Chickens kept at home in the backyard produce eggs of varying size and colour, yet their nutritional quality, just like the uniform supermarket eggs, is determined by the bird’s diet. For instance, eggs that are laid by pasture-fed birds eat green grass and  grubs which is necessary for the synthesis of omega-3 fatty acids, while grain-fed birds produce eggs that are high in omega-6 fatty acid instead.

The golden yokes of eggs obtained from pasture-fed birds testifies to their nutritional worth. The yolk contains nutrients such as protein, fats, cholesterol, carbohydrate, minerals and vitamins, while the white contains about 90% water, as well as proteins such as albumin and globulin, trace minerals, vitamins and glucose. As a result, eggs are very nutritious and a good source of high quality protein for people who can’t afford to consume meat regularly.

‘How many eggs can I eat?’ is a frequently asked question in clinic, and when I look at the patient’s finger nails, skin and tongue I know that they would love to eat more. So how did we get to the unfortunate point where people fearfully suppress a natural desire to eat this nutrient-dense wholefood but feel unashamed eating as much margarine, sugar and white bread as they like?

In 1968 it was recommended by the American Heart Association that people should consume no more than 300 mg of dietary cholesterol per day, which amounts to little more than one egg. This recommendation was based on the state of the research at the time which had severe limitations. The data, associating dietary cholesterol with blood cholesterol levels, came from three sources: firstly, animal studies using herbivores such as rabbits, which are much more sensitive to dietary cholesterol than dogs or humans; secondly, epidemiology statistics which involved simple correlations of dietary cholesterol and heart disease; and thirdly, clinical studies in which very large quantities of egg cholesterol was used.¹

The animal studies date back to experiments in Germany in 1912 by Nikolay Anitchkov, who fed egg cholesterol to rabbits and subsequently produced arterial plague. Six decades later the experiments could not be reproduced by American researchers until they realised that the cholesterol had been inadvertently oxidised in the lab while separated from the rest of the egg, before it was fed to the animals. This pre-oxidation, as you find in most highly processed foods, turned out to be central to the problem. In fact, egg cholesterol produces ‘32 auto-oxidation products some of which have lethal toxic effects on the arterial walls leading to atheroma.’²

Recent research has also found no significant relationship between dietary cholesterol from eggs and heart disease risk. An analysis of data from two famous studies, the Nurses’ Health Study and the Health Professionals Study, found no difference in risk between eating one egg per day and one egg per week—there is in fact no risk at all unless perhaps you are diabetic.³

Saturated fat, once called the leading ‘dietary villain’ by Dr. Ancel Keys has also since been found to have no significant association with heart disease risk.⁴ The slow-acting Australian Heart Foundation still recommends a maximum of 6 eggs per week, also recommending that people replace butter with margarine and canola oil. This is considered ‘prudent’ by the experts, but it is actually counterproductive because these type of modified factory-fats have the worst profile of all fats when related to heart disease or stroke.⁵

The original study behind the ‘prudent diet’ recommendations, also known as the ‘anti-coronary club’, involved 814 men divided into two groups. One was on a standard American diet and the other an experimental diet. The experimental diet included low-fat protein, low-fat dairy, the avoidance of butter, a limit on egg yolks to four per week, an increase in fish intake, and the increased consumption of polyunsaturated vegetable oil (mostly corn).⁶ This diet resulted in a marked lowering of serum cholesterol over six months in the first phase, and again at 5 years, along with a reduction in obesity and hypertension. It all looked exceptionally good, with 12 coronary ‘events’ in the control group compared to only 8 in the active experimental group on the prudent diet; however, of the 8 in the experimental group, plus a further 8 cleverly sequestered in another ‘inactive’ experimental group, half died. What is significant for the reader is that none died in the control group on the standard American diet.

People dying on an experimental diet is usually considered a stark failure, indicating its hazardous nature. This outcome would normally stop a trial and inform the experimenters that either a successful lowering of cholesterol was harmful in the long-term, and therefore unethical, or that there was a more complex picture and variables to be explored, or both. The startling effect on mortality was instead ignored and the diet was vaunted, in a more limited sense for its undeniable influence on lowering serum cholesterol, as ‘efficacious’ by the medical journals, indicating an intractable ideological position.⁷

Statin drugs suffer from the same institutional bias, evident by the low efficacy in reducing heart disease risk (1-2%), that is despite their apparent ability to lower cholesterol dramatically.⁸ The Framingham Heart Study (1948-) in fact confirmed that high or low serum cholesterol had no effect on heart disease risk for healthy men and women over the age of fifty.⁹ The current generation of anti-cholesterol drugs such as evolocumab (an injectable antibody) are a natural successor to this approach with an even more potent effect on lowering cholesterol but with no concurrent improvement in mortality. But industry scientists can’t keep this obfuscation up forever, and fortunately for those suffering unnecessary dietary restrictions and the imposition of long-term drug regimes, the field has matured. In 2015 the unsupportable recommendation for a limit on egg consumption and total dietary cholesterol was dropped by The British Heart Foundation as well as The American Heart Foundation, meaning an end to forty-eight years of bias against eggs.

As it turns out, cholesterol is now known to be only a only part of a cascade of events including inflammation, oxidation, vascular damage and nutrient deficiencies, which eventually leads to plaque formation in arteries. As a consequence conventional medicine, at the behest of the pharmaceutical industry, is steadily moving away from prescribing statins based on the overly-simplistic assessment of cholesterol levels, and moving instead to the unstable ground of prescribing based on statistical risk factors.¹⁰ This means patients will be prescribed a statin based on a questionnaire looking for symptoms of diabetes, obesity, heart disease etc., a strategy which is even more dubious, but one which cleverly broadens the market by billions of dollars. (The upper limit for systolic blood pressure to be defined as hypertension was also lowered from 140 to 130 mmHg).

A more realistic level to measure, better reflecting underlying degenerative disease processes, would be oxidised LDL-C or perhaps vitamin status and homocysteine. The unavoidable result would be a restriction on ultra-processed convenience foods, not the prescription of statins which come with a legion of side-effects that in some cases have to be endured for decades.

By comparison to pharmaceutical drugs, eggs actually contain protective bioactive compounds such as the carotenoids lutein and zeaxanthin, in addition to phospholipids and some very interesting proteins. Phospholipids from the yolk have been found to be preferentially incorporated in HDL cholesterol, contributing to the elevation of this so-called ‘good’ cholesterol. Carotenoids are responsible for the yellow colour in the yolk and are reliant on the hen’s diet, and consumption of these protective antioxidants are then reflected in elevated blood levels of these protective carotenoids. The yolk also contains lecithin which is known as a cholesterol solubiliser. Furthermore, the egg white contains proteins that are antimicrobial in activity and protective of the immune system.

Apparently in Canada it is common for people to only eat the white of the egg and discard the ‘problematic’ yellow, a practice probably inspired by the Pritikin diet. The original Pritikin diet was mostly high-fibre vegetarian but it was fanatically low in fat even to the point of excluding most nuts, so it is certainly was deficient in crucial omega-3 essential fatty acids and fat-soluble vitamins, something corrected in later versions. This is because Pritikin considered all fats harmful, unlike Dr. Ancel Keys who was mostly just against saturated animal fat. Nevertheless, It helped the pedantic engineer reverse his heart disease, as well as that of many other people, and no small part of the success can be attributed to the exclusion of refined sugar, margarine, alcohol, caffeine, artificial sweeteners and therefore nearly all inflammatory American factory-foods from the Pritikin diet.¹¹

While isolated egg cholesterol may have properties contributing to plaque formation in the rabbit model this practice does not take into account the fact that it is usually eaten as a whole egg in human models and therefore is consumed with a protective phospholipid matrix.¹² Whole eggs may also be eaten in the context of a protective wholefood diet rich in protective phytonutrients which prevent oxidation and inflammation. Cholesterol absorption is also important because it relates significantly to the level of fibre in the diet, gut health in general as well as liver function, something not controlled for in animal trials because lab animals are not fed wholefoods.

It seems therefore, that far from being dangerous, whole eggs either cause no harm according to the current view of scientists, or are actually protective against heart disease if you take into account the role of protective phospholipids on supporting good HDL cholesterol, as well as that of antioxidants that prevent LDL oxidation—a startling reversal!

If you have a cholesterol or plaque problem you got there via the factory-food diet, a sedentary lifestyle, smoking, stress or an underactive thyroid, unless of course you have familial hypercholesterolemia. In alternative medicine there are several prudent strategies available as an alternative to statin use: increase vitamin C intake to support vessel integrity, bile acid synthesis and anti-oxidant status;¹³ increase the intake of omega-3 fatty acids sourced from oily fish or flax oil; reduce polyunsaturated omega-6 consumption derived from vegetable oils or grains; use extra-virgin olive oil as a staple; improve fibre intake from fruit, vegetables, bran and oats; support cholesterol metabolism by using bitter herbs such as artichoke, dandelion and milk thistle; drink green tea instead of carbonated caffeine drinks; eat lots of garlic, turmeric, avocado, nuts, pomegranate and lecithin; and finally, avoid all refined sugar.

Disclaimer: this article is intended for the purpose of general education only, and is not a substitute for diagnosis, treatment advice, or a prescription that is given in a consultation with a qualified physician.

References:

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2.         Constant J. The role of eggs, margarines and fish oils in the nutritional management of coronary artery disease and strokes. Keio J Med 2004;53:131–6.

3.         Hu FB, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999;281:1387–94.

4.         Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med 2014;160:398–406.

5.         Micha R, Mozaffarian D. Trans fatty acids: effects on cardiometabolic health and implications for policy. Prostaglandins Leukot Essent Fatty Acids 2008;79:147–52.

6.         Jolliffe N, Rinzler SH, Archer M. The anti-coronary club; including a discussion of the effects of a prudent diet on the serum cholesterol level of middleaged men. Am J Clin Nutr 1959;7:451–62.

7.         Singman HS, Berman SN, Cowell C, Maslansky E, Archer M. The Anti-Coronary Club: 1957 to 1972. Am J Clin Nutr 1980;33:1183–91.

8.         ALLHAT Officers. Major outcomes in moderately hypercholesterolemic, hypertensive patients randomized to pravastatin vs usual care: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). JAMA 2002;288:2998–3007.

9.         Anderson KM, Castelli WP, Levy D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 1987;257:2176–80.

10.       Gulati M, Merz CNB. New cholesterol guidelines and primary prevention in women. Trends Cardiovasc Med 2015;25:84–94.

11.       Pritikin N. The Pritikin Program For Diet & Exercise. Grosset & Dunlap; 1979.

12.       Andersen CJ. Bioactive Egg Components and Inflammation. Nutrients 2015;7:7889–913. 13.       Chambial S, Dwivedi S, Shukla KK, John PJ, Sharma P. Vitamin C in disease prevention and cure: an overview. Indian J Clin Biochem IJCB 2013;28:314–28.