The 2012 Atherosclerosis egg study: More smoking is associated with more plaque, unless you eat more eggs

I blogged before about the study by David Spence and colleagues, published online in July 2012 in the journal Atherosclerosis (). This study attracted a lot of media attention (e.g., ). The article is titled: “Egg yolk consumption and carotid plaque”. The study argues that “regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease”. It hints at egg yolks being unhealthy in general, possibly even more so than cigarettes.

I used the numbers in Table 2 of the article (only 5 rows of data, one per quintile; i.e., N=5) to conduct a type of analysis that is rarely if ever conducted in health studies – a moderating effects analysis. A previous blog post summarizes the results of one such analysis using WarpPLS (). It looked into the effect of the number of eggs consumed per week on the association between blood LDL cholesterol and plaque (carotid plaque). The conclusion, which is admittedly tentative due to the small sample (N=5), was that plaque decreased as LDL cholesterol increased with consumption of 2.3 eggs per week or more ().

Recently I ran an analysis on the moderating effect of number of eggs consumed per week on the association between cumulative smoking (measured in “pack years”) and plaque. As it turns out, if you fit a 3D surface to the five data points that you get for these three variables from Table 2 of the article, you end up with a relatively smooth surface. Below is a 3D plot of the 5 data points, followed by a best-fitting 3D surface (developed using an experimental algorithm).

Based on this best-fitting surface you could then generate a contour graph, shown below. The “lines” are called “isolines”. Each isoline refers to plaque values that are constant for a set of eggs per week and cumulative smoking combinations. Next to the isolines are the corresponding plaque values. The first impression is indeed that both egg consumption and smoking are causing plaque buildup, as plaque clearly increases as one moves toward the top-right corner of the graph.

But focus your attention on each individual isoline, one at a time. It is clear that plaque remains constant for increases in cumulative smoking, as long as egg consumption increases. Take for example the isoline that refers to 120 mm2 of plaque area. An increase in cumulative smoking from about 14.5 to 16 pack years leads to no increase in plaque if egg consumption goes up from about 2 to 2.3 eggs per week.

These within-isoline trends, which are fairly stable across isolines (they are all slanted to the right), clearly contradict the idea that eggs cause plaque buildup. So, why does plaque buildup seem to clearly increase with egg consumption? Here is a good reason: egg consumption is very strongly correlated with age, and plaque increases with age. The correlation is a whopping 0.916. And I am not talking about cumulative egg consumption, which the authors also measure, through a variable called “egg-yolk years”. No, I am talking about eggs per week. In this dataset, older folks were eating more eggs, period.

The correlation between plaque and age is even higher: 0.977. Given this, it makes sense to look at individual isolines. This would be analogous to what biostatisticians often call “adjusting for age”, or analyzing the effect of egg consumption on plaque buildup “keeping age constant”. A different technique is to “control for age”; this technique would be preferable had the correlations been lower (say, lower than 0.7), as collinearity levels might have been below acceptable thresholds.

The underlying logic of the “keeping age constant” technique is fairly sound in the face of such a high correlation, which would make “controlling for age” very difficult due to collinearity. When we “keep age constant”, the results point at egg consumption being protective among smokers.

But diehard fans of the idea that eggs are unhealthy could explain the results differently. Maybe egg consumption causes plaque to go up, but smoking has a protective effect. Again taking the isoline that refers to 120 mm2 of plaque area, these diehard fans could say that an increase in egg consumption from 2 to 2.3 eggs per week leads to no increase in plaque if cumulative smoking goes up from about 14.5 to 16 pack years.

Not too long ago I also blogged about a medical case study of a man who ate approximately 25 eggs (20 to 30) per day for over 15 years (probably well over), was almost 90 years old (88) when the case was published in the prestigious The New England Journal of Medicine, and was in surprisingly good health (). This man was not a smoker.

Perhaps if this man smoked 25 cigarettes per day, and ate no eggs, he would be in even better health eh!?

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Does tallness cause heart disease? No, but sex does

Popular beliefs about medical issues are sometimes motivated by a statistical phenomenon known as “spurious relationship”, among other names. Two variables X and Y are influenced by a third variable C, which leads to X and Y being correlated and thus the impression that X and Y are causally associated.

Take a look at the table below, which I blogged about in a previous post (). This table shows that there is a strong unadjusted correlation between height and arterial stiffness, a marker of heart disease. The likelihood that the correlation is due to chance is lower than one tenth of a percentage point (P<.001).

Interestingly, the authors of the study even use height as a control variable to narrow down the “true” causes of arterial stiffness (column with adjusted results), assuming that height did indeed influence arterial stiffness and what they found to be a key predictor of arterial stiffness, 2-hour postprandial glucose.

But there is no convincing evidence that height causes heart disease, with exception of pathological extremes – e.g., acromegaly. Extremes tend to influence statistical results somewhat, leading to conflicting conclusions that end up being disseminated by the popular media (). This is one of the sources of popular beliefs about medical issues.

Another, more important, source are real confounders. And this takes us back to the issue of height being associated with heart disease. In fact, height will typically be significantly associated with heart disease in almost any study that includes men and women and does not control for biological sex.

One of the reasons is that women overall tend to have a significantly lower incident of heart disease than men. The other is that height is significantly lower among women than men, on average, even though there are several women who are taller than the average man.

The table above was from a study including both sexes. Therefore, the strong association between height and arterial stiffness is a “reflection” of the strong association between being male and increased arterial stiffness. If one were to add a variable coded as 0 for male and 1 for female, and use it in a multivariate analysis of predictor of arterial stiffness, together with height, the effect of height would probably “disappear”.

Biological sex is the control variable, the “confounder”, that the authors should have used to narrow down the “true” causes of arterial stiffness (second column in the table). In the absence of biological sex, controlling for height accomplished something similar, but in a “wobbly” way, leaving many readers scratching their heads in confusion.

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No fat gain while eating well during the Holiday Season: Palatability isolines, the 14-percent advantage, and nature’s special spice

Like most animals, our Paleolithic ancestors had to regularly undergo short periods of low calorie intake. If they were successful at procuring food, those ancestors alternated between periods of mild famine and feast. As a result, nature allowed them to survive and leave offspring. The periods of feast likely involved higher-than-average consumption of animal foods, with the opposite probably being true in periods of mild famine.

Almost anyone who adopted a low carbohydrate diet for a while will tell you that they find foods previously perceived as bland, such as carrots or walnuts, to taste very sweet – meaning, to taste very good. This is a special case of a more general phenomenon. If a nutrient is important for your body, and your body is deficient in it, those foods that contain the nutrient will taste very good.

This rule of thumb applies primarily to foods that contributed to selection pressures in our evolutionary past. Mostly these were foods available in our Paleolithic evolutionary past, although some populations may have developed divergent partial adaptations to more modern foods due to recent yet acute selection pressure. Because of the complexity of the dietary nutrient absorption process, involving many genes, I suspect that the vast majority of adaptations to modern foods are partial adaptations.

Modern engineered foods are designed to bypass reward mechanisms that match nutrient content with deficiency levels. That is not the case with more natural foods, which tend to taste good only to the extent that the nutrients that they carry are needed by our bodies.

Consequently palatability is not fixed for a particular natural food; it does not depend only on the nutrient content of the food. It also depends on the body’s deficiency with respect to the nutrient that the food contains. Below is what you would get if you were to plot a surface that best fit a set of data points relating palatability of a specific food item, nutrient content of that food, and the level of nutrient deficiency, for a group of people. I generated the data through a simple simulation, with added error to make the simulation more realistic.

Based on this best-fitting surface you could then generate a contour graph, shown below. The curves are “contour lines”, a.k.a. isolines. Each isoline refers to palatability values that are constant for a set of nutrient content and nutrient deficiency combinations. Next to the isolines are the corresponding palatability values, which vary from about 10 to 100. As you can see, palatability generally goes up as one moves toward to right-top corner of the graph, which is the area where nutrient content and nutrient deficiency are both high.

What happens when the body is in short-term nutrient deficiency with respect to a nutrient? One thing that happens is an increase in enzymatic activity, often referred to by the more technical term “phosphorylation”. Enzymes are typically proteins that cause an acute and targeted increase in specific metabolic processes. Many diseases are associated with dysfunctional enzyme activity. Short-term nutrient deficiency causes enzymatic activity associated with absorption and retention of the nutrient to go up significantly. In other words, your body holds on to its reserves of the nutrient, and becomes much more responsive to dietary intake of the nutrient.

The result is predictable, but many people seem to be unaware of it; most are actually surprised by it. If the nutrient in question is a macro-nutrient, it will be allocated in such a way that less of it will go into our calorie stores – namely adipocytes (body fat). This applies even to dietary fat itself, as fat is needed throughout the body for functions other than energy storage. I have heard from many people who, by alternating between short-term fasting and feasting, lost body fat while maintaining the same calorie intake as in a previous period when they were steadily gaining body fat without any fasting. Invariably they were very surprised by what happened.

In a diet of mostly natural foods, with minimal intake of industrialized foods, short-term calorie deficiency is usually associated with short-term deficiency of various nutrients. Short-term calorie deficiency, when followed by significant calorie surplus (i.e., eating little and then a lot), is associated with a phenomenon I blogged about before here – the “14-percent advantage” of eating little and then a lot (, ). Underfeeding and then overfeeding leads to a reduction in the caloric value of the meals during overfeeding; a reduction of about 14 percent of the overfed amount.

So, how can you go through the Holiday Season giving others the impression that you eat as much as you want, and do not gain any body fat (maybe even lose some)? Eat very little, or fast, in those days where there will be a feast (Thanksgiving dinner); and then eat to satisfaction during the feast, staying away from industrialized foods as much as possible. Everything will taste extremely delicious, as nature’s “special spice” is hunger. And you may even lose body fat in the process!

But there is a problem. Our bodies are not designed to associate eating very little, or not at all, with pleasure. Yet another thing that we can blame squarely on evolution! Success takes practice and determination, aided by the expectation of delayed gratification.

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Zero Waste Europe - my top 10 favourite blogposts

So, did you know it's the European Week for Waste Reduction?  I guess it's not the most snappy of names to roll off the tongue, but I love the fact there is one week in the year that's dedicated towards bringing our diverse continent together in the fight against waste.

It also makes me feel that my dusty old degree in Modern European Studies from (cough) the 1980s, still has some relevance to my life today.  The concluding motto in 1989 was that 'Europe is a unity through its diversity'.  I can't remember what I made of that back then, but when it comes to tackling our mountain of waste, it's certainly relevant to today's range of initiatives - diverse yet united towards the same goal, that of waste minimisation.

So for EWWR, (a much snappier title), I thought I'd kick off with an introduction to one of my favourite Zero Waste blogs, Zero Waste Europe, and my top ten favourite blogposts, revealing some of the great ideas that are taking place on the continent as well as inspiration from further afield.

The association of Italian Zero Waste towns has been created

Little Museum of Bad Industrial Design

Kretsloppsarken. Recycling or amusement park?

A Zero Waste month in Sweden: 4 people = less than 1kg of waste!

The first European university to ban bottled water?

Retorna – When waste has a value it stops being waste

Repair café – a project to make friends, not waste

The art of Zero Waste!

David Andersen Copenhagen; designing waste out of fashion
 
On the Road to Zero Waste: Lessons from around the world


But seriously, don't stop there.  There are plenty of other great posts, including some wonderful examples of waste reduction activities in the UK too, such as Nappy Ever After and Unpackaged.

For anyone who wants to explore the wider approach to Zero Waste, Zero Waste Europe really is a great place to start.

And on that note, as you travel virtually from country to country, perhaps all that's left to say, is 'Bon Voyage!'



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European Week for Waste Reduction runs from 17-25 November.  More information can be found at www.ewwr.eu.  To follow events and discussion on Twitter, use the hashtag #ewwr.

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The Rubbish Diet could be coming to a town near you!

The Rubbish Diet team visiting Nesta!

Please excuse my tardiness in sharing this VERY EXCITING news with you. 

I should have done it last week, but with news of my mum falling ill, then rushing to Wales to see her, then losing my laptop en route, and continued worries about her health, understandably this blog has had to take a back seat.

However, I can't keep it quiet any longer!  What's happening with The Rubbish Diet is far too exciting to keep tucked away in my desk drawers and if you follow me on Twitter, you may have indeed caught a few snippets of the news.

So to the sound of an imaginary drum-roll, I am chuffed to pieces to announce that my Rubbish Diet challenge has been selected as a semi-finalist in a national waste reduction competition, which could see the 'slimming club' analogy rolled out to villages, towns and cities, right across the UK, helping communities achieve an amazing impact on reducing their rubbish.

The Waste Reduction Challenge, run by Nesta, the UK’s innovation foundation, and funded by the Cabinet Office, aims to identify new ideas that can influence and mobilise communities to make significant reductions in waste and impact behaviour for years to come.

In partnership with the Zero Waste Alliance UK (working with Katy Anderson, pictured above), the Rubbish Diet competition entry proposes to engage with established community groups around the UK, including schools, Transition Towns and W.I. branches, to help them organise their own waste-busting challenges, following an 8-week plan of fun and lively events that will help to empower households to slim their bins.

The idea is, of course, based on the very roots of this blog, when I took St Edmundsbury Borough Council's Zero Waste Week Challenge almost five years ago, (remember that plaster?), and which then developed into the online Rubbish Diet Challenge 2012, where I mentored 8 households through the process of slimming their bins, by at least 50%, at the beginning of this year.


Building on that, I have since been busy with Transition Shrewsbury, which has already launched its Rubbish Diet Shropshire community pilot, where 20 households have signed up to reduce their waste.  This is just the first stage. The Rubbish Diet Shropshire project, which is being managed locally, will launch even wider in the new year,  with events run by the community for the community, with households just like yours and mine, sharing knowledge about how they reduce their waste and attempting to overcome the hurdles that arise.

And it's that process, which the Nesta Waste Reduction Challenge will help to replicate around the UK.

So, we're in the semi-finals!  What next?

This is where even more hard work begins, in putting together an ambitious but realistic plan to roll-out the Rubbish Diet challenge next year, featuring a communications strategy, participant engagement, measuring & monitoring procedures and lots of other exciting things that will help communities launch their own slimming clubs for bins.

So, there really really could be a fun Rubbish Diet challenge coming to an area near you.  Just imagine!

We just need to get through the next round! But, boy, is the competition tough! So please keep watching this space for further news.

And of course, if you think your community would like to join in, then do get in touch.

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The Waste Reduction Challenge Prize is offering a prize for the innovation that achieves the biggest measureable reduction in waste, by providing new opportunities for communities to come together to give time, skills and resources.

The semi-finalists (which also includes a Mattress Recycling Scheme in my home county of Suffolk) will be supported to develop a detailed plan for their idea. In January, five concepts for each, with the potential for sustainability and scale, will be selected to test their ideas. They will receive up to £10,000 and professional advice to set up and test their projects before a winner for each challenge is selected in September 2013 and awarded £50,000.

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The bipolar disorder pendulum: Depression as a compensatory adaptation

As far as explaining natural phenomena, Darwin was one of the best theoretical researchers of all time. Yet, there were a few phenomena that puzzled him for many years. One was the evolution of survival-impairing traits such as the peacock’s train, the large and brightly colored tail appendage observed in males.

Tha male peacock’s train is detrimental to the animal’s survival, and yet it is clearly an evolved trait ().

This type of trait is known as a “costly” trait – a trait that enhances biological fitness (or reproductive success, not to be confused with “gym fitness”), and yet is detrimental to the survival of the individuals who possess it (). Many costly traits have evolved in animals because of sexual selection. That is, they have evolved because they are sexy.

Costly traits seem like a contradiction in terms, but the mechanisms by which they can evolve become clear when evolution is modeled mathematically (, ). There is evidence that mental disorders may have evolved as costs of attractive mental traits (); one in particular, bipolar disorder (a.k.a. manic-depression), fits this hypothesis quite well.

Ironically, a key contributor to the mathematics used to understand costly traits, George R. Price (), might have suffered from severe bipolar disorder. Most of Price’s work in evolutionary biology was done in the 1970s; toward the end of his life, which was untimely ended by Price himself. For many years he was known mostly by evolutionary biologists, but this has changed recently with the publication of Oren Harman’s superb biographical book titled “The Price of Altruism: George Price and the Search for the Origins of Kindness” ().

Bipolar disorder is a condition characterized by disruptive mood swings. These swings are between manic and depressed states, and are analogous to the movement of a pendulum in that they alternate, seemingly gravitating around the "normal" state. See the figurative pendulum representation below, adapted from a drawing on Thinkquest.org.

Bipolar disorder is generally associated with creative intelligence, which is a very attractive trait (). Moreover, the manic state of the disorder is associated with hypersexuality and exaggerated generosity (). So one can clearly see how having bipolar disorder may lead to greater reproductive success, even as it creates long-term survival problems.

On one hand, a person may become very energetic and creative while in the manic state. This could be one of the reasons why many who suffer from bipolar disorder have fairly successful careers in fields that require creative intelligence (), which are many and not restricted to fields related to the fine and performing arts. Creative intelligence is highly valued in most knowledge-intensive professions ().

On the other hand, sustained acute mania or depression are frequently associated with serious health problems (). This is why the clinical treatment of bipolar disorder often starts with an attempt to keep the pendulum from moving too far in one direction or another. This may require medication, such as clinical doses of the elemental salt lithium, prior to cognitive behavioral therapy. The focus of cognitive behavioral therapy is on changing the way one sees and thinks about the world, particularly one’s “social world”.

Prolonged acute mania, usually accompanied by severely impaired sleep, may lead to psychosis. This, psychosis, is an extreme state characterized by hallucinations and/or delusions, leading to hospitalization in most cases. It has been theorized that depression is an involuntary compensatory adaptation () aimed at moving the pendulum in the other direction, out of the manic state, before more damage ensues ().

Elaborate approaches have been devised to treat and manage bipolar disorder treatment that involve the identification of mania and depression “prodromes” (), which are signs that a full-blown manic or depressive episode is about to start. Once prodromes are identified, cognitive behavioral therapy techniques are employed to prevent the pendulum from moving further in one direction or the other. The main goal of these techniques is to change one’s way of thinking about various issues (e.g., fears, pessimism). These techniques take years of practice to be used effectively.

Identification of prodromes and subsequent use of cognitive behavioral therapy seems to be particularly effective when dutifully applied with respect to manic episodes (). The reason for this may be related to one interesting fact related to bipolar disorder: manic episodes are not normally dreaded as much as depression episodes.

In fact, many sufferers avoid taking medication because they do not want to give up the creative and energetic bursts that come with manic episodes, even though they absolutely do not want the pendulum to go in the other direction. The problem is that, if depression is indeed a compensatory adaptation to mania, it seems reasonable to assume that extreme manic episodes are likely to be followed by extreme episodes of depression. Perhaps the key to avoid prolonged acute depression is to avoid prolonged acute mania.

As someone with bipolar disorder becomes more and more excited with novel and racing thoughts (a prodrome of mania), it would probably make sense to identify and carry out calming activities – to avoid a fall into despairing depression afterwards.

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The man who ate 25 eggs per day: What does this case really tell us?

Many readers of this blog have probably heard about the case of the man who ate approximately 25 eggs (20 to 30) per day for over 15 years (probably well over), was almost 90 years old (88) when the case was published in the prestigious The New England Journal of Medicine, and was in surprisingly good health ().

The case was authored by the late Dr. Fred Kern, Jr., a widely published lipid researcher after whom the Kern Lipid Conference is named (). One of Kern’s research interests was bile, a bitter-tasting fluid produced by the liver (and stored in the gallbladder) that helps with the digestion of lipids in the small intestine. He frames the man’s case in terms of a compensatory adaptation tied to bile secretion, arguing that this man was rather unique in his ability to deal with a lethal daily dose of dietary cholesterol.

Kern seemed to believe that dietary cholesterol was harmful, but that this man was somehow “immune” to it. This is ironic, because often this case is presented as evidence against the hypothesis that dietary cholesterol can be harmful. The table below shows the general nutrient content of the man’s daily diet of eggs. The numbers in this and other tables are based on data from Nutritiondata.com (), in some cases triangulated with other data. The 5.3 g of cholesterol in the table (i.e., 5,300 mg) is 1,775 percent the daily value recommended by the Institute of Medicine of the U.S. National Academy of Sciences ().

As you can see, the man was on a very low carbohydrate diet with a high daily intake of fat and protein. The man is described as an: “… 88-year-old man who lived in a retirement community [and] complained only of loneliness since his wife's death. He was an articulate, well-educated elderly man, healthy except for an extremely poor memory without other specific neurologic deficits … His general health had been excellent, without notable symptoms. He had mild constipation.”

The description does not suggest inherited high longevity: “His weight had been constant at 82 to 86 kg (height, 1.87 m). He had no history (according to the patient and his personal physician of 15 years) of heart disease, stroke, or kidney disease … The patient had never smoked and never drank excessively. His father died of unknown causes at the age of 40, and his mother died at 76 … He kept a careful record, egg by egg, of the number ingested each day …”

The table below shows the fat content of the man’s daily diet of eggs. With over 14 g of omega-6 fat intake every day, this man was probably close to or in “industrial seed oils territory” (), as far as daily omega-6 fat intake is concerned. And the intake of omega-3 fats, at less than 1 g, was not nearly enough to balance it. However, here is a relevant fact – this man was not consuming any industrial seed oils. He liked his eggs soft-boiled, which is why the numbers in this post refer to boiled eggs.

This man weighed between 82 to 86 kg, which is about 180 to 190 lbs. His height was 1.87 m, or about 6 ft 1 in. Therefore his body mass index varied between approximately 23 and 25, which is in the normal range. In other words, this person was not even close to obese during the many years he consumed 25 eggs or so per day. In the comments section of a previous post, on the sharp increase in obesity since the 1980s (), several readers argued that the sharp increase in obesity was very likely caused by an increase in omega-6 fat consumption.

I am open to the idea that industrialized omega-6 fats played a role in the sharp increase in obesity observed since the 1980s. When it comes to omega-6 fat consumption in general, including that in “more natural” foods (e.g., poultry and eggs), I am more skeptical. Still, it is quite possible that a diet high in omega-6 fats in general is unhealthy primarily if it is devoid of other nutrients. This man’s overall diet might have been protective not because of what he was not eating, but because of what he was eating.

The current debates pitting one diet against another often revolve around the ability of one diet or another to eliminate or reduce the intake of a “bad thing” (e.g., cholesterol, saturated fat, carbohydrates). Perhaps the discussion should be more focused on, or at least not completely ignore, what one diet or another include as protective factors. This would help better explain “odd findings”, such as the lowest-mortality body mass index of 26 in urban populations (). It would also help better explain “surprising cases”; such as this 25-eggs-a-day man’s, vegetarian-vegan “ageless woman” Annette Larkins’s (), and the decidedly carnivore De Vany couple’s ().

The table below shows the vitamin content of the man’s daily diet of eggs. The vitamin K2 content provided by Nutritiondata.com was incorrect; I had to get what seems to be the right number by triangulating values taken from various publications. And here we see something interesting. This man was consuming approximately the equivalent in vitamin K2 that one would get by eating 4 ounces of foie gras () every day. Foie gras, the fatty liver of overfed geese, is the richest known animal source of vitamin K2. This man’s diet was also high in vitamin A, which is believed to act synergistically with vitamin K2 – see Chris Masterjohn’s article on Weston Price’s “activator X” ().

Kern argued that the very high intake of dietary cholesterol led to a sharp increase in bile secretion, as the body tried to “get rid” of cholesterol (which is used in the synthesis of bile). However, the increased bile secretion might have been also been due to the high fat content of this man’s diet, since one of the main functions of bile is digestion of fats. Whatever the case may be, increased bile secretion leads to increased absorption of fat-soluble vitamins, and vitamins K2 and A are fat-soluble vitamins that seem to be protective against cardiovascular disease, cancer and other degenerative diseases.

Finally, the table below shows the mineral content of the man’s daily diet of eggs. As you can see, this man consumed 550 percent the officially recommended daily intake of selenium. This intake was slightly lower than the 400 micrograms per day purported to cause selenosis in adults (). Similarly to vitamins K2 and A, selenium seems to be protective against cardiovascular disease, cancer and other degenerative diseases. This man’s diet was also rich in phosphorus, needed for healthy teeth and bones.

Not too many people live to be 88 years of age; many fewer reach that age in fairly good health. The country with the highest average life expectancy in the world at the time of this writing is Japan, with a life expectancy of about 82 years (79 for men, and 86 for women). Those who think that they need a high HDL cholesterol and a low LDL cholesterol to be in good health, and thus live long lives, may be surprised at this man’s lipid profile: “The patient's plasma lipid levels were normal: total cholesterol, 5.18 mmol per liter (200 mg per deciliter); LDL, 3.68 mmol per liter (142 mg per deciliter); and HDL, 1.17 mmol per liter (45 mg per deciliter). The ratio of LDL to HDL cholesterol was 3.15.”

If we assume that this man is at least somewhat representative of the human species, and not a major exception as Kern argued, this case tells us that a diet of 25 eggs per day followed by over 15 years may actually be healthy for humans. Such diet has the following features:

- It is very high in dietary cholesterol.

- It involves a high intake of omega-6 fats from animal sources, with none coming from industrial seed oils.

- It involves a high overall intake of fats, including saturated fats.

- It is fairly high in protein, all of which from animal sources.

- It is a very low carbohydrate diet, with no sugar in it.

- It is a nutritious diet, rich in vitamins K2 and A, as well as in selenium and phosphorus.

This man ate 25 eggs per day apparently due to an obsession tied to mental problems. Repeated attempts at changing his behavior were unsuccessful. He said: “Eating these eggs ruins my life, but I can't help it.”

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