I really have got better things to do than to continually dissect articles from so called scientists, but, when the item under attack is the super food called egg, someone has to leap to its defence. So here goes….
I have a copy of the full article – sadly it’s not on free view. You can see the abstract on this link. The abstract tells us that 1,262 people were involved in the study with an average age of 61.5. 47% were women. (The full article says that 1,231 participants were involved – discrepancies like this should be corrected before publication.)
The results were summarised as: “Carotid plaque area increased linearly with age after age 40, but increased exponentially with pack-years of smoking and with egg-yolk years. Plaque area in patients consuming < 2 eggs per week (n=388) was 125± 129mm2, versus 132 ± 142 mm2 in those consuming 3 or more eggs per week (n=603).”
The Canadian authors – David Spence, David Jenkins and Jean Davignon concluded: “Our findings suggest that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease.”
The authors have invented the term “egg-yolk years”, which is defined as egg yolks consumed per week times number of years of consumption. They compare this with “pack-years of smoking”, which is defined as number of packs per day times number of years smoking. Yes – this article really does place one of the most nutritious foods on the planet alongside one of the most harmful man-made drugs – and conclude that they are just about equally evil…
“Our data suggest a strong association between egg consumption and carotid plaque burden. The exponential nature of the increase in TPA by quintiles of egg consumption follows a similar pattern to that of cigarette smoking. The effect of the upper quintile of egg consumption was equivalent in terms of atheroma development to 2/3 of the effect of the upper quintile of smoking. In view of the almost unanimous agreement on the damage caused by smoking, we believe our study makes it imperative to reassess the role of egg yolks, and dietary cholesterol in general, as a risk factor for CHD.”
The entire study is about egg yolks. There is no evidence presented in the paper that these 1,231 people throw away egg whites. The paper has simply assumed that there can be nothing in egg whites that could cause any concern whatsoever so we don’t need to even think about egg whites. As someone interested in nutrition, here is the comparative nutritional information for whole eggs (which normal people eat); egg whites (which people who don’t value vitamins and minerals eat) and egg yolks (which people who do value vitamins and minerals eat).
|(All per 100g of product)||USA RDA/AI||Whole egg||Egg yolk||Egg white|
|B1 (Thiamin) (mg)||1.2mg||0.1||0.2||0|
|B2 (Riboflavin) (mg)||1.3mg||0.5||0.5||0.4|
|B3 (Niacin) (mg)||16mg||0.1||0||0.1|
|B5 (Pantothenic Acid) (mg) (AI)||5mg (AI)||1.4||3||0.2|
|Folic Acid (Folate) (mcg)||400mcg||47||146||4|
|B12 (mcg)||2.4 mcg||1.3||1.9||0.1|
|D (IU) (AI)||400IU (AI)||35||107||0|
|K (mcg) (AI)||120mcg (AI)||0.3||0.7||0|
|Calcium (mg) (AI)||1000-1200mg (AI)||53||129||7|
|Potassium (mg) (AI)||4700mg (AI)||134||109||163|
|Sodium (mg) (AI)||1500mg (AI)||140||48||166|
|Manganese (mg) (AI)||2.3mg (AI)||0.0||0.1||0|
|Selenium (mcg)||55 mcg||31.7||56||20|
So the egg yolk is where we find the nutrition in an egg. Please bear this in mind as we go on to talk about egg-yolk years alongside pack-years of smoking…
Table 2 at the end of the paper has the baseline characteristics of participants in the study (1,231 people) by quintile of egg-yolk eaters.
|Egg yolk years||<50||50-110||110-150||150-200||>200|
|Age at first visit||55.70||57.97||56.82||64.55||69.77|
|Eggs per week||0.41||1.37||2.30||2.76||4.68|
|Smoking (pack years)||14.14||14.37||16.57||13.88||17.00|
|Plaque area (mm2)||101.45||110.35||113.58||135.76||175.77|
The article notes that: “carotid atherosclerotic plaque burden increases linearly after age 40“. This means that plaque area increases directly with age – this is not surprising and by far the most obvious relationship in all of these variables. (Please note that the plaque itself is not the root cause of problems. Plaque forms over damage to the arterial walls in much the same way that a scab forms over a cut on the skin. The original source of that damage is what we need to understand. Chief suspects should be smoking, sugar, stress, chemicals and apparently we now need to add egg yolks to this list!)
The above table has columns A to E categorised into these invented egg-yolk years. The plaque area rises from columns A to E. However the age of the participants at first visit also rises from A to E. The average age in column A is under 56; the average age in column E is 70. That’s a 14 year difference! Surely the single biggest determinant of plaque area?
Column E has 24% more incidence of diabetes than column A – could that impact plaque area? (Please note that the association between plaque area and diabetes does not follow a uniform relationship – Columns C and D buck the trend).
Column E has 20% higher smoking pack years than column A – could that impact plaque area? (Please note that the association between plaque area and smoking pack years does not follow a uniform relationship – Column D bucks the trend).
The data – Plaque builds up with age
I look at the above table and conclude that the strongest relationship is between age and plaque – as one would expect.
If you consume a particular food regularly over more years you will amass more ‘food-years’. The authors could have picked broccoli and measured broccoli years and the top quintile group of 70 year olds would have had 14 years more broccoli consumption than the 56 year olds!
But when you are funded by drug companies, to continue the cholesterol/lipid hypothesis you’ll pick on a cholesterol rich food and not broccoli. Scroll down to “Conflict of interest” and you’ll see: “Dr Spence and Dr Davignon have received honoraria and speaker’s fees from several pharmaceutical companies manufacturing lipid-lowering drugs, and Dr Davignon has received support from Pfizer Canada for an annual atherosclerosis symposium; his research has been funded in part by Pfizer Canada, AstraZeneca Canada Inc and Merck Frosst Canada Ltd.”
The data – Eggs & cholesterol levels
The other thing I take from the table above is that egg consumption has bugger all to do with blood cholesterol levels – unless we want to note the inverse association. People eating an average 4.68 egg yolks per week have lower total cholesterol, lower triglycerides, higher HDL and lower LDL than people eating an average of 0.41 egg yolks per week. Omelette anyone?
However, this also doesn’t display a consistent relationship – total cholesterol is highest at the mid range of egg yolk consumption – an average of 2.3 per week. Triglycerides and LDL are also highest at the midpoint of egg yolk consumption – an average of 2.3 per week. (Not that I care about any ‘cholesterol levels’ – but just to comment on the data in the article from people who do care about ‘cholesterol levels’).
BMI, by the way, peaks at the midpoint of egg consumption and is lowest at the highest level of egg consumption. Low carbers know why.
In all of this please note that even the highest egg consumers are not eating even one egg a day. The very top egg consumers are consuming an average two thirds of an egg a day.
What plausible mechanism is there?
Any study not only has to show an association, it has to show that this association is plausible. I can observe that more people who wear blue socks have a larger plaque area than people who wear red socks. However this is a meaningless observation unless I can offer a rationale for why this might be.
For this study to suggest an association between egg yolks and carotid plaque (which is analogous for heart disease in effect in the article) there needs to be a plausible mechanism. Interestingly the study has ruled out cholesterol as a mechanism. Hence the conventional view that cholesterol is ‘clogging up arteries’ cannot be used because no association with cholesterol holds (the association is inverse, if anything).
So what is the mechanism by which egg yolks are supposed to build carotid plaque? We don’t know. The article is conspicuously silent on any possible pathway, let alone any plausible pathway.
Let’s see what happens when we eat to see how ludicrous this study really is…
One large egg yolk (c. 17g) has 9g water, 3g protein and 5g of fat – the majority of the fat is unsaturated with monounsaturated fat being the single largest fat in egg (and egg yolk). The protein is digested in the stomach – broken down into amino acids. I’ve not yet seen any suggestion that protein clogs up arteries so let’s focus on the fat. (Plus – if the Canadians do come back and suggest that the protein element of egg yolks is an issue then we can talk about egg whites.)
The fat passes from our mouth very quickly into the pharynx (the part of the throat that goes from behind the nose to the start of the oesophagus) and then into the oesophagus (the muscular tube through which food travels from the mouth to the stomach). From there it goes into the stomach (the main area for food ‘short-term’ storage and digestion of protein and carbohydrate). Fat is not digested until it passes from the stomach into the small intestine (where almost all nutrients are absorbed) and, from there, it passes into the large intestine (the main function of which is to transport waste out of the body and to absorb water from the waste before it leaves). So, our egg yolk fat has quite a journey through our digestive system and we haven’t yet started to describe how it can go anywhere near our arteries.
Chylomicrons (the largest lipoproteins) are formed in the intestine, as a result of digestion, and chylomicrons are the transport mechanism for taking dietary fat (and cholesterol) from the digestive system into the blood stream and from there to the different parts of the body to do their vital work. As any young biology student will know, arteries pump blood around the body from the heart. There is no artery to take dietary fat away from the intestines.
The chain length of fatty acids determines how they are transported out of the digestive system. If a fatty acid has fewer than 12 carbon atoms, it will “probably travel through the portal vein that connects directly to the liver. If the fatty acid is a more typical long-chain variety, it must be reformed into a triglyceride and enter circulation via the lymphatic system.”[i]
The composition (by weight) of the most prevalent fatty acids in egg yolk is typically as follows:[ii]
Unsaturated fatty acids: Oleic acid, 47% (18 carbon atoms); Linoleic acid, 16% (18 carbon atoms); Palmitoleic acid, 5% (16 carbon atoms); Linolenic acid, 2% (18 carbon atoms) and
Saturated fatty acids: Palmitic acid, 23% (16 carbon atoms); Stearic acid, 4% (18 carbon atoms); Myristic acid, 1% (14 carbon atoms)
Egg yolks thus have no short chain fatty acids that may even head off in the portal vein to the liver (not that this should cause concern anyway). The longer chain fats (saturated and unsaturated) are packaged into chylomicrons, released into the lymphatic system and they glide from there into the blood stream to carry the vital nutrients around the body to do their vital work.
So, assuming that egg yolks have not been injected into our arteries, egg yolks have not gone into any arteries through any less invasive route. Egg yolks have gone on a normal digestive process journey, probably taking a few hours for fat, still without going into an artery. Yet, the world is now led to believe, thanks to the imagination of some Canadians, that eating egg yolks is going to clog up our arteries. I’d love to hear the process by which the authors think that the post digestion component parts of egg yolks leap out of chylomicrons, find their way into an artery and lay themselves down in the name of plaque. Or maybe they do inject egg yolks in Canada?!
[i] Gordon Wardlaw, Anne Smith, Contemporary Nutrition, seventh edition, McGraw Hill (2009).
[ii] ] (National Research Council, 1976, Fat Content and Composition of Animal Products, Printing and Publishing Office, National Academy of Science, Washington, D.C., ISBN 0-309-02440-4; p. 203)