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.”

The 14-percent advantage of eating little and then a lot: Putting it in practice

In my previous post I argued that the human body may react to “eating big” as it would to overfeeding, increasing energy expenditure by a certain amount. That increase seems to lead to a reduction in the caloric value of the meals during overfeeding; a reduction that seems to gravitate around 14 percent of the overfed amount.

And what is the overfed amount? Let us assume that your daily calorie intake to maintain your current body weight is 2,000 calories. However, one day you consume 1,000 calories, and the next 3,000 – adding up to 4,000 calories in 2 days. This amounts to 2,000 calories per day on average, the weight maintenance amount; but the extra 1,000 on the second day is perceived by your body as overfeeding. So 140 calories are “lost”.

The mechanisms by which this could happen are not entirely clear. Some studies contain clues; one example is the 2002 study conducted with mice by Anson and colleagues (), from which the graphs below were taken.

In the graphs above AL refers to ad libitum feeding, LDF to limited daily feeding (40 percent less than AL), IF to intermittent (alternate-day) fasting, and PF to pair-fed mice that were provided daily with a food allotment equal to the average daily intake of mice in the IF group. PF was added a control condition; in practice, the 2-day food consumption was about the same in AL, IF and PF.

After a 20-week period, intermittent fasting was associated with the lowest blood glucose and insulin concentrations (graphs a and b), and the highest concentrations of insulin growth factor 1 and ketones (graphs c and d). These seem to be fairly positive outcomes. In humans, they would normally be associated with metabolic improvements and body fat loss.

Let us go back to the 14 percent advantage of eating little and then a lot; a pattern of eating that can be implemented though intermittent fasting, as well as other approaches.

So, as we have seen in the previous post (), it seems that if you consume the same number of calories, but you do that while alternating between underfeeding and overfeeding, you actually “absorb” 14 percent fewer calories – with that percentage applied to the extra calorie intake above the amount needed for weight maintenance.

And here is a critical point, which I already hinted at in the previous post (): energy expenditure is not significantly reduced by underfeeding, as long as it is short-term underfeeding – e.g., about 24 h or less. So you don’t “gain back” the calories due to a possible reduction in energy expenditure in the (relatively short) underfeeding period.

What do 140 calories mean in terms of fat loss? Just divide that amount by 9 to get an estimate; about 15 g of fat lost. This is about 1 lb per month, and 12 lbs per year. Does one lose muscle due to this, in addition to body fat? A period of underfeeding of about 24 h or less should not be enough to lead to loss of muscle, as long as one doesn’t do glycogen-depleting exercise during that period ().

Sounds good? It actually gets better. Underfeeding tends to increase the body’s receptivity to both micronutrients and macronutrients. This applies to protein, carbohydrates, vitamins etc. For example, the activity of liver and muscle glycogen synthase is significantly increased by underfeeding (the scientific term is “phosphorylation”), particularly carbohydrate underfeeding, effectively raising the insulin sensitivity of those tissues.

The same happens, in general terms, with a host of other tissues and nutrients; often mediated by enzymes. This means that after a short period of underfeeding your body is primed to absorb micronutrients and macronutrients more effectively, even as it uses up some extra calories – leading to a 14 percent increase in energy expenditure.

There are many ways in which this can be achieved. Intermittent fasting is one of them; with 16-h to 24-h fasts, for example. Intermittent calorie restriction is another; e.g., with a 1/3 and 2/3 calorie consumption pattern across two-day periods. Yet another is intermittent carbohydrate restriction, with other macronutrients kept more or less constant.

If the same amount of food is consumed, there is evidence suggesting that such practices would lead to body weight preservation with improved body composition – same body weight, but reduced fat mass. This is what the study by Anson and colleagues, mentioned earlier, suggested ().

A 2005 study by Heilbronn and colleagues on alternate day fasting by humans suggested a small decrease in body weight (); although the loss was clearly mostly of fat mass. Interestingly, this study with nonobese humans suggested a massive decrease in fasting insulin, much like the mice study by Anson and colleagues.

Having said all of the above, there are several people who gain body fat by alternating between eating little and a lot. Why is that? The most likely reason is that when they eat a lot their caloric intake exceeds the increased energy expenditure.

The 14-percent advantage of eating little and then a lot: Is it real?

When you look at the literature on overfeeding, you see a number over and over again – 14 percent. That is approximately the increase in energy expenditure you get when you overfeed people; that is, when you feed people more calories that they need to maintain their current weight.

This phenomenon is related to another interesting one: the nonlinear increase in body weight and fat mass following overfeeding after a period starvation, illustrated by the top graph below from an article by Kevin Hall (). The data for the squares on the top graph is from the Minnesota Starvation Experiment (). The graph at the bottom is based mostly on the results of a simulation, and doesn’t clearly reflect the phenomenon.

Due to the significant amount of weight lost in what is called above the semistarvation stage (SS), the controlled refeeding period (CR) actually involved significant overfeeding. Nevertheless, weight was not gained right away, due to a sharp increase in energy expenditure. That is illustrated by the U-curve shape of the weight gain in response to overfeeding. Initially the gain is minimal, increasing over time, and continuing through the ad libitum refeeding stage (ALR).

Interestingly, overfeeding leads to increased energy expenditure almost immediately after it starts happening. It seems that even one single unusually big meal will significantly increase energy expenditure. Also, the 14 percent is usually associated with meals with a balanced amount of macronutrients. That percentage seems to go down if the balance is significantly shifted toward dietary fat (), probably because the metabolic “cost” of converting dietary fat into body fat is low. In other words, large meals with a lot of fat in them tend to cause a reduced increase in energy expenditure – less than 14 percent. Shifting the balance to protein appears to have the opposite effect, increasing energy expenditure even more, probably because protein is the jack-of-all-trades among macronutrients ().

The calorie surplus used in experiments where the 14 percent increase in energy expenditure is observed is normally around 1,000 calories, but the percentage seems to hold steady when people are overfed to different degrees () (). Let us assume that one is overfed 1,000 calories. What happens? About 140 calories are “lost” due to overfeeding.

What does this have to do with eating little, and then a lot, in an alternate way? It allows for some reasonable speculation, based on a simple pattern: when you alternate between underfeeding and overfeeding, you reduce food consumption for short period of time (usually less than 24 h), and then eat big, because you are hungry.

It is reasonable to assume, based on the empirical evidence on what happens during overfeeding, that the body reacts to “eating big” as it would to overfeeding, increasing energy expenditure by a certain amount. That increase leads to a reduction in the caloric value of the meals during overfeeding; a reduction of about 14 percent of the overfed amount.

But the body does not seem to significantly decrease energy expenditure if one reduces food consumption for a short period of time, such as 24 h. So you have the potential here for some steady fat loss without a reduction in caloric intake. Keeping a calorie intake up above a certain point is more important than many people think, because a calorie intake that is too low may lead to nutrient deficiencies (). This is possibly one of the reasons why carrying a bit of extra weight is associated with increased longevity in relatively sedentary populations ().

Is this 14-percent effect real, or just another mirage? If yes, what does it possibly translate into in terms of fat loss? More on these issues is coming in the next post.

The lowest-mortality BMI: What is the role of nutrient intake from food?

In a previous post (), I discussed the frequently reported lowest-mortality body mass index (BMI), which is about 26. The empirical results reviewed in that post suggest that fat-free mass plays an important role in that context. Keep in mind that this "BMI=26 phenomenon" is often reported in studies of populations from developed countries, which are likely to be relatively sedentary. This is important for the point made in this post.

A lowest-mortality BMI of 26 is somehow at odds with the fact that many healthy and/or long-living populations have much lower BMIs. You can clearly see this in the distribution of BMIs among males in Kitava and Sweden shown in the graph below, from a study by Lindeberg and colleagues (). This distribution is shifted in such a way that would suggest a much lower BMI of lowest-mortality among the Kitavans, assuming a U-curve shape similar to that observed in studies of populations from developed countries ().

Another relevant example comes from the China Study II (see, e.g., ), which is based on data from 8000 adults. The average BMI in the China Study II dataset, with data from the 1980s, is approximately 21; for an average weight that is about 116 lbs. That BMI is relatively uniform across Chinese counties, including those with the lowest mortality rates. No county has an average BMI that is 26; not even close. This also supports the idea that Chinese people were, at least during that period, relatively thin.

Now take a look at the graph below, also based on the China Study II dataset, from a previous post (), relating total daily calorie intake with longevity. I should note that the relationship between total daily calorie intake and longevity depicted in this graph is not really statistically significant. Still, the highest longevity seems to be in the second tercile of total daily calorie intake.

Again, the average weight in the dataset is about 116 lbs. A conservative estimate of the number of calories needed to maintain this weight without any physical activity would be about 1740. Add about 700 calories to that, for a reasonable and healthy level of physical activity, and you get 2440 calories needed daily for weight maintenance. That is right in the middle of the second tercile, the one with the highest longevity.

What does this have to do with the lowest-mortality BMI of 26 from studies of samples from developed countries? Populations in these countries are likely to be relatively sedentary, at least on average, in which case a low BMI will be associated with a low total calorie intake. And a low total calorie intake will lead to a low intake of nutrients needed by the body to fight disease.

And don’t think you can fix this problem by consuming lots of vitamin and mineral pills. When I refer here to a higher or lower nutrient intake, I am not talking only about micronutrients, but also about macronutrients (fatty and amino acids) in amounts that are needed by your body. Moreover, important micronutrients, such as fat-soluble vitamins, cannot be properly absorbed without certain macronutrients, such as fat.

Industrial nutrient isolation for supplementation use has not been a very successful long-term strategy for health optimization (). On the other hand, this type of supplementation has indeed been found to have had modest-to-significant success in short-term interventions aimed at correcting acute health problems caused by severe nutritional deficiencies ().

So the "BMI=26 phenomenon" may be a reflection not of a direct effect of high muscularity on health, but of an indirect effect mediated by a high intake of needed nutrients among sedentary folks. This may be so even though the lowest mortality is for the combination of that BMI with a relatively small waist (), which suggests some level of muscularity, but not necessarily serious bodybuilder-level muscularity. High muscularity, of the serious bodybuilder type, is not very common; at least not enough to significantly sway results based on the analysis of large samples.

The combination of a BMI=26 with a relatively small waist is indicative of more muscle and less body fat. Having more muscle and less body fat has an advantage that is rarely discussed. It allows for a higher total calorie intake, and thus a higher nutrient intake, without an unhealthy increase in body fat. Muscle mass increases one's caloric requirement for weight maintenance, more so than body fat. Body fat also increases that caloric requirement, but it also acts like an organ, secreting a number of hormones into the bloodstream, and becoming pro-inflammatory in an unhealthy way above a certain level.

Clearly having a low body fat percentage is associated with lower incidence of degenerative diseases, but it will likely lead to a lower intake of nutrients relative to one’s needs unless other factors are present, e.g., being fairly muscular or physically active. Chronic low nutrient intake tends to get people closer to the afterlife like nothing else ().

In this sense, having a BMI=26 and being relatively sedentary (without being skinny-fat) has an effect that is similar to that of having a BMI=21 and being fairly physically active. Both would lead to consumption of more calories for weight maintenance, and thus more nutrients, as long as nutritious foods are eaten.

The lowest-mortality BMI: What is its relationship with fat-free mass?

Do overweight folks live longer? It is not uncommon to see graphs like the one below, from the Med Journal Watch blog (), suggesting that, at least as far as body mass index (BMI) is concerned (), overweight folks (25 < BMI < 30) seem to live longer. The graph shows BMI measured at a certain age, and risk of death within a certain time period (e.g., 20 years) following the measurement. The lowest-mortality BMI is about 26, which is in the overweight area of the BMI chart.



Note that relative age-adjusted mortality risk (i.e., relative to the mortality risk of people in the same age group), increases less steeply in response to weight variations as one becomes older. An older person increases the risk of dying to a lesser extent by weighing more or less than does a younger person. This seems to be particularly true for weight gain (as opposed to weight loss).

The table below is from a widely cited 2002 article by Allison and colleagues (), where they describe a study of 10,169 males aged 25-75. Almost all of the participants, ninety-eight percent, were followed up for many years after measurement; a total of 3,722 deaths were recorded.



Take a look at the two numbers circled in red. The one on the left is the lowest-mortality BMI not adjusting for fat mass or fat-free mass: a reasonably high 27.4. The one on the right is the lowest-mortality BMI adjusting for fat mass and fat-free mass: a much lower 21.6.

I know this may sound confusing, but due to possible statistical distortions this does not mean that you should try to bring your BMI to 21.6 if you want to reduce your risk of dying. What this means is that fat mass and fat-free mass matter. Moreover, all of the participants in this study were men. The authors concluded that: “…marked leanness (as opposed to thinness) has beneficial effects.”

Then we have an interesting 2003 article by Bigaard and colleagues () reporting on a study of 27,178 men and 29,875 women born in Denmark, 50 to 64 years of age. The table below summarizes deaths in this study, grouping them by BMI and waist circumference.



These are raw numbers; no complex statistics here. Circled in green is the area with samples that appear to be large enough to avoid “funny” results. Circled in red are the lowest-mortality percentages; I left out the 0.8 percentage because it is based on a very small sample.

As you can see, they refer to men and women with BMIs in the 25-29.9 range (overweight), but with waist circumferences in the lower-middle range: 90-96 cm for men and 74-82 cm for women; or approximately 35-38 inches for men and 29-32 inches for women.

Women with BMIs in the 18.5-24.9 range (normal) and the same or lower waists also died in small numbers. Underweight men and women had the highest mortality percentages.

A relatively small waist (not a wasp waist), together with a normal or high BMI, is an indication of more fat-free mass, which is retained together with some body fat. It is also an indication of less visceral body fat accumulation.

BMI puts young Asian-American women at risk of being "skinny fat"

As if we needed any more reason to pick on Body Mass Index (BMI): new research finds that this most accepted approach for assessing overweight and obesity based on height and weight could lead to misclassification of young Asian-American women as healthy when they're really "skinny fat," which could put them at greater risk for type 2 diabetes and cardiovascular disease.

In my last post, I discussed the scary, growing problem of sarcopenic obesity (aka "skinny fat") in older adults, described as age-related muscle loss in combination with the accumulation of body fat. One common result of sarcopenic obesity is a misclassification using BMI as "normal-weight" in these aged individuals. Misclassification in older adults with sarcopenic obesity is just one reason why BMI is loathed by those interested in public health.

Sadly, I learned at Experimental Biology, misclassification also occurs frequently across all ages depending on ethnicity. Asian Americans with normal weight sarcopenic obesity, for example, are often misclassified even in a college-aged population, according to nutritional epidemiologist Catherine Carpenter, an associate professor from University of California, Los Angeles.

In a symposium organized by the American Society for Nutrition to discuss the topic of obesity and BMI classification, Carpenter presented findings of a yet-to-be-published cross-sectional study that evaluated BMI and percent body fat measured by biolectrical impedance analysis among on the multi-ethnic college students on campus. The study's findings were that college-aged Asian American women were most likely to be misclassified by BMI.

Kindly, Carpenter provided me with further details about the study after the event. The study included 940 college students recruited over four consecutive years. The average participant was 21.4 years old with an average normal weight BMI of 22.9 kilogram over meter squared (kg/m2). The average percent body fat was 24.8 percent. The ethnic samples consisted of four ethnic groups: 49 percent Asian, 23 percent Caucasian, 7 percent Hispanic, and 21 percent as Other.

Among the college-age students, Asian-American women had the lowest BMI (21.5 kg/m2), but the second highest percent body fat (27.8 percent). In comparison, Hispanic women had the highest percent body fat (29.9 percent) and the highest BMI (23.5 kg/m2).

These findings suggest Asian-American women are most likely to be misclassified by BMI, which could mean greater likelihood risk of normal-weight obesity gone unnoticed. Ultimately, greater risk of obesity-related chronic disease such as type 2 diabetes and cardiovascular disease is the result.

No question, studies like these will continue to reveal the limitations of BMI. Once again, I'll repeat that it may be better to focus physical activity and amount of skeletal muscle mass (along with or maybe more than dietary calories or macronutrients like sugar) for prevention of obesity and chronic disease.

Skeletal muscle is critical as a large site for fat burning, glucose disposal, and metabolic rate. Sarcopenia in college-age adults should be most disturbing! It's much easier to hold on to muscle than it is to gain it back. Prevention, as usual, is key; and, prevention can be achieved with daily physical activity and a balanced diet -- with sufficient daily intake of quality protein, especially after exercise and throughout the day.

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Men who are skinny-fat: There are quite a few of them

The graph below (from Wikipedia) plots body fat percentage (BF) against body mass index (BMI) for men. The data is a bit old: 1994. The top-left quadrant refers to men with BF greater than 25 percent and BMI lower than 25. A man with a BF greater than 25 has crossed into obese territory, even though a BMI lower than 25 would suggest that he is not even overweight. These folks are what we could call skinny-fat men.

The data is from the National Health and Nutrition Examination Survey (NHANES), so it is from the USA only. Interesting that even though this data is from 1994, we already could find quite a few men with more than 25 percent BF and a BMI of around 20. One example of this would be a man who is 5’11’’, weighing 145 lbs, and who would be technically obese!

About 8 percent of the entire sample of men used as a basis for the plot fell into the area defined by the top-left quadrant – the skinny-fat men. (That quadrant is one in which the BMI measure is quite deceiving; another is the bottom-right quadrant.) Most of us would be tempted to conclude that all of these men were sick or on the path to becoming so. But we do not know this for sure. On the standard American diet, I think it is a reasonably good guess that these skinny-fat men would not fare very well.

What is most interesting for me regarding this data, which definitely has some measurement error built in (e.g., zero BF), is that it suggests that the percentage of skinny-fat men in the general population is surprisingly high. (And this seems to be the case for women as well.) Almost too high to characterize being skinny-fat as a disease per se, much less a genetic disease. Genetic diseases tend to be rarer.

In populations under significant natural selection pressure, which does not include modern humans living in developed countries, genetic diseases tend to be wiped out by evolution. (The unfortunate reality is that modern medicine helps these diseases spread, although quite slowly.)  Moreover, the prevalence of diabetes in the population was not as high as 8 percent in 1994, and is not that high today either; although it tends to be concentrated in some areas and cluster with obesity as defined based on both BF and BMI.

And again, who knows, maybe these folks (the skinny-fat men) were not even the least healthy in the whole sample, as one may be tempted to conclude.

Maybe being skinny-fat is a trait, passed on across generations, not a disease. Maybe such a trait was useful at some point in the not so distant past to some of our ancestors, but leads to degenerative diseases in the context of a typical Western diet. Long-living Asians with low BMI tend to gravitate more toward the skinny-fat quadrant than many of their non-Asian counterparts. That is, long-living Asians generally tend have higher BF percentage at the same BMI (see a discussion about the Okinawans on this post).

Evolution is a deceptively simple process, which can lead to very odd results.

This “trait-not-disease” idea may sound like semantics, but it has major implications. It would mean that many of the folks who are currently seen as diseased or disease-prone, are in fact simply “different”. At a point in time in our past, under a unique set of circumstances, they might have been the ones who would have survived. The ones who would have been perceived as healthier than average.

Low bone mineral content in older Eskimos: Meat-eating or shrinking?

Mazess & Mather (1974) is probably the most widely cited article summarizing evidence that bone mineral content in older North Alaskan Eskimos was lower (10 to 15 percent) than that of United States whites. Their finding has been widely attributed to the diet of the Eskimos, which is very high in animal protein. Here is what they say:

“The sample consisted of 217 children, 89 adults, and 107 elderly (over 50 years). Eskimo children had a lower bone mineral content than United States whites by 5 to 10% but this was consistent with their smaller body and bone size. Young Eskimo adults (20 to 39 years) of both sexes were similar to whites, but after age 40 the Eskimos of both sexes had a deficit of from 10 to 15% relative to white standards.”

Note that their findings refer strictly to Eskimos older than 40, not Eskimo children or even young adults. If a diet very high in animal protein were to cause significant bone loss, one would expect that diet to cause significant bone loss in children and young adults as well. Not only in those older than 40.

So what may be the actual reason behind this reduced bone mineral content in older Eskimos?

Let me make a small digression here. If you want to meet quite a few anthropologists who are conducting, or have conducted, field research with isolated or semi-isolated hunter-gatherers, you should consider attending the annual Human Behavior and Evolution Society (HBES) conference. I have attended this conference in the past, several times, as a presenter. That gave me the opportunity to listen to some very interesting presentations and poster sessions, and talk with many anthropologists.

Often anthropologists will tell you that, as hunter-gatherers age, they sort of “shrink”. They lose lean body mass, frequently to the point of becoming quite frail in as early as their 60s and 70s. They tend to gain body fat, but not to the point of becoming obese, with that fat replacing lean body mass yet not forming major visceral deposits. Degenerative diseases are not a big problem when you “shrink” in this way; bigger problems are  accidents (e.g., falls) and opportunistic infections. Often older hunter-gatherers have low blood pressure, no sign of diabetes or cancer, and no heart disease. Still, they frequently die younger than one would expect in the absence of degenerative diseases.

A problem normally faced by older hunter-gatherers is poor nutrition, which is both partially caused and compounded by lack of exercise. Hunter-gatherers usually perceive the Western idea of exercise as plain stupidity. If older hunter-gatherers can get youngsters in their prime to do physically demanding work for them, they typically will not do it themselves. Appetite seems to be negatively affected, leading to poor nutrition; dehydration often is a problem as well.

Now, we know from this post that animal protein consumption does not lead to bone loss. In fact, it seems to increase bone mineral content. But there is something that decreases bone mineral content, as well as muscle mass, like nothing else – lack of physical activity. And there is something that increases bone mineral content, as well as muscle mass, in a significant way – vigorous weight-bearing exercise.

Take a look at the figure below, which I already discussed on a previous post. It shows a clear pattern of benign ventricular hypertrophy in Eskimos aged 30-39. That goes down dramatically after age 40. Remember what Mazess & Mather (1974) said in their article: “… after age 40 the Eskimos of both sexes had a deficit of from 10 to 15% relative to white standards”.

Benign ventricular hypertrophy is also known as athlete's heart, because it is common among athletes, and caused by vigorous physical activity. A prevalence of ventricular hypertrophy at a relatively young age, and declining with age, would suggest benign hypertrophy. The opposite would suggest pathological hypertrophy, which is normally induced by obesity and chronic hypertension.

So there you have it. The reason older Eskimos were found to have lower bone mineral content after 40 is likely not due to their diet.  It is likely due to the same reasons why they "shrink", and also in part because they "shrink". Not only does physical activity decrease dramatically as Eskimos age, but so does lean body mass.

Obese Westerners tend to have higher bone density on average, because they frequently have to carry their own excess body weight around, which can be seen as a form of weight-bearing exercise. They pay the price by having a higher incidence of degenerative diseases, which probably end up killing them earlier, on average, than osteoporosis complications.

Reference

Mazess R.B., & Mather, W.W. (1974). Bone mineral content of North Alaskan Eskimos. American Journal of Clinical Nutrition, 27(9), 916-925.

How lean should one be?

Loss of muscle mass is associated with aging. It is also associated with the metabolic syndrome, together with excessive body fat gain. It is safe to assume that having low muscle and high fat mass, at the same time, is undesirable.

The extreme opposite of that, achievable though natural means, would be to have as much muscle as possible and as low body fat as possible. People who achieve that extreme often look a bit like “buff skeletons”.

This post assumes that increasing muscle mass through strength training and proper nutrition is healthy. It looks into body fat levels, specifically how low body fat would have to be for health to be maximized.

I am happy to acknowledge that quite often I am working on other things and then become interested in a topic that is brought up by Richard Nikoley, and discussed by his readers (I am one of them). This post is a good example of that.

Obesity and the diseases of civilization

Obesity is strongly associated with the diseases of civilization, of which the prototypical example is perhaps type 2 diabetes. So much so that sometimes the impression one gets is that without first becoming obese, one cannot develop any of the diseases of civilization.

But this is not really true. For example, diabetes type 1 is also one of the diseases of civilization, and it often strikes thin people. Diabetes type 1 results from the destruction of the beta cells in the pancreas by a person’s own immune system. The beta cells in the pancreas produce insulin, which regulates blood glucose levels.

Still, obesity is undeniably a major risk factor for the diseases of civilization. It seems reasonable to want to move away from it. But how much? How lean should one be to be as healthy as possible? Given the ubiquity of U-curve relationships among health variables, there should be a limit below which health starts deteriorating.

Is the level of body fat of the gentleman on the photo below (from: ufcbettingtoday.com) low enough? His name is Fedor; more on him below. I tend to admire people who excel in narrow fields, be they intellectual or sport-related, even if I do not do anything remotely similar in my spare time. I admire Fedor.

Let us look at some research and anecdotal evidence to see if we can answer the question above.

The buff skeleton look is often perceived as somewhat unattractive

Being in the minority is not being wrong, but should make one think. Like Richard Nikoley’s, my own perception of the physique of men and women is that, the leaner they are, the better; as long as they also have a reasonable amount of muscle. That is, in my mind, the look of a stage-ready competitive natural bodybuilder is close to the healthiest look possible.

The majority’s opinion, however, seems different, at least anecdotally. The majority of women that I hear or read voicing their opinions on this matter seem to find the “buff skeleton” look somewhat unattractive, compared with a more average fit or athletic look. The same seems to be true for perceptions of males about females.

A little side note. From an evolutionary perspective, perceptions of ancestral women about men must have been much more important than perceptions of ancestral men about women. The reason is that the ancestral women were the ones applying sexual selection pressures in our ancestral past.

For the sake of discussion, let us define the buff skeleton look as one of a reasonably muscular person with a very low body fat percentage; pretty much only essential fat. That would be 10-13 percent for women, and 5-8 percent for men.

The average fit look would be 21-24 percent for women, and 14-17 percent for men. Somewhere in between, would be what we could call the athletic look, namely 14-20 percent for women, and 6-13 percent for men. These levels are exactly the ones posted on this Wikipedia article on body fat percentages, at the time of writing.

From an evolutionary perspective, attractiveness to members of the opposite sex should be correlated with health. Unless we are talking about a costly trait used in sexual selection by our ancestors; something analogous to the male peacock’s train.

But costly traits are usually ornamental, and are often perceived as attractive even in exaggerated forms. What prevents male peacock trains from becoming the size of a mountain is that they also impair survival. Otherwise they would keep growing. The peahens find them sexy.

Being ripped is not always associated with better athletic performance

Then there is the argument that if you carried some extra fat around the waist, then you would not be able to fight, hunt etc. as effectively as you could if you were living 500,000 years ago. Evolution does not “like” that, so it is an unnatural and maladaptive state achieved by modern humans.

Well, certainly the sport of mixed martial arts (MMA) is not the best point of comparison for Paleolithic life, but it is not such a bad model either. Look at this photo of Fedor Emelianenko (on the left, clearly not so lean) next to Andrei Arlovski (fairly lean). Fedor is also the one on the photo at the beginning of this post.

Fedor weighed about 220 lbs at 6’; Arlovski 250 lbs at 6’4’’. In fact, Arlovski is one of the leanest and most muscular MMA heavyweights, and also one of the most highly ranked. Now look at Fedor in action (see this YouTube video), including what happened when Fedor fought Arlovski, at around the 4:28 mark. Fedor won by knockout.

Both Fedor and Arlovski are heavyweights; which means that they do not have to “make weight”. That is, they do not have to lose weight to abide by the regulations of their weight category. Since both are professional MMA fighters, among the very best in the world, the weight at which they compete is generally the weight that is associated with their best performance.

Fedor was practically unbeaten until recently, even though he faced a very high level of competition. Before Fedor there was another professional fighter that many thought was from Russia, and who ruled the MMA heavyweight scene for a while. His name is Igor Vovchanchyn, and he is from the Ukraine. At 5’8’’ and 230 lbs in his prime, he was a bit chubby. This YouTube video shows him in action; and it is brutal.

A BMI of about 25 seems to be the healthiest for long-term survival

Then we have this post by Stargazey, a blogger who likes science. Toward the end the post she discusses a study suggesting that a body mass index (BMI) of about 25 seems to be the healthiest for long-term survival. That BMI is between normal weight and overweight. The study suggests that both being underweight or obese is unhealthy, in terms of long-term survival.

The BMI is calculated as an individual’s body weight divided by the square of the individual’s height. A limitation of its use here is that the BMI is a more reliable proxy for body fat percentage for women than for men, and can be particularly misleading when applied to muscular men.

The traditional Okinawans are not super lean

The traditional Okinawans (here is a good YouTube video) are the longest living people in the world. Yet, they are not super lean, not even close. They are not obese either. The traditional Okinawans are those who kept to their traditional diet and lifestyle, which seems to be less and less common these days.

There are better videos on the web that could be used to illustrate this point. Some even showing shirtless traditional karate instructors and students from Okinawa, which I had seen before but could not find again. Nearly all of those karate instructors and students were a bit chubby, but not obese. By the way, karate was invented in Okinawa.

The fact that the traditional Okinawans are not ripped does not mean that the level of fat that is healthy for them is also healthy for someone with a different genetic makeup. It is important to remember that the traditional Okinawans share a common ancestry.

What does this all mean?

Some speculation below, but before that let me tell this: as counterintuitive as it may sound, excessive abdominal fat may be associated with higher insulin sensitivity in some cases. This post discusses a study in which the members of a treatment group were more insulin sensitive than the members of a control group, even though the former were much fatter; particularly in terms of abdominal fat.

It is possible that the buff skeleton look is often perceived as somewhat unattractive because of cultural reasons, and that it is associated with the healthiest state for humans. However, it seems a bit unlikely that this applies as a general rule to everybody.

Another possibility, which appears to be more reasonable, is that the buff skeleton look is healthy for some, and not for others. After all, body fat percentage, like fat distribution, seems to be strongly influenced by our genes. We can adapt in ways that go against genetic pressures, but that may be costly in some cases.

There is a great deal of genetic variation in the human species, and much of it may be due to relatively recent evolutionary pressures.

Life is not that simple!

References

Buss, D.M. (1995). The evolution of desire: Strategies of human mating. New York, NY: Basic Books.

Cartwright, J. (2000). Evolution and human behavior: Darwinian perspectives on human nature. Cambridge, MA: The MIT Press.

Miller, G.F. (2000). The mating mind: How sexual choice shaped the evolution of human nature. New York, NY: Doubleday.

Zahavi, A. & Zahavi, A. (1997). The Handicap Principle: A missing piece of Darwin’s puzzle. Oxford, England: Oxford University Press.

Body mass index and cancer deaths in various US states

Ancel Keys is often heavily criticized for allegedly originating the fat phobia that we see today in the US and other countries, perhaps with good reason. But he has also made many important contributions to the health sciences.

One of them was the index known as body mass index (BMI), calculated based on a person's weight and height. Unlike other measures, such as body fat percentage and body fat mass, BMI is very easy to calculate; divide your weight (kg) by your height (m) squared.

BMI is strongly correlated with body fat percentage, and body fat mass. Very muscular people are exceptions; they may have a high BMI and yet reduced body fat.

Excessive body fat mass leads to chronic inflammation, due in part to elevated circulating levels of pro-inflammatory hormones such as tumor necrosis factor-alpha (cute name eh?).

Chronic inflammation, in turn, leads to increased incidence of cancer.

Thus it should be no surprise that having a BMI above 30 (obesity level) is strongly correlated with cancer death rates; see graph below (click on it to enlarge), from: Florida, 2009 (full reference at the end of this post).

The correlation for the graph above is a high 0.702, calculated as the square-root of the R-squared value shown at the bottom-right. The R-squared is the percentage of explained variance for cancer deaths, meaning that nearly 50 percent of the cancer deaths are "explained", or caused, by the BMI percentages.

One more reason to bring body fat down to healthy levels.

How do you do that? A good way to start is to replace refined carbohydrates and sugars with natural sources of protein and fat in your diet; eggs included, no need to worry about dietary cholesterol.

Reference:

Florida, R. (2009). The geography of obesity. Creative Class, Nov. 25.