph.D., director of the McMaster Centre for Nutrition, Exercise, and Health Research] said … 

[T]he researchers noted there may be measurement error because the diet data was based on recall … Not only can this type of self-reported data be unreliable, but also, researchers assessed this only once … and assumed it didn’t change in an average of 17 years of follow-up.

Also, they stated that all cohorts used different dietary assessment tools, leading them to implement their own methodology to harmonize diet data. Finally, the study findings are observational, so while they can suggest a relationship, they can’t prove that one thing caused the other.”

Andrew Mente, Ph.D., principal investigator for the Epidemiology Program at the Population Health Research Institute, pointed out a clear contradiction in the data, telling Runner’s World:⁹

“The primary hypothesis here is that eggs increase your bad cholesterol, and the more you eat, the worse it gets. But buried way down in the appendix is a note that they found higher egg intake is related to a reduction in LDL, your bad cholesterol. So, what’s driving the association in this research? It seems like there’s a contradiction with the findings.”

I interviewed Dr. Malcolm Kendrick, author of “Doctoring Data: How to Sort Out Medical Advice From Medical Nonsense,” right after the study was published and he echoed Mente’s concerns above. Below is a slice of my upcoming interview with him.

Zoe Harcombe, who has a Ph.D., in public health nutrition, went a step further, listing no less than 10 different problems, including the following:^10,11

The study found an association between egg consumption and CVD, but not coronary heart disease, which is a major part of CVD.

The meta-analysis included six studies, one of which was dominant, and all of which looked at American populations only, which means findings are not applicable to non-Americans, as dietary patterns are not generalizable between populations.

Association does not mean causation, and according to Harcombe, “17 percent is too small to get off the ground for Bradford Hill criteria,” also known as Hill’s criteria for causation.12 This refers to a set of nine principles commonly referred to when trying to establish evidence of a causal relationship between a proposed cause and an observed effect. The nine criteria include effect size (strength of association), reproducibility of effects, specificity, temporality, biological gradient, plausibility, coherence, experimental evidence and analogous evidence.

Harcombe explains the 17 percent relative risk saying, “It would equate to an absolute risk difference of 17 versus 15 events (i.e., two events) per 1,000 person years to use the event rate from the dominant study” of the six studies included in the analysis.

The study did not evaluate pure egg consumption. “It was a study of ‘Ingredients in mixed dishes,’” Harcombe says, “which — for eggs — means a long list of junk food from cakes to ice cream.”

They also did not adjust for significantly different CVD risk factors. Instead, it was assumed that different characteristics could have been caused by eggs and/or cholesterol.

Interestingly, people reporting the lowest intake of dietary cholesterol also had significantly lower energy intake overall — a mere one-third of the energy intake of those with the highest cholesterol intake. Harcombe suggests, “Maybe people weren’t eating more eggs or dietary cholesterol — they were just more honest about, or better at recalling, their food intake!”

The researchers also resorted to a strangely random selection when it came time to calculate the risk of harm from each additional half egg. “[S]ub-group analysis revealed that this only applied to specific, but random, groups of participants, e.g., women, but not men; slim, but not overweight people.”

And now for the BIG one — conflicts of interest — Harcombe points out they’re “the who’s who of statin manufacturers,” adding, “The paper appears to have as its core purpose resurrection of the diet-cholesterol-heart myth — the dietary cholesterol part of which was rejected … at least 65 years ago.”