Eggs and your arteries–yolk or no yolk

Here we go again. The popular press gets ahold of a scientific study, misinterprets it, and runs a scary story. Of course, it’s much worse if the scientific study published in a respected journal seems to also misinterpret the study. As I mentioned before, a true skeptic needs to critically analyze whatever is written in the press by going to the original study whenever possible; but what happens if that study requires some critical analysis? Well, I never said it was easy. If you want easy, denialism is really easy!

So back to the eggs. All across the news during the past week or so, you probably saw a story that eating egg yolks cause arteriosclerosis, a chronic condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol. Some people may have already believed that anecdotally, but a new article published in AtherosclerosisEgg yolk consumption and carotid plaque, concluded that, 

Our findings suggest that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease. This hypothesis should be tested in a prospective study with more detailed information about diet, and other possible confounders such as exercise and waist circumference.

Well, newspapers and other news outlets jumped on this articles with full-throated arguments that we needed to avoid eggs. The Los Angeles Times published an article, No yolk: eating the whole egg as dangerous as smoking? As dangerous as smoking? Really? Nevertheless, the article reported that:

Smoking tobacco and eating egg yolks increased carotid wall thickness in similar fashion — which is to say, the rate of increase accelerated with each stair-step up in cigarette smoking or yolk consumption. By contrast, for those who did not smoke, or who rarely consumed egg yolks, carotid wall thickness increased after 40, but at a slow-steady rate.

Of course, smoking has other health effects like lung cancer, but sure, this might make sense. And of course, eating eggs may have benefits, according to the LA Times,

In recent years, nutritionists have begun to agree with egg purveyors that chicken eggs — cheap and packed with protein — have gotten a bad rap as a dangerous source of cholesterol. Some studies have suggested that eggs may increase HDL, or “good cholesterol” that protects against heart disease, even as it contributes to the artery-clogging LDL cholesterol, making egg consumption something of a wash. And regular egg-eaters may form larger lipoprotein particles that help clear the blood of fat particles and are not as likely to settle in artery walls.

So what are the facts? What’s really going on with eggs? Let’s go back to the Atherosclerosis article by J. David SpenceDavid J.A. Jenkins, and Jean Davignon. Unfortunately, it’s behind a pay wall (one day, these science articles need to be open-access, if we’re going to have open discussion of issues, but that’s a debate for another day), but the good people at Science Based Medicine just published a review of the Spence et al. article, Eggs and Atherosclerosis, and gave us an interesting graph with some data that seems to poke a few holes in the eggs are bad story. 

To interpret this chart, “egg group years” is the number of egg yolks eaten per week times the number of years, so more eggs are eaten in each patient grouping across the chart. As you can see, the plaque area (in the last line) increases as more eggs are eaten which would seem to imply that as you eat more eggs, the more closed the carotid artery becomes in these groups of patients. That’s not good and is a very important indicator of cardiovascular disease. But there’s a really serious issue with this data, and that is that triglycerides, HDL cholesterol (what is considered the “good” cholesterol) and LDL (“bad” cholesterol) are unchanged across the groups. Though plaque area is significantly different, the assumed cause of the plaque change, bad cholesterol, isn’t changing as a result of the increase in eating eggs.

This goes to the age old problem in science of “correlation does not imply causation.” Maybe the authors missed some other factor that is causative, such as…nothing seems to be clear with this data. As Steven Novella says at Science Based Medicine, “This strongly suggests the association is not causal but is incidental or spurious – unless an alternate mechanism can be proposed and supported by evidence.” About the only thing I would consider is that eating more eggs could mean a higher calorie diet when combined with a more sedentary lifestyle might lead to higher plaque formation, but none of this data would be supportive of that conclusion.

It is so frustrating that these food myths are invented based on cursory reading of data. But it’s even more frustrating when the scientific study seems to make a conclusion that isn’t supported by the data that it presents.

But what do other studies say. Well, a British Medical Journal article, Dietary fat intake and prevention of cardiovascular disease: systematic review, in 2001  stated that:

There is a small but potentially important reduction in cardiovascular risk with reduction or modification of dietary fat intake, seen particularly in trials of longer duration.

And a Cochrane Review, Reduced or modified dietary fat for preventing cardiovascular disease, concludes that:

The findings are suggestive of a small but potentially important reduction in cardiovascular risk on modification of dietary fat, but not reduction of total fat, in longer trials. Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates. The ideal type of unsaturated fat is unclear. 

The results seem a bit equivocal, and it’s suggestive of a general lifestyle change that include dietary changes that are not of the level of what was suggested in the “eggs are as dangerous as smoking” article in the Los Angeles Times

Published articles that directly studied effects of eggs on overall cardiovascular health are all over the place:

So what’s the overall conclusion? I don’t see any definitive data (I don’t even see equivocal data) that there is anything wrong with eating eggs in healthy adults. I don’t even see definitive data that eating eggs in those individuals with chronic diseases are increasing their risks, although the extra calories might not be necessarily a good thing. Once again, dietary claims seem to be more shrouded in myth and magic than it is in science. Once you look for evidence in dietary claims, you either find contrary evidence or varying evidence (which, unless it is conclusive, does not mean you can pick out the evidence that supports your on beliefs). 

Eat eggs if you want, but eat them in moderate quantities. Get exercise. Burn more calories than you consume. It’s not that hard.

 

The Original Skeptical Raptor
Chief Executive Officer at SkepticalRaptor
Lifetime lover of science, especially biomedical research. Spent years in academics, business development, research, and traveling the world shilling for Big Pharma. I love sports, mostly college basketball and football, hockey, and baseball. I enjoy great food and intelligent conversation. And a delicious morning coffee!

16 Replies to “Eggs and your arteries–yolk or no yolk”

  1. Is It Time to 'Eggsonerate' Eggs? By James J. Kenney, PhD, RD, FACN.

    Dietary cholesterol has been shown to elevate LDL-cholesterol levels and has been associated with an increased risk of developing atherosclerosis and coronary heart disease (CHD). This has led the American Heart Association, the National Cholesterol Education Program, and the US Dietary Guidelines to all recommend that Americans should limit their intake of dietary cholesterol and eggs. With eggs being the single greatest source of dietary cholesterol in the American diet, such advise is obviously not conducive to the sale of more eggs. Not surprisingly the commercial egg industry is less than thrilled with recommendations to limit dietary cholesterol and/or eggs. In a long running propaganda campaign led by the Egg Nutrition Center there has been a steady stream of media reports for decades mostly orchestrated by the Egg Nutrition Center proclaiming that dietary cholesterol and eggs have little impact on serum cholesterol levels and are not responsible for CHD. For example, the Fall 2011 issue of the Nutrition Close-Up newsletter from the Egg Nutrition Center has a blurb titled "Rethinking Dietary Cholesterol" in which they sum up an opinion article published in Current Opinion in Clinical Nutrition and Metabolic Care by Dr. Fernandez, stating "… the lack of a relationship between dietary cholesterol and CHD should be sufficient to support the policy of no upper limit for dietary cholesterol." Already based on the flawed arguments of apologists for the egg industry have seen several European countries, Korea, India, Australia, and Canada have removed the limits of dietary cholesterol from their dietary guidelines. Could pseudoscientific arguments espoused by Dr. Fernandez and propaganda from the American Egg Board result in the "eggsoneration" of dietary cholesterol and eggs from the limits placed on their intake by the AHA and public health agencies in the US? Perhaps but should it happen and Americans started eating more eggs and cholesterol there is little doubt that this would raise total and LDL-cholesterol levels.1 Indeed, a study of vegetarian college students showed in a double-blind controlled clinical trial that increasing their dietary cholesterol with more eggs from 97mg to 418mg per day raised LDL-cholesterol levels by an average of 12% in 3 weeks.2 In addition to elevated fasting cholesterol levels there is growing data showing that eating more eggs and cholesterol damages arteries by altering postprandial blood lipids, increasing inflammation, and impairing endothelial function.3 1 AJCN 1981;34:2092-9 2 Lancet, March 1984:647-9 3 Can J Cardiol 2010;26:e336-e339.

    1. Though I'm no fan of the "Big Egg" or "Big Pharma" ad hominem, fundamentally I would agree there should be limits on consumption. I need to read the articles, but comparing vegetarians or vegans over 3 weeks sounds like a impossibly short period of time to make a serious physiological conclusion. Since you're the expert on these mechanisms, I bet you could tell me why the numbers go up, and what MIGHT be predicted in 12 months in a normal healthy adult who switches from pure vegan to eating say 10 eggs a week. Maybe there's some temporary adaptive response. In fact, I might bet on it, but I'm not knowledgeable on what might happen. But I'm just very skeptical that a 3 week response has any medical validity.

  2. Dietary fat & cholesterol is absorbed via chylomicrons. Chylomicrons are similar to triglyceride-rich VLDL particles generated by the liver. As chylomicorns and VLDL particles give up their triglyceride content and lose some of their apoproteins and other proteins they degrade into cholesterol-rich remnant particles. Both chylomicron remnants and VLDL-remnants (a.k.a. LDL) are known to get into the artery wall and promote atherosclerosis. So chylomicron remnants get enriched in cholesterol from dietary cholesterol and some of this ends up in the artery wall. Chylomicrons also give up cholesterol and Apo-CIII to HDL particles rendering them proatherogenic. So when you say there is no plausible explanantion as to how dietary cholesterol might promote atherosclerosis absent significant adverse changes in fasting blood lipids that is not entirely correct. Primates generally do not develop much atherosclerotic plaque without dietary cholesterol so assuming humans are unique among primates also seems questionable. I think we can agree that we need more data on these relationships but in the interim given the totality of what we know and strongly suspect promotes atherosclerosis I think it prudent to discourage people at risk of CVD events from eating eggs (and other foods high in cholesterol and/or saturated fat).

    1. First, I'm not sure where I mentioned that humans were unique amongst primates. In fact, I would never mention that because I wouldn't actually believe that. I consider primate models to possibly be proxies for human diets:

      http://www.skepticalraptor.com/skepticalraptorblog.php/eating-great-ape-relatives/

      Maybe you read that somewhere else, and thought I wrote it.

      Furthermore, I was specifically debunking the Spence article which was creating a conclusion from correlation without providing causation. Though you have provided a plausible mechanism of causality, it is unsupported by the data specifically provided by the Spence article because even triglyceride levels were flat across the egg eating groups. Absent any other information, yes it would be prudent to discourage individuals at risk for CVD events to reduce fats, if at the minimum to reduce calorie intake. But in general, eggs aren't dangerous, and certainly your and Spence's hypotheses are unsupported by the data in this paper, which is the only one I really considered.

    2. I think you my point with primates. All I was pointing out that dietary cholesterol added to their diets does promte the growth of atherosclerosis. There also seems some confusion regarding TG levels being flat having some relevance to the atherogenic impact of dietary cholesterol. It does not as dietary cholesterol has no real impact on either postprandial or fasting TG levels. What dietary cholesterol does is enrich the chylomicron particles with cholesterol (not TG). Now dietary fat does increase postprandial TG levels markedly but this is largely ignored as most MDs measure only fasting blood lipid levels.

      What is a bit perplexing about the Spence article is the fact that higher dietary cholesterol intake was not correlated with higher serum Total-C and LDL-C levels. The evidence is overwhelming that dietary cholesterol raises both total-C and LDL-C. It may also raise HDL-C a bit but it may do so by increasing the transfer of cholesterol from the chylomicrons to HDLs and also dietary may down regulate Scanvanger receptor B1 in the liver. We know that dietary saturated fat down regulates these SR-B1 receptors and can raise HDL-C. However, while fewer SR-B1s may increase HDL-C by slowing its clearance from the blood this is not a good thing as the SR-B1s are largely responsible for reverse cholesterol transport. That plus an increase in Apo-CIII attached to HDL-C is why some people with high HDL-C levels still develop a lot of atherosclerosis. Are you familiar with the recent studies showing that there is "bad" HDL particles thast actually promote atherosclerosis?

      Certainly we agree that the Spence data in a vacuum would hardly be sufficient to make warrant telling people to limit dietary cholesterol. However, when viewed in context of all the other data linking increased dietary cholesterol with more atherosclerosis it is certainly yet one more bit of data suggesting that it may be wise to limit dietary cholesterol intake if one wants to reduce the risk of CVD events. So when you say you don't even see any equivocal data linking egg intake with any disease I would beg to differ.

    3. James Kenney You actually prove a more general point I make about science. It's impossible for someone in the biomedical sciences to be an expert in all fields. I actually have a substantial background in cardiology, but in a very specific area of it, and you're making points that I wouldn't know. Once again, I'm with you on CVD disease, but once again, the Spence article would never convince me of your point-of-view!

      The evidence, however, for eggs causing atheriosclerosis in a healthy adult, absent other risk factors, is just equivocal. I posted in my article rather well done reviews and meta-reviews (trying to avoid primary data) of eggs vs. CVD, and there just seems to be no correlation that we can say "yes, there it is."

      I remain highly skeptical of the science of diets in general, and just as skeptical here. But, you have given me some pause for reevaluation, and you have provided a reasonable and plausible biochemical mechanism, but the data remains equivocal from my review.

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