In April 1995 an article appeared in the journal Current Anthropology that was an intellectual tour de force and, in my view, an example of a perfect theoretical paper.  “The  Expensive-Tissue Hypothesis” (ETH) by Leslie Aiello and Peter Wheeler demonstrated by a brilliant thought experiment that our species didn’t evolve to eat meat but evolved because it ate meat.

The ETH is an example of the kind of scientific detective work that I love.  In fact, this paper is one of my all time favorites.  (An amazing bit of trivia about this paper is that it almost didn’t get published.  I had the opportunity to talk with Leslie Aiello at a meeting a few months ago, and she told me that the journal was reluctant to publish the paper because they thought it too technical for their readers.  I suspect they also found it too controversial.  Now I’m sure they’re glad they published because I would imagine it is the most cited of all the papers ever published in Current Anthropology.)  The authors methodically lay the scientific foundation for their experiment, then, like Sherlock Holmes, progress step by step, accumulating little pieces of data until they reach the ineluctable conclusion that meat eating made us human. I would like to walk us all through their thought processes as laid out in their brilliant paper.

Let’s start with the problem.

For years anthropologists have speculated about why humans developed such large brains so quickly – from softball size to what we have now in just a short 2 million years.  Below is a graphic showing hominid/human brain growth over time.

A number of hypotheses have arisen to answer this question.  Some say that humans developed large brains because they had to contend with problems involving group size, others posit that large brains came about as a consequence of developing complex foraging strategies, others yet say the development of a social or Machiavellian  intelligence was the driving factor.  And even others say that the complexities of learning to hunt expanded brain size.

Any or all of these hypotheses may be valid, but the problem isn’t really as much a matter of why as it is a matter of how.  Other primates deal with groups and have complex foraging strategies; and many deal with social problems within their groups, and some even hunt.  Yet they still have small brains.  (Granted, their brains are larger for their size than those of other mammals, but primates sport small brains as compared to humans.)  How did the human brain grow?

This isn’t an easy question to answer because of the thermogenics involved.  Brains consume a large amount of fuel and, consequently, throw off an enormous amount of heat for their size.  The metabolic rate of brain tissue is nine times that of the average of  the metabolic rate of the rest of the body.

So what? you may say.  So we’ve got a big, hot-running, energy-burning brain.  What difference does that make?  It’s reflected in our overall metabolic rate, right?  Well, sort of, and therein lies the crux of the problem.  As we will see below, our total metabolic rate – even with our huge brains – is the same as that of any other animal our size. Or to say it another way, animals our size with much smaller brains have the same metabolic rate that we do with our huge brains.  This fact was the starting point for the authors of the ETH.  So let’s start there as well.

In keeping with a great scientific tradition, Aiello and Wheeler were able to see what they saw because they stood on the shoulders of giants who came before them.  In their case the giant was Max Kleiber, an animal physiologist working at the University of California at Davis, who published a groundbreaking paper in 1947 and a scholarly text titled The Fire of Life in 1961.  Kleiber’s work involved the meticulous measurement of the metabolic rates of numerous animals, including humans.  As he plotted the various metabolic rates, he discovered an extremely strong correlation between the mass of an animal and its metabolic rate.  Kleiber found that this relationship held constant across numerous species.  His October 1947 paper in Physiological Reviews simply titled “Body Size and Metabolic Rate” was a classic.  By using the equations Kleiber worked out, the metabolic rate of virtually any animal could be determined simply by knowing the animal’s body size.  Or, as Kleiber put it in the paper:

Does a horse produce more heat per day than a rat or do some rats produce more heat than do some horses?  Almost anybody who understands what is meant by “heat production per day” will not hesitate to give the correct answer and will even be convinced that the daily rate of heat production of men or sheep is greater than that of rats, but smaller than that of horses.  Thus most people (among those who understand the question) are convinced that in general the bigger  homeotherms produce more heat per day than the smaller homeotherms, that, in other words, the metabolic rate of homeotherms is positively correlated to body size.

The answer to the next question: “does a horse produce more heat per day per kilogram of body weight than a rat?” requires some biological training.  Most biologists, however, will not hesitate to answer that the rate of heat production per unit body weight of the big animal is less than that of the small animal.

The positive correlation between metabolic rate and body size, and the negative correlation between metabolic rate per unit weight and body size, establish two limits between which we expect to find the rate of heat production [basal metabolic rate] of a horse if we know the rate of heat production of a rat.  We expect the metabolic rate of the horse to be somewhere between that of the rat, and that of the rat times the the ratio of horse weight to rat weight, provided of course that we do not regard these two correlations as simply accidental.

If we are firmly convinced that the metabolic rate of horses, and other homeotherms of similar size, is never outside these two limits, then we admit to recognize a natural law between body size and metabolic rate.

This natural law, carefully calculated by Kleiber, is now known as Kleiber’s law.  Below is Kleiber’s law graphed out by him as it appeared in his seminal paper.  And this is exactly as it appeared in the journal, but with the addition here of colors for better legibility.  Since their was no Excel nor graphics software in Kleiber’s time, the graph was hand drawn and appeared in the pages of Physiological Reviews as such.  How times have changed.

As you look along the line running from lower left to upper right, you can find rats and horses and a host of other mammals including humans.  Over the years, mammals that Kleiber didn’t have the opportunity to work on have been measured, and they all fit nicely along Kleiber’s line, following Kleiber’s law.  Because of this tight correlation, Kleiber’s equations can be used to precisely estimate the metabolic rate of any animal just by knowing its size.

Aiello and Wheeler used Kleiber’s law as the jumping off point for their grand thought experiment.

Since all animals measured have conformed to Kleiber’s law, Aiello and Wheeler postulated that animals now extinct – including our human and pre-human predecessors – would have fallen along the same line. Using skeletal remains paleontologists have been able to calculate body sizes of extinct animals along with pre-Homo and early-Homo species.  Then using Kleiber’s law, it is possible to closely estimate the metabolic rates of these creatures.  And here’s where it gets interesting.

According to Kleiber’s law, an australopithecine weighing 80 pounds would have the same metabolic rate as a human weighing 80 pounds despite the disparity in brain size between the two.  The much larger brain of the human would have 4-5 times the metabolic rate of the brain of the australopithecine, yet would have the same overall metabolic rate.  What gives?

That’s precisely what the authors of “The Expensive-Tissue Hypothesis” wondered.

Because the human brain costs so much more in energetic terms than the equivalent average mammalian brain, one might expect the human BMR [basal metabolic rate] to be correspondingly elevated.  However, there is no significant correlation between relative basal metabolic rate and relative brain size in humans and other encephalized animals.

Where does the energy come from to fuel the encephalized brain?

The authors postulated a solution.

One possible answer to the cost question is that the increased energetic demands of a larger brain are compensated for by a reduction in the mass-specific metabolic rates of other tissues.

In other words, if one organ – the brain, for example – is chewing up a lot of energy and contributing a disproportionate amount of the basal metabolic rate for the animal as a whole, then maybe another organ or group of organs are consuming less energy to compensate.  The heart, the kidneys, the liver, the skeletal muscles, the GI tract – all consume energy and contribute to metabolic rate.  Maybe one of these organs became smaller as the brain became larger over time.

We can hone our analysis a little finer if we begin to look at an energy-balance equation, but an energy-balance equation of a different kind.  I have written a number of times in this blog about the energy-balance equation that applies to weight loss: change in weight equals energy in minus energy out.  That is not the equation we’ll be talking about here.  The other energy-balance equation says that the total metabolic rate is the sum of all the metabolic rates of the various organs and tissues in the body.  If you add the metabolic rates of the kidneys, the heart, the brain, the muscles, the digestive tract and so on together, you will get the total metabolic rate of the body, which makes sense because it is the sum of the parts.

Total BMR = brain BMR + heart BMR + kidney BMR + GI tract BMR + liver BMR + the remainder of the body’s tissues.

The authors of the ETH set out to look at the metabolic rates of the various organs.  By a diligent search of the literature, they found that along with the brain, the the heart, the kidneys, the liver and the gastro-intestinal tract account for the vast majority of the total BMR.  They dubbed these organs as ‘expensive tissues’ because they consume a large amount of energy as compared to their size.  (Surprisingly, muscle mass doesn’t contribute all that much to the total metabolic rate (skin and bone contribute even less), which gives the lie to that old notion — that I, myself, have fallen prey to — that replacing fat with muscle increases metabolism significantly.)

Aiello and Wheeler reasoned that if the total metabolic rate stayed the same while the energy-expensive brain grew over time some other expensive tissue had to get smaller.  There could be no other solution.

But which of the expensive tissues got smaller?

Aiello and Wheeler examined the data on the metabolic rates and sizes of the various expensive tissues and learned that for a 65 kg primate, the heart, the kidneys, and the liver were approximately the same size as those of a 65 kg (143 lb) human.  The greater metabolic rate of the large human brain was compensated for by a GI tract significantly decreased in size.  It turns out that the GI tract of a 65 kg human is just a little over half the size of the GI tract of a similar sized primate.

The combined mass of the metabolically expensive tissues for the reference adult human is remarkably close to that expected for the average 65-kg primate, but the contributions of individual organs to this total are very different from the expected ones.  Although the human heart and kidneys are both close to the size expected for a 65-kg primate, the mass of the splanchnic organs (the abdominal organs) is approximately 900 g less that expected.  Almost all of this shortfall is due to a reduction in the gastro-intestinal tract, the total mass of which is only 60% of that expected for a similar-sized primate.  Therefore, the increase in mass of the human brain appears to be balanced by a almost identical reduction in size of the gastro-intestinal tract.

Below is a graphic from the ETH showing the sizes of the different organs as based on predictions from a 65-kg primate and the observed size in humans.

So we know that as humans evolved larger brains they simultaneously co-evolved smaller guts in order to maintain a set BMR.  And this is where the story gets interesting. Why?  Because

the logical conclusion is that no matter what is selecting for brain-size increase, one would expect a corresponding selection for reduction in the relative size of the gut.

Some researchers believe that increasingly complex activities drove the brain to enlarge.  As the authors of the ETH summarized it:

The relationship between relative brain size and diet is often mentioned in the literature on primate encephalization and is generally explained in terms of the different degrees of intelligence needed to exploit various food resources.  For example, [some] have argued that a relatively large brain and neocortical size correlates with omnivorous feeding in primates , which requires relatively complicated strategies for extracting high-quality foodstuffs.  Alternatively, [others] have suggested that frugivores have relatively large brain sizes because they have relatively larger home ranges than folivores, necessitating a more sophisticated mental map for location and exploitation of the food resources.

But it doesn’t matter whether our brains got big because our predecessors were socialized, developed complex foraging strategies, lived in and had to deal with groups or were skilled hunters, in order to obey Kleiber’s law, something had to force our guts to get smaller at the same time.  What could that be?

According to Aiello and Wheeler, it is increased diet quality that allowed the gut to get smaller while still absorbing the necessary nutrients to fuel the metabolism.  As they put it

The results presented here [in the ETH] suggest that the relationship between relative brain size and diet is primarily a relationship between relative brain size and relative gut size, the latter being determined by dietary quality.  This would imply that a high-quality diet is necessary for this encephalization, no matter what may be selecting for that encephalization.  A high-quality diet relaxes the metabolic constraints on encephalization by permitting a relatively smaller gut, thereby reducing the considerable metabolic cost of this tissue.

What the authors are saying is that it doesn’t matter how much more brain power was required, the brain couldn’t enlarge without something else giving.  What obviously gave was the size of the GI tract, and the only way a smaller GI tract could provide the fuel for the body was to have a higher-quality diet. How did the our most ancient relatives the early hominids increase the quality of their diets?

A considerable problem for the early hominids would have been to provide themselves, as large-bodied species, with sufficient quantities of high-quality food to permit the necessary reduction of the gut.  The obvious solution would have been to include increasingly large amounts of animal-derived food in the diet.

Increasing the amount of easily-digested food of animal origin allowed us to shrink our guts while expanding our brains.  Had we remained on a diet high in vegetation, we would no doubt not have been able to expand our brains irrespective of how much more thinking those brains would have needed to do.  It just wouldn’t have been possible to do so without violating Kleiber’s law.

Take the gorilla, for example, almost pure vegetarians that spend their entire ‘working’ day foraging and eating, which they have to do to get enough calories to maintain their enormous bulk.  They have large guts and pay for it by having small brains.  Even smaller than that of our most primitive ancestors, the australophthecines.

Gorilla has one of the lowest levels of encephalization of any haplorhine primate, and the much higher level of encephalization of all the australopithecines suggests a diet of significantly higher quality than that of this genus.

Which makes sense when you consider that carbon 13 isotope analysis has shown that Australopithecus africanus (the species that came right after Lucy) consumed meat.  As you go up the lineage from Australopithecus and through Homo, you find that more and more meat was consumed the higher up the tree you go.

It’s easy to see that, as compared to humans, chimps and gorillas have large, protuberant bellies, which supports the fact that they have larger GI tracts, but what about our ancient ancestors.  All we have to go on are skeletal remains, which show nicely that their heads (and brains) were much smaller than ours, but what about their guts?  How do we really know their guts were larger?  According to Kleiber, they would have to be, but how to we really know they were?

The large gut of the living pongids gives their bodies a somewhat pot-bellied appearance, lacking a discernible waist.  This is because the rounded profile of the abdomen is continuous with that of the lower portion of the rib cage, which is shaped like an inverted funnel, and also because the lumbar region is relatively short (three to four lumber vertebrae).

The drawing below from the ETH shows the inverted-funnel shape of the ribcage of the chimpanzee on the left.  You can mentally draw the lines downward from these ribs and envision the pot-bellied look of the abdomen that these primates evidence.  Looking at the image on the right, you can see that Australopithecus afarensis (Lucy’s species) has the same inverted-funnel shaped rib cage, indicating a large belly and a low-quality diet.

The drawing in the middle is of a modern human.  If you extrapolate the lines down from the human rib cage, you can see that they lead to a more narrow waist.  Makes you think more of a lean, rangy wolf or other slim-waisted carnivore, whereas the other two don’t.

The authors conclude:

If an encephalized animal does not have a correspondingly elevated BMR [which according to Kleiber, it can’t], its energy budget must be balanced in some other way.  The expensive-tissue hypothesis suggested here is that this balance can be achieved by a reduction in size of one of the other metabolically expensive organs in the body (liver, kidney, heart of gut).  We argue that this can best be done by the adoption of a high-quality diet, which permits a relatively small gut and liberates a significant component of BMR for the encephalized brain.  No matter what was selecting for encephalization, a relatively large brain could not be achieved without a correspondingly [sic] increase in dietary quality unless the metabolic rate was correspondingly increased.

At a more general level, this exercise has demonstrated other important points.  First, diet can be inferred from aspects of anatomy other than teeth and jaws.  For example, an indication of the relative size of the gastro-intestinal tract and consequently the digestibility of the food stuffs being consumed is provided by the morphology of the rib cage and pelvis.  Second, any dietary inference for the hominids must be consistent with all lines of evidence.  Third, the evolution of any organ of the body cannot be profitably studied in isolation.  Other approaches to understand the costs of encephalization have generally failed because they have tended to look at the brain in isolation from other tissues.  The expensive-tissue hypothesis profitably emphasizes the essential interrelationship between the brain, BMR, and other metabolically expensive body organs.

I hope you are now armed with enough knowledge to be able to see through these articles and/or charts that are all too common showing how the GI tract of humans is closer to that of a gorilla than it is to that of a cat or some other carnivore.  It seems to me that Aiello and Wheeler have pretty thoroughly demolished the notion that humans are actually designed by the forces of natural selection to be vegetarians.  Based on the data and the argument they present, it is actually the opposite:  we evolved to be meat eaters.

It was our gradual drift toward the much higher quality diet provided by food from animal sources that allowed us to develop the large brains we have.  It was hunting and meat eating that reduced our GI tracts and freed up our brains to grow.  As I wrote at the start of this post, the evidence indicates that we didn’t evolve to eat meat – we evolved because we ate meat.

Lierre Keith had it right in The Vegetarian Myth:

The wild herds of aurochs and horses invented us out of their bodies, their nutrient-dense tissues gestating the human brain.

If we evolved because we ate meat, why would we want to stop now?

Note: I found the full text of this article available on Scribd.  If it gets taken down, let me know, and I’ll put it up here.  I’m just trying to save space on my server.

Painting at top: Monkey Before Skeleton by Gabriel Cornelius von Max

But I have just recently been disabused of that notion.

My friend Tim Ferriss put up an excerpt of our new book The 6-Week Cure on his site a few days ago and asked me if I would mind answering a few of the commenters.  I told him I wouldn’t mind at all, but I didn’t realize what I was getting myself into.

Tim’s blog isn’t really a nutritional blog – it’s a lifestyle design blog (said term invented by Tim himself).  There is a little nutrition thrown in here and there, but mainly the blog is focused in other directions.  As a consequence, it attracts mainly youngish readers who enjoy following Tim’s adventures and want to learn how to model their lifestyles after his.  My blog is specifically directed to folks more interested in nutrition who are willing to put up with my digressions into other areas from time to time, so I expect them to be more nutritionally aware.

I wasn’t prepared for what I got in the comments on Tim’s post.  Surprisingly, there were a fair number of commenters – maybe even a majority – who would feel right at home on my blog.  But there were also a fair number who made me realize that nutritional sophistication is far from a universal phenomenon.  You can take a trip over to the comments section of his blog to see what I mean.  I pretty much answered only those who I thought were totally off track, so you’ll be able to read my comments, then track back to the comment I was responding to and see what I mean.

The experience made me realize just how much of a void there is in good info out there explaining why humans really are meat eaters at heart, so I’ve decided to do a couple of posts on the subject to be able to refer to in the future when this issue arises.  While I was mulling this idea over, I received a link to a piece of sheer idiocy that really pushed me over the edge.  It made me realize that if this kind of stuff is out there circulating, it’s no wonder these people have such bizarre notions of what constitutes a rational diet.

I’m going to start off this first part by examining some of this nonsense, and I’ll finish off in the second part by going through one of the classic papers of all time showing why we humans aren’t just meat eaters, but we are humans because we eat meat.

The link I had sent by a friend of mine is one I’ve seen referred to on a couple of other low-carb or Paleo sites.  I didn’t give it much thought until the Tim Ferriss blog experience (which, BTW, is still going on.  I just got binged on my email that Tim approved another 15 or so comments that I need to take a look at, so keep checking his blog) made me realize that there were really people out their buying into this nonsense.

The piece from AlterNet starts out with a big, bold headline:

Eating Meat Is Not Natural

No equivocating there.  A categorical statement if I’ve ever seen one.  Let’s see how the author of the piece – Kathy Freston – backs it up.  She starts out with a short introductory paragraph that ends with another categorical statement.  I’ve noticed that these folks love to write these things with such authority.  Same with the people on Tim’s blog.  There is no doubt in their minds that they’re correct.  But they are operating in an informational void.

Which brings to mind a great quote from Lierre Kieth’s book:

I was on the side of righteousness, and like any fundamentalist, I could only stay there by avoiding information.

Here is the intro paragraph to the AlterNet piece:

Going through the reader feedback on some of my recent articles, I noticed the frequently stated notion that eating meat was an essential step in human evolution. While this notion may comfort the meat industry, it’s simply not true, scientifically. [My italics]

No hesitance there.  “It’s simply not true, scientifically.”  Not even a smidgen of doubt.

How does our author prove it’s not true?  By referring to the writings of people who present themselves as scientists but who are ideological vegetarians.

Dr. T. Colin Campbell, professor emeritus at Cornell University and author of The China Study (please check out the link), explains that in fact, we only recently (historically speaking) began eating meat, and that the inclusion of meat in our diet came well after we became who we are today. He explains that “the birth of agriculture only started about 10,000 years ago at a time when it became considerably more convenient to herd animals. This is not nearly as long as the time [that] fashioned our basic biochemical functionality (at least tens of millions of years) and which functionality depends on the nutrient composition of plant-based foods.”

Ah, our old friend Dr. T. Colin Campbell and the China study.  Many commenters on Tim’s blog referenced this study as if were gospel.  Before we get into The China Study, I’ve got a disclosure to make.  I’ve never read the thing.  So how can I talk about it intelligently?  Because I have appeared on the podium with Dr. Campbell.  A few years ago we both spoke at a symposium somewhere (I can’t even remember where now), and his talk preceded mine.  As I sat on the stage, I listened intently and made notes as I watched his slides.  What I realized right off the bat is that his whole shtick is nothing but an epidemiologic or observational study, which, as I’ve written about in these pages  before, proves no causality and serves only to derive hypotheses.  He spent his entire presentation trying to prove his thesis with studies that can’t he used to prove diddly.  Since I spent an hour listening, watching and then rebutting, I figure I’ve earned a pass from reading the book.

If you want to read more on The China Study, I suggest you take a look at two sources.  First, read Chris Masterjohn’s review, then you can read Dr. Campbell’s rebuttal, then Chris’s response to that.  And you can read my good friend Anthony Colpo’s review of the book.  The China Study is a pretty sorry piece of work and, since it is an observational study (the results of which are misrepresented in the pop science book available), it doesn’t prove squat.  I certainly wouldn’t rush out and become a vegetarian because of it.  Yet if you read some of the comments on Amazon, you would think this book is the Second Coming.  These poor people who have been so gulled simply don’t realize how worthless such studies are.

In the quote above, Dr. Campbell is obviously unaware that the birth of agriculture involved primarily the turn from a hunting/gathering subsistence to the growing of grain.  The agricultural revolution wasn’t a change from a herbivore existence to the herding of animals for food.  This kind of clap trap shows just how misguided these kind of folks are and how they twist the historical facts to suit their purposes.

The next ‘authority’ trotted out by our author is none other than Dr. Neal Barnard, the president of the inappropriately named Physician’s Committee for Responsible Medicine and himself a vegetarian.

That jibes with what Physicians Committee for Responsible Medicine President Dr. Neal Barnard says in his book, The Power of Your Plate, in which he explains that “early humans had diets very much like other great apes, which is to say a largely plant-based diet, drawing on foods we can pick with our hands. Research suggests that meat-eating probably began by scavenging — eating the leftovers that carnivores had left behind. However, our bodies have never adapted to it. To this day, meat-eaters have a higher incidence of heart disease, cancer, diabetes, and other problems.”

This is the Dr. Barnhard of the much-ballyhooed (by him, at least) ‘study’ of the ill effects of low-carb diets that I rebutted a few years back.

He is correct in saying that the earliest of men probably begin to eat meat by scavenging.  The paleontological record seems to bear that out.  But the line about our bodies never adapting to it and the statement that meat-eaters have higher incidences of all the diseases mentioned is pure malarky.  If Dr. Barnhard were asked to come up with references for these statements, all he could possible produce would be a few observational studies, which, as we all know, don’t prove anything.  And for each one he could come up with, I could come up with just as many showing the opposite.

Now we get to the big gun: Richard Leakey.

There is no more authoritative source on anthropological issues than paleontologist Dr. Richard Leakey, who explains what anyone who has taken an introductory physiology course might have discerned intuitively — that humans are herbivores. Leakey notes that “[y]ou can’t tear flesh by hand, you can’t tear hide by hand … We wouldn’t have been able to deal with food source that required those large canines” (although we have teeth that are called “canines,” they bear little resemblance to the canines of carnivores).

Hmmm.  I wonder if Leakey has ever seen the canines of a gorilla?  They certainly have the appearance of the canines of a carnivore yet gorillas are pure vegetarians.  But let’s go on.

In fact, our hands are perfect for grabbing and picking fruits and vegetables. Similarly, like the intestines of other herbivores, ours are very long (carnivores have short intestines so they can quickly get rid of all that rotting flesh they eat).  We don’t have sharp claws to seize and hold down prey.  And most of us (hopefully) lack the instinct that would drive us to chase and then kill animals and devour their raw carcasses. Dr. Milton Mills builds on these points and offers dozens more in his essay, “A Comparative Anatomy of Eating.”

All this anatomical stuff is pure gibberish, yet many people not skilled in the art of critical thinking buy into it.  In part II of this post, I’ll address many of these anatomical issues, so we’ll leave it until then.  If you’re bored, you might want to take a look at the Comparative Anatomy of Eating, which is a not-very-successful attempt to push a square peg into a round hole.  Dr. Milton really has to stretch to get the anatomy to fit with his notions of what it is designed for.  I’ve seen so many variations on this theme – people showing minor anatomical differences to prove that humans are really herbivores – that I’ve lost count.

The author now turns to her last expert, a big time, mainstream doctor.

The point is this: Thousands of years ago when we were hunter-gatherers, we may have needed a bit of meat in our diets in times of scarcity, but we don’t need it now.  Says Dr. William C. Roberts, editor of the American Journal of Cardiology, “Although we think we are, and we act as if we are, human beings are not natural carnivores.  When we kill animals to eat them, they end up killing us, because their flesh, which contains cholesterol and saturated fat, was never intended for human beings, who are natural herbivores.”

This guy really goes off the rails.  He tells us that “when we kill animals to eat them, they end up killing us,…”  A strong statement that he has absolutely nothing but his own opinion to back it up with.  Then he really takes a leap.  These animals we kill to eat do us in “because their flesh, which contains cholesterol and saturated fat, was never intended for human beings, who are natural herbivores.”  Oh, really.  That cholesterol will do us in, eh?  Why is it that we have cholesterol ourselves and plants don’t?  Why is every cell in our bodies capable of making cholesterol?  Because we don’t need it?  The depth of his dumbth is unfathomable.  Realizing that this guy is the editor of a major cardiology journal lets you know really quickly why such journals publish such biased articles.

Our author goes on.

Sure, most of us are “behavioral omnivores” — that is, we eat meat, so that defines us as omnivorous. But our evolution and physiology are herbivorous, and ample science proves that when we choose to eat meat, that causes problems, from decreased energy and a need for more sleep up to increased risk for obesity, diabetes, heart disease, and cancer.

Here again with the meat causes obesity, diabetes, heart disease and cancer.  Instead of the “ample science” she claims, there is no proof whatsoever.  She uses an interesting expression: she describes us humans as “behavioral omnivores,” which I think is a good definition, but she’s using it incorrectly.  She means that we are really herbivores, but we’ve learned to become omnivores, therefore we are behavioral omnivores, not real omnivores.  I agree with her, but with a twist.  I think we are designed as carnivores and have adapted to an omnivore existence, so we are behavioral omnivores, just not the way she thinks we are.  Gorillas are behavioral vegetarians.  They have the GI tracts from teeth to the other end of carnivores – and they do fine being fed meat in zoos – but they culturally are vegetarians or behavioral vegetarians.

Old habits die hard, and it’s convenient for people who like to eat meat to think that there is evidence to support their belief that eating meat is “natural” or the cause of our evolution. For many years, I too, clung to the idea that meat and dairy were good for me; I realize now that I was probably comforted to have justification for my continued attachment to the traditions I grew up with.

But in fact top nutritional and anthropological scientists from the most reputable institutions imaginable say categorically that humans are natural herbivores, and that we will be healthier today if we stick with our herbivorous roots. It may be inconvenient, but it alas, it is the truth.

She ends by summarizing all the twaddle she presented earlier.  And she relies on what others say to ‘prove’ her points – all the top scientists at all the most reputable institutions – which is a dead give away that she hasn’t gone to any original sources herself and is simply relying on hearsay.  But, hey, she’s a journalist, not a scientist, so she’s got to rely on the scientists to tell her what’s going on, right?  To a point, but she should also check with some other “top scientists” from other “reputable institutions” to perhaps provide counter opinions.

It almost defies belief that people can be so gullible as to put any credence whatsoever in an article such as this one, yet, after dealing with Tim’s blog, it’s apparent that many do.

One journalist who doesn’t, however, is my friend Amy Alkon, better known as The Advice Goddess who writes a syndicated column that I never miss.  In her latest, published in the Orange County Register, she gives advice to a vegan who has come a cropper in a burgeoning email romance with a non-vegetarian.  As you read the request for advice from the vegan, you can see her innate sense of moral authority start to bleed through.  Amy’s advice is priceless. (It was Amy, in fact, who emailed me the link (after some zealot had sent it to her) to the article above that I’ve just spent three pages dissecting.)

While you’re at it, read her advice to the next seeker after the vegan.  My favorite line:

People say the best things in life – love, friendship, moonlight – are free, but so are the worst things: lymphoma, a really big overbite, and road kill.

How true, how true.

The next post is going to be free, and I hope it will fall into the good kind of free category.  We’ll go over a famous paper from the anthropological literature making a virtually watertight case that it was eating meat that made us human.

Felis silvestris lybica Photo by Noorderlicht

When you get right down to it, house cats are pretty useless. If you’re overrun with mice, cats can be a help, but that’s pretty much it.  They are fiercely  independent and, unlike dogs, which have a want-to-please-their-master nature, cats don’t really give a flip.  They don’t fetch, they don’t roll over, they don’t sit up and beg, and, for the most part, they don’t come when called. If you had a kid who acted like a cat, you would probably put him/her up for adoption. So why are they the most popular house pet in the world today?

Scientists using DNA analysis have determined that virtually all house cats alive today are descended from a specific line of wild cats, Felis silvestris lybica, that are indigenous to the Middle East.  Although there are a number of lines of wildcats throughout the world, mitochondrial DNA analysis of all breeds of house cats appears to indicate they all descended from this one branch of the wildcat family.

With the geography and an approximate age of the initial phases of cat domestication established, we could begin to revisit the old question of why cats and humans ever developed a special relationship. Cats in general are unlikely candidates for domestication. The ancestors of most domesticated animals lived in herds or packs with clear dominance hierarchies. (Humans unwittingly took advantage of this structure by supplanting the alpha individual, thus facilitating control of entire cohesive groups.) These herd animals were already accustomed to living cheek by jowl, so provided that food and shelter were plentiful, they adapted easily to confinement.

Cats, in contrast, are solitary hunters that defend their home ranges fiercely from other cats of the same sex (the pride-living lions are the exception to this rule). Moreover, whereas most domesticates feed on widely available plant foods, cats are obligate carnivores, meaning they have a limited ability to digest anything but meat—a far rarer menu item. In fact, they have lost the ability to taste sweet carbohydrates altogether. And as to utility to humans, let us just say cats do not take instruction well. Such attributes suggest that whereas other domesticates were recruited from the wild by humans who bred them for specific tasks, cats most likely chose to live among humans because of opportunities they found for themselves.

Turns out that the answer to the domestication question is that cats were useful to our ancestors for the same reason they are useful to use: their mousing ability.  When humans turned to agriculture and started storing quantities of grain, rodents became a problem because they bred like flies and overran the human food supply.  Cats, which don’t eat grain but do eat rodents, were the solution, so we hired them on despite their quirks.

So are today’s cats truly domesticated? Well, yes—but perhaps only just. Although they satisfy the criterion of tolerating people, most domestic cats are feral and do not rely on people to feed them or to find them mates. And whereas other domesticates, like dogs, look quite distinct from their wild ancestors, the average domestic cat largely retains the wild body plan. It does exhibit a few morphological differences, however—namely, slightly shorter legs, a smaller brain and, as Charles Darwin noted, a longer intestine, which may have been an adaptation to scavenging kitchen scraps.

Unlike dogs, which exhibit a huge range of sizes, shapes and temperaments, house cats are relatively homogeneous, differing mostly in the characteristics of their coats. The reason for the relative lack of variability in cats is simple: humans have long bred dogs to assist with particular tasks, such as hunting or sled pulling, but cats, which lack any inclination for performing most tasks that would be useful to humans, experienced no such selective breeding pressures.

As a little diversion let me demonstrate the difference between art and science.  The article on the domestication of cats took up five pages of text in Scientific American.  J.R.R. Tolkien (yes, he of Lord of the Rings fame) pretty much transmitted the same information in a short poem.  I came across this poem in my youth and was mesmerized by it.  I loved the rhyming pattern and was amazed that so much information could be compressed into what seemed to be just a little piece of doggerel.

Cat

The fat cat on the mat
may seem to dream
of nice mice that suffice
for him, or cream;
but he free, maybe,
walks in thought
unbowed, proud, where loud
roared and fought
his kin, lean and slim,
or deep in den
in the East feasted on beasts
and tender men.
The giant lion with iron
claw in paw,
and huge ruthless tooth
in gory jaw;
the pard dark-starred,
fleet upon feet,
that oft soft from aloft
leaps upon his meat
where woods loom in gloom –
far now they be,
fierce and free,
and tamed is he;
but fat cat on the mat
kept as a pet
he does not forget.

As I said, on the surface it appears to be a little nursery-type of poem, but it’s not really.  The rhyme sequence is astonishingly complex for such a small poem.  The odd lines rhyme at the end while the even lines each have three internal rhymes, and it’s all done in just a few words.  Yet is conveys the essential nature of cats better than the long Scientific American article without seeming to stretch to make any of the rhymes work.

It’s hard to believe that Tolkien wrote such a gem intending to include it in The Lord of the Rings, but decided not to.  It ended up being kind of a throw away.

We, ourselves, like cats, walked “in thought unbowed, proud, where loud roared and fought [our] kin, lean and slim, or deep in den in the East [and] feasted on beasts” in a time long past.  And just like fat cats on mats everywhere, we remember, too, those “fierce and free” primal days, if not in our conscious brains, at least in our DNA.  We are hardwired to gobble meat with “huge ruthless tooth in gory jaw.”  If you don’t believe me, take a look at this YouTube of chimps, our nearest genetic ancestor hunting and eating meat.

Beware.  And I’m not kidding.  This video is not for the squeamish, so be forewarned.

I’m not nearly as clever with verse as J.R.R. Tolkien, so I won’t attempt to capture the feelings this video engenders with poetry.  But it should be obvious from the watching what hunts must have been like in our own past.  I suspect not too different than the one you just saw.  And, friends, that is the primitive circuitry deep inside of us all; we differ from the chimps you saw by a mere 6 percent of genes.  That means that we have 94 percent of our genes in common with them.  Au contraire to what our vegetarian friends would have us believe, we have the GI tracts of carnivores, not herbivores, and we were designed by nature to use every last speck of the nutrients in meat.  We can survive on all-meat diets just fine, whereas we can’t survive on an all-plant diet without supplementation.

We’ve developed our large brains and our social instincts as a consequence of meat eating.  I’m planning a post on this subject in the near future, so you can see how our very humanness arose because we developed a taste for meat.  We are carnivores to our very cores – were we not, we would still be roaming the savannas with brains the size of grapefruits.

We may sleep and dream of larger houses, bigger cars and vacations to exotic locations, but our insides still remember when we were “fleet upon feet” and leapt upon our meat “where woods loom in gloom.”  It was this memory that drove Paleolithic Man, with whom we have 100 percent of genes in common, to hunt to extinction all the large beasts (whose skeletons fill natural history museums everywhere) to extinction from the Bering Strait to Tierra del Fuego in about 1000 years. They didn’t make this effort because they used meat as a condiment.

Whether we like it or not, we are hard wired to our past.

Photo of F.s lybica by Noorderlicht

H/T to Richard Nikoley for alerting me to the YouTube video

When I wrote the Overcoming the Curse of the Mummies chapter in Protein Power, I wrote mainly about the evidence of disease found in the mummies of ancient Egyptians and correlated this disease with their high-carbohydrate diet.  Along with all the material on mummies, which is the part everyone seems to remember, I wrote about a study done in the United States in the 1970s that persuasively demonstrated the superiority of the hunter diet as compared to an agricultural diet, which no one seems to remember.  I came across that study a couple of days ago and decided to present it in a little more detail than I was able to in Protein Power.

The anthropological record of early man clearly shows health took a nosedive when populations made the switch from hunting and gathering to agriculture. It takes a physical anthropologist about two seconds to look at a skeleton unearthed from an archeological site to tell if the owner of that skeleton was a hunter-gatherer or an agriculturist.

Unlike the Egyptian mummy data, there is usually no soft tissue material left when remains of early man are found.  But the skeletal remains of hunter-gatherers show them to be much healthier than agriculturalists.  Hunter-gatherers had better bones, had no signs of iron-deficiency anemia, no signs of infection, few (if any) dental cavities, fewer signs of arthritis and were in general larger and more robust than their agriculture-following contemporaries.  One of the theories as to why postulates that hunter-gatherers lived in smaller, more mobile societies.  Consequently, they weren’t as likely to get communicable diseases and were able to travel to find food, whereas agriculturists were rooted to one spot, lived in larger groups, making the spread of disease more likely, and they were subject to lack of food if a drought or other natural disaster decimated their crops.

The study we’re going to look at today is unusual in several respects.  First, there is a large amount of data, i.e., a lot of skeletons of both groups.  Second, it compares sedentary hunter-gatherers to sedentary agriculturalists.  And it compares peoples who probably had the same genetic heritage to one another.  Finally, it compares hunter-gatherers to agriculturalists living in the same general area.  The only real difference between the two groups of people is the time in which they lived and diet.

The group of agriculturalists lived in an area called Hardin Village, which is a famous archeological site located in Kentucky on the bank of the Ohio River across from the current day city of Portsmouth, Ohio.  These people farmed the area from about 1500 AD to 1675 AD.  There is no indication in the archeological record of any European contact with these Hardin Villagers.

The hunter-gatherers lived in the same general area in an archeological site called Indian Knoll, which is a large midden (an ancient refuse heap) located on the Green River in western Kentucky.  Carbon-14 dating dates the age of habitation of these hunter-gatherers to about 5000 years ago.  Based on the excavation of the deep midden, these people lived at this site for a long period of time, i.e., they stayed in one spot instead of roving as most hunter-gatherers did.

Writes Claire Cassidy, Ph.D., author of the study:

Available fauna and flora, water, and climate were so similar in the two areas that it may be assumed that whatever natural stresses existed at one site were probably existent at the other also, and therefore, in themselves, these should not affect the health and nutrition differently.

Population size and degree of sedentarism affect disease spread.  In the cases of the Hardin Village and Indian Knoll, since both are sedentary or semisedentary, this variable should be negligible in explaining differences in disease experience between the sites.

Archeological-reconstructable variability in material culture is also fairly small (though Indian Knollers used the spear-thrower and spear, while Hardin Villagers had pottery, permanent houses, and the bow and arrow).  Thus, in all probability the most significant difference between these two populations is in subsistence technique, with agriculture at the later site, and hunting-gathering at the earlier.

So, we have two societies who both lived in the same area and didn’t move around much, if at all.  One lived by agriculture and one lived by hunting and gathering.  Genetically they were probably the same, although there is no way to tell for sure.  Both groups had the same climate, weather, water, etc.  Neither group had contact with Europeans, so there is no contamination that way.  The groups are separated by only diet and time.  The hunter-gatherers lived in the area approximately 3500 years before the farmers did and had a substantially different diet.

(When I first went through this paper, I went nuts trying to remember whether the Hardin Villagers were the agriculturalists or whether the Indian Knollers were.  After whipping back to the start of the paper a half dozen times to check and recheck on it, I decided to come up with a mnemonic for it.  I started thinking of the Villagers part of Hardin Village as being farmers.  Village = farm.  Farmers live in villages – at least they do in my mind, so it’s easy for me to remember that the Hardin VILLAGERS are farmers.  Readers of this blog are probably smarter than I am and won’t have to go to such lengths, but if any do, this will help.)

What did these folks eat?

At Hardin Village, primary dependence was on corn, beans, and squash.  Wild plants and animals (especially deer, elk, small mammals, wild turkey, box turtle) provided supplements to a largely agricultural diet.  It is probable that deer was not a quantitatively important food source…  At Hardin Village, remains of deer were sparse.

At Indian Knoll it is clear that very large quantities of river mussels and snails were consumed.  Other meat was provided by deer, small mammals, wild turkey, box turtle and fish; dog was sometimes eaten ceremonially.

There are several other dietary differences.  The Hardin Village diet was high in carbohydrates, while that at Indian Knoll was high in protein.  In terms of quality, [some] believe that primitive agriculturalists got plenty of protein from grain diets, most recent [researchers] emphasize that the proportion of essential amino-acids is the significant factor in determining protein-quality of the diet, rather than simply the number of grams of protein eaten.  It is much more difficult to achieve a good balance of amino-acids on a corn-beans diet than when protein is derived from meat or eggs.  The lack of protein at the Hardin Village signaled by the archaeological data should prepare us for the possibility of finding evidence of protein deficiency in the skeletal material.

The Hardin Village site yielded 296 skeletons and the Indian Knoll site 285.

What did this skeletal data show?  Let’s take a look.

Based on the ages of the people whose skeletons were found (anthropologists can easily tell age from skeletal remains), the life expectancies for people of both sexes and all ages were lower at Hardin Village as compared to Indian Knoll.  And infant mortality was higher at Hardin Village as well.

Iron-deficiency anemia of sufficient duration to cause bone changes was present at Hardin Village but absent at Indian Knoll.  And half the cases of serious iron-deficiency anemia occurred in children at Hardin Village.

Iron-deficiency anemia is a true deficiency disease, often an accompaniment of low-meat diets, long-term infection, or chronic disease.  It is also frequently found in cases of protein-energy malnutrition. The classic sign of iron-deficiency anemia presents as a couple of conditions seen in the skull called porotic hyperostosis and cribra orbitalia.   8.2 percent of the Hardin Villagers had iron-deficiency anemia severe enough to cause one or both of these conditions.  These conditions are extremely painful and those afflicted had to have been miserable, especially the children, most of whom were under five years old.

Porotic hyperostosis

cribra orbitalia

There were signs of malnutrition in both populations, but the signs differed between them.

There are a couple of ways anthropologists look for periods of malnutrition.  One is by examining the tibias (lower leg bones) with X-ray looking for a finding called Harris lines (or growth arrest lines).

Harris lines

All these Harris lines indicate is that an episode of malnutrition occurred during childhood while the bones were developing, causing a period of growth arrest that lasted at least ten days or more.  But since these lines appear after the period of malnutrition, they can’t provide information as to the total duration of the lack of food.  The total number of lines found tells approximately how many episodes of dietary lack occurred that were serious enough to halt bone growth.

To determine the severity of periods of malnutrition, anthropologists look for enamel hypoplasia.  Enamel hypoplasia derives from periods of ill-health or hunger lasting long enough to interrupt the deposition of enamel on the teeth.  These defects, like Harris lines, represent periods of growth arrest in childhood, but unlike Harris lines, enamel hypoplasia quantifies the severity of the period of malnutrition.  The worse the defect, the worse the malnutrition.

Enamel hypoplasia

Enamel hypoplasia

Interestingly, there were more Harris lines found in the specimens from Indian Knoll, but these lines were regularly spaced, “indicating that malnutrition occurred at periodic intervals, perhaps as a “normal part of life.”  There were an equal number of jaws at both sites demonstrating teeth with enamel hypoplasia, “but the frequency of severe episodes of arrest was significantly higher at Hardin Village.”

The most parsimonious interpretation of this information is that mild food shortages occurred at regular intervals at Indian Knoll; perhaps late winter was a time of danger.  [Researchers] using growth arrest lines [Harris lines] and … archaeological data, have similarly concluded that in the hunter-gatherer populations they studied, food shortages occurred regularly, probably on a yearly basis.  At Hardin Village growth arrest was caused by illnesses or crop failure which resulted in long-lasting, but randomly-occurring episodes of growth arrest.

Bones can also exhibit signs of certain types of infection.  Bone infections affected an equal number of people at both sites, but affected significantly more children at Hardin Village than at Indian Knoll.

A specific type of infectious disease showing up in skeletal remains and identified as the syndrome of periosteal inflammation was present at both sites, but was thirteen times more common at Hardin Village.  No one knows for sure what causes this disorder, but it is thought to be caused by a treponematosis, a disease caused by a similar but not identical agent as that that causes yaws, pinta or even syphilis.

The author of this study attributes the greatly increased incidence of this disease in the Hardin Villagers to “lack of resistance in the host because of poor diet and general health.”

Teeth are often a window into the diet of ancient populations.  Based on the wear patterns and number of caries (dental cavities), teeth can provide much information on the quality of the diet.  Teeth ridden with decay are typically associated with poor quality diets, and the unhealthy teeth themselves can be a major factor in the overall poor health of an individual.

Tooth decay was rampant at Hardin Village, but uncommon at Indian Knoll.  Adult males at Hardin Village had an average of 6.74 carious teeth per mouth, while at Indian Knoll the corresponding frequency was 0.73 per mouth.  For women the rates were 8.52 and 0.91 per mouth respectively.  No Indian Knoll children under twelve years of age had caries, whereas some Hardin Village children already had developed caries in milk teeth in their second year of life.  Tooth decay is closely associated with sugar content and consistency of food, occurring with higher frequency in sweet or high carbohydrate diets which are soft and sticky.

Dental caries

Here is the summary of the findings of this analysis of skeletal data as tabulated by the author:

1.    Life expectancies for both sexes at all ages were lower at Hardin Village than at Indian Knoll.
2.    Infant mortality was higher at Hardin Village.
3.    Iron-deficiency anemia of sufficient duration to cause bone changes was absent at Indian Knoll, but present at Hardin Village, where 50 percent of cases occurred in children under age five.
4.    Growth arrest episodes at Indian Knoll were periodic and more often of short duration and were possibly due to food shortage in late winter; those at Hardin Village occurred randomly and were more often of long duration, probably indicative of disease as a causative agent.
5.    More children suffered infections at Hardin Village than at Indian Knoll.
6.    The syndrome of periosteal inflammation was more common at Hardin Village than at Indian Knoll.
7.    Tooth decay was rampant at Hardin Village and led to early abscessing and tooth loss; decay was unusual at Indian Knoll and abscessing occurred later in life because of severe wear to the teeth.  The differences in tooth wear and caries rate are very likely attributable to dietary differences between the two groups.

Her analysis based on this data:

Overall, the agricultural Hardin Villagers were clearly less healthy than the Indian Knollers, who lived by hunting and gathering.

The author raises a couple of interesting questions about the diet of early populations and the drive to eat carbohydrates in place of real food once the taste is acquired.  Before we get to these interesting issues, however, I want to delve into a sad situation that obviously prevailed in the Hardin Villagers and continues to be present in some modern day agriculturalists.

Below is a chart from the paper showing the life expectancies by age of people living in Hardin Village and Indian Knoll.  Look at the enormous increase in mortality in the agricultural Hardin Villagers between the ages of two to four.

Why this rapid increase in mortality in these young children.  The author tells us:

The health and nutrition situation at Hardin Village may profitably be compared with that in modern peasant villages.  In may of these, children are typically fairly healthy until weaned.  At this time they are introduced to a soft diet consisting largely of carbohydrates (in much of Africa and Central America, a pap is made of sugar, water, and maize flour: in Jamaica green bananas replace maize).  In many cases, within a few weeks or months these children develop diarrhea, lose weight, suffer multiple infections, and may eventually develop the form of protein-energy malnutrition called kwashiorkor.   In this disorder caloric intake is usually adequate, but protein and other nutrient intakes are extremely limited; without modern hospital care many victims die.

At Hardin Village the highest rate of death occurs between the second and fourth years of life.  This is typical for a population experiencing weaning problems.  Considering the softness of the adult diet and the high caries rate of both children and adults, it is not unlikely that the children were weaned onto a corn pap of some type.

The high prevalence of childhood infection, severity of growth arrest in the first few years of life, and the existence of iron-deficiency anemia all point to a situation at Hardin Village analogous to those in modern peasant villages.  In other words the evidence supports a hypothesis that malnutrition began with weaning at Hardin Village, sometimes resulted in kwashiorkor, and continued at low level – just enough to reduce the resistance of the population to infectious disease – throughout the life of the individual.

Think about this the next time you hear a pediatrician recommend that babies who are being weaned start out on some sort of Pablum or other processed cereal for infants.  And they virtually all recommend it.  Our grandchildren’s pediatrician recommended it, but MD and I interceded after the first feeding.  From then on they all got pureed turkey, pork, chicken or other meat along with pureed vegetables.  They had no grain.

Dr. Cassidy, the author of this fascinating paper, speculates in the discussion section about why a society would abandon hunting and gathering for agriculture when the diet quality provided by an agricultural subsistence is so inferior.  She writes about the possibility of all the game being decimated by over hunting, and she mentions the possibility of inter tribal warfare reducing the male hunting population to the point that those remaining standing couldn’t provide enough food for all by hunting alone.  Then she gets to the heart of the matter, and asks some questions that are pertinent not just to ancient agricultural societies, but to us today.

Thus population expansion, inefficient hunting techniques, loss of game from the area by migration and overkill, and warfare, all may have contributed to force the Hardin Villagers to become more and more dependent on a small number of high-carbohydrate agricultural foods of limited quality, and this may have been so even were they aware of an increase in physical ill-health in the group.

Finally, we must also wonder if people didn’t ultimately begin to prefer corn and beans to meats?  There is some evidence that carbohydrates can become so palatable to humans that they eat them in preference to other foods; such a situation may have further limited the appeal of hunting.

If this is the case, the Hardin Villagers are not the only society in history who have chosen carbohydrates in preference to other foods.  And they certainly aren’t the only ones to prefer corn and beans to meats.  I would venture that most people today prefer carbs to meat, a notion that is confirmed in the nutritional data.  Carbs play a far larger role in the American diet than do meats of all kinds.  And if many so-called nutritional experts had their way, we would all eat even more.

The next time you may be tempted by the siren song of the high-carb pushers, remember what happened to the Hardin Villagers and do the Nancy Reagan: Just say no.

*Cassidy CM. Nutrition and health in agriculturalists and hunter-gatherers: a case study of two prehistoric populations. in Nutritional Anthropology. Eds Jerome NW et al. 1980 Redgrave Publishing Company, Pleasantville, NY pg 117-145

Dr. George Bray's model of obesity

In July 2008 I posted on Dr. George Bray’s critique of Gary Taubes’ book Good Calories, Bad Calories that appeared in Obesity Reviews.  Included in my post was a copy of Gary’s response.  Now Dr. Bray is back with a rebuttal to Gary’s response to his (Bray’s) original critique.  In conversation, Gary told me he has elected to drop the issue because the discussion is going nowhere.  Gary makes substantive points; Bray obfuscates the issues and will continue to do so.  I, however, am not going to drop the case.  Maybe I’ll have the last word here.

I want to go over Dr. Bray’s response to Gary’s letter in some detail because it is emblematic of all that is wrong with obesity research today and clearly demonstrates why we will never get anywhere until the people of Bray’s generation fade away. I don’t know that I’ve ever seen so many instances of one writer missing the point as often as Dr. Bray does in this short reply.  The entirety of his response is an example of either shoddy thinking or intellectual dishonesty.  Or maybe both. It brings to mind Mary McCarthy’s famous quote about Lillian Hellman: “Every word she writes is a lie, including ‘and’ and ‘the’.

(You can read Dr. Bray’s original critique of Good Calories, Bad Calories along with Gary’s response in my July 2008 post.  The full-text of Dr. Bray’s letter of reply we’ll be discussing in today’s post can be found here.  You should pull it down in pdf and print it so you can follow along.)

Right off the bat, in the very first line, Bray leads off with his first porkie.

In his nearly 5000-word response to my book review, Mr. Taubes has raised a number of issues.

Gary’s response was slightly under 2000 words.  You might think this just simply a typo, and normally I would too, but the entire piece is filled with so many inaccuracies seemingly designed to denigrate Gary’s response that I don’t think so.  Why even put the number of words?  Why not simply say: In his response to my book review…?  By quantifying the number of words the way he does, Bray casts a pejorative shadow on Gary’s response from the get go.

If you read Gary’s letter, you will see that he methodically refutes Dr. Bray’s criticisms of GCBC and identifies those issues in which he feels Bray misses the point.  In his response, Bray says Gary’s critique of his (Bray’s) review of GCBC

opened the door for [him] to contrast [Taubes’] hypothesis for obesity with [his own].

It’s a kind of disingenuous way for Bray to get his own hypothesis of obesity into play in what amounts to a review of Gary’s book, but let’s take a look at what he has to say.  First, he completely simplifies and basically mischaracterizes Gary’s hypothesis of obesity.  Here is Gary’s hypothesis of obesity and his proposed treatment as interpreted by Dr. Bray:

As you can see, it appears pretty simplistic, which, I’m sure, was the intent.  Not shown are all the feedback loops and intricacies Gary has described at length in GCBC .

In referring to this diagram, Dr. Bray admits that it is based on “two sentences from the letter,” which doesn’t seem like a lot out of a 5,000-word letter (or even the 2,000-word letter that it was).  Then he goes on to use three sentences to establish the basis for the diagram.  (See what Mary McCarthy meant about even ‘and’ and ‘the’?)

After giving short shrift to Gary’s hypothesis of obesity, Dr. Bray then goes on to lay out in great detail his own theory of obesity as represented by the Rube Goldbergesque diagram at the top of this post.  Bray’s entire hypothesis, for which he recruits leptin, insulin, the brain, glucocorticoids, and God knows what else to help make his point, is based on a faulty premise.  But it’s a faulty premise he has accepted uncritically.

His hypothetical model of obesity, he authoritatively states

starts with the First Law of Thermodynamics, which states that the change of energy in a closed system is the difference between the heat added to the system and the work done by the system.

Dr. Bray then restates this hypothesis (and the First Law) in the form of this equation:

Δ E = Heat (q) – Work (w)

Readers of this blog know this as the energy balance equation, which looks like this in its more familiar form:

Δ Weight (the Δ means change) = Energy in (food) – Energy out (exercise plus metabolism)

The fatal flaw in Dr. Bray’s hypothesis (which is a flaw we’ve discussed often in these pages) is that he doesn’t understand that the components on the right side of the equal sign are not independent variables.  They are dependent variables.  If one eats less, the rate of metabolism falls to compensate.  If one exercises more, the appetite increases, and one eats more to compensate.

Were these components truly independent variables, life would be easier (but we may not have survived).  According to Dr. Bray, Anthony Colpo, and countless others, however, these components are independent variables.  Eat less, say they, and you’ll lose weight.  Which is true, to a point.  But once the energy-out component of the equation kicks in, weight loss stalls, even if you are eating less, a fact everyone who has ever dieted knows.  Exercise more, they pontificate, and you’ll lose weight.  Which, again, works (maybe) in the very short term.  But once appetite kicks in, you unconsciously eat enough more to compensate for your increase in exercise, as anyone knows who has tried to lose weight by walking or other exercise alone without consciously restraining eating.

Now don’t get me wrong, it is possible to lose weight by decreasing food intake and increasing exercise.  It worked well in the concentration camps in WWII and in Ancel Keys’ starvation studies in the 1940s.  But in those cases, people were under lock and key.  It doesn’t work for the long term for the majority of people unless they are coerced.

This fairly obvious observation that the energy in/energy out components are not independent variables seems to elude most (if not all) obesity researchers, including George Bray.  These people persist on basing the foundation of any obesity treatment on the admonition to eat less and exercise more, which is a total folly.  Yet Bray and his ilk continue to clothe this folly in the garments of academic respectability and work to pass it off as the latest fashion in scientific thinking.

Dr. Bray believes that the reason so many people are fat is twofold. First, he thinks  humans have a ‘hedonic’ drive that inexorably pushes them to increase their food intake.  And, second, he reckons that this ‘hedonic’ drive also overrides the “appropriate negative feedback signals to stop eating.”  What stimulates this ‘hedonic’ drive?  According to Dr. Bray

It is caused by the pleasurable effects of high-fat, high-sugar foods.

Well, at least he’s half right on that one.  No one binges on pure fat.  It’s impossible because of feedback inhibition to eat a lot of pure fat at a sitting.  Try sometime to sit down and eat some butter all by itself.  See how much you can choke down.  I can guarantee you it won’t be much.  Then add a little sugar to the mix and see what happens.  Suddenly the butter is converted to frosting, and you can put away a lot of it.  What’s the difference?  It’s the sugar.  Sugar – and carbohydrates in general – override the stop-eating center in the brain.  That’s why all binge eaters binge on a combination of fat and carbohydrate.  That’s also why you can go out to dinner, eat ‘til your stuffed, not be able to eat another bite of any kind of meat or other real food, yet perk up when the dessert tray comes around.  As the old saying goes: there’s always room for dessert.  Why? Because your brain knows the stop-eating center will be overridden by the sugar and carb in the dessert.

Dr. Bray would have been more accurate had he said that the stimulus for the ‘hedonic’ drive is carbohydrate.

But he doesn’t.  He is trapped in the fat-is-bad paradigm.

In experimental animals, highly palatable food or a high-fat diet is one of the easiest ways to disturb this homeostatic system [as defined by Dr. Bray], and this may apply to human beings as well.

Dr. Bray seems to believe that we live in a toxic world in food terms.  We are unable to help ourselves, and are therefore destined to be fat because of our ‘hedonic’ drive.  We are helpless.  There is no cure save eating less and exercising more, which even he more or less admits doesn’t work despite his entire model being based on the idea.  As I have discussed in another post, Dr. Bray is a major proponent of drug therapy to treat obesity.

In a way, I agree with him about the idea that we live in a toxic world, one with all kinds of the wrong kinds of food available to tempt us 24/7.  Problem is that Bray and his ilk are a major part of the reason we live in such a world.  But that’s a topic I’ll leave for a future post.

Dr. Bray makes a bizarre case for why he thinks the majority of dietary studies show better results in those subjects following low-carb diets than in those consuming low-fat regimens.  I’m going to use his own words, so you won’t think I’m making this up.

the principal studies that directly support this model [Taubes’ theory on low-carb dieting] included the word ‘Atkins’ in their clinical trial. When similar low-carbohydrate diets were tested without using this ‘name’, the low-carbohydrate diets had no more effect than those to which they were compared.

There you have it.  All you have to do to make a diet work is include the name ‘Atkins’ in the title.  I wish MD and I had known that when we wrote Protein Power.

What is truly ironic about this nonsense is that in this very same issue of Obesity Reviews containing Bray’s rebuttal is a long review article titled Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities.  This article takes an in depth look at studies comparing low-carb diets to low-fat diets.  Here is the conclusion as written in the abstract:

There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year.

Dr. Bray lists five other issues about Gary’s letter to which he wishes to respond, but before he gets to the list, he makes one last flippant point.

I thus conclude that if any diet ‘cured’ obesity as their proponents often claim, there would be no obesity and thus no need for the next diet. Yet the past 150 years, since the publication of Banting’s first popular diet, have seen a continuing stream of new diet books.

The reason, of course, is that we dieting fish all swim in waters that have been polluted by Bray and his brethren, more about which in a later post.

Now to the list.

1.    Near the end of the letter, Mr Taubes suggests that my review of his book may be a ‘conflict of interest’. He says ‘I [Bray] may be defending what my scientific research has led me to believe’. If this is a conflict of interest, then all scientists have a conflict of interest.

This first short point of only three sentences tells you everything you need to know about Dr. Bray’s scientific credibility.  I have no problem with the first sentence.  The second sentence is purportedly a quote from Gary Taubes letter.  It isn’t.  It is a paraphrase…sort of, but put in quotation marks.  This is a real no no.  It was done so for a particularly egregious reason, which was for a set up for Bray’s final sentence.  But that sentence even further diminishes his credibility.  Scientists are supposed to constantly challenge their own hypotheses, not accept them as fact simply because they’ve spent their careers enraptured with them.   All true scientists don’t have this conflict of interest.

2.    The first paragraph of his letter dealt with lipoproteins that I said he had not covered. The issue was not the lipoproteins but their receptors, from which we have learned so much in the past 30 years.

This one is a real copout.  In Bray’s original critique he wrote:

As I read through Good Calories, Bad Calories, I found a number of errors of omission or commission that are important when relating diet to heart disease.  There is no mention in the Diet-Heart section of low-density lipoprotein-cholesterol (‘bad cholesterol’) or of high-density lipoprotein-cholesterol (‘good cholesterol’).

The issue may have been the receptors and not the lipoproteins, but as you can see from his direct quote above, that’s not how Bray characterized it.  Gary set him straight with a list of about two dozen pages and groups of pages where LDL and HDL were mentioned, yet Bray weasels instead of admitting his mistake.  When I read his first letter, it made me wonder if he had even read the book.

3.    In his letter he mentions doubly labelled water only to conclude that we knew this already from the 19th and early 20th century and he did not need to discuss it in his book. I would submit that we did not know that people under-report their intake by as much as they do and that overweight people under-report more than normal-weight people do.

Okay.  There’s a total non sequitur.  What does the second sentence have to do with the first?  Weird.  Was Bray on dope when he wrote this?

4.    Mr. Taubes say ‘the goal of science is to determine causality…’

(What Gary actually wrote was ‘The goal of science is to correctly determine causality,’ but who’s counting?)

Then Bray wades into this strange discourse about the theories of Karl Popper, whom he misnames as Hans Popper.  (Does this guy ever bother to look anything up?)

This is significantly different from the views of Hans Popper, the philosopher of science, whose search is for ‘reality’ rather than ‘causality’. Popper says ‘there is a reality behind the world as it appears to us, possibly a many-layered reality, of which the appearances are the outermost layers. What the great scientist does is boldly to guess, daringly to conjecture, what these inner realities are like. Popper also espouses the concept of ‘falsification’, which is at the heart of rationalist thought. To quote him again –’a false theory may be as great an achievement as a true one. And many false theories have been more helpful in our search for truth than some less interesting theories which are still accepted’.

If you can make sense of this gibberish, you’re a better man than I am.  All I know is that Bray misses Popper’s point about falsification in a major way.  (We discussed Popper and his theory of falsification in an earlier post.  And it ain’t anything like Bray makes it out to be. I seriously doubt he has even read Popper’s work.)

The last sentence of the above paragraph I find particularly interesting.  Writes Bray, apropos of nothing really:

And many theories have been more helpful in our search for truth than some less interesting theories which are still accepted.

I don’t know about the search for truth, but I can tell you that the inability of Bray and the rest of the academic obesity ‘experts’ to shake loose from their own ‘less interesting theories’ have led us into the obesity epidemic we’re in the throes of now.

Dr. Bray’s fifth comment, which I’m not going to reproduce in full, is a world-class case of totally missing the point.  After commending Gary for proposing an experiment to validate his hypothesis, he goes on to quote Gary’s rebuttal letter:

He says ‘the positive energy balance hypothesis of obesity asserts that the only way to lose excess fat is to eat less and/or exercise more – that without consciously inducing a negative energy balance we will not lose weight’. His hypothesis is ‘the carbohydrate/insulin hypothesis asserts that if we restrict carbohydrates in the diet/and or improve the quality of the carbohydrates consumed then insulin levels will be lowered, reducing the accumulation of fat in the fat tissue independent of the nutrition state of the subject’. I would take exception to his use of the word ‘consciously’ in his statement of the energy balance hypothesis. For example, the current level of oil prices may increase human energy expenditure through more walking as it decreases automobile use. This is not a ‘conscious’ choice in the sense used above but would have the same effect.

Say what?!?!?!

Let me get this straight.  Dr. Bray thinks if we walk more because we decrease automobile use as a consequence of the high price of gasoline that we’ll lose weight because we are unconsciously exercising instead of volitionally exercising?  As I say, he misses the point, which is that the two components on the right side of the energy balance equation are not independent variables, but are dependent variables.  It doesn’t matter if one walks as a part of exercise or because one can’t afford the gas, the body compensates by increasing food intake.

Dr. Bray ends his response by resorting to the old conservation of energy principle, which all the eat-less, exercise-more folks hew to.  They seem to believe that no one who advocates low-carb diets can understand the laws of thermodynamics when it is they themselves who don’t understand them as applied to diet.  There is nothing inconsistent with Gary’s theories of the cause and treatment of fat accumulation and the laws of thermodynamics.  It’s Bray and friends’ lack of understanding of these laws and/or their refusal to accept the dependent nature of the energy in/energy out components of the energy balance equation that are the heart of the problem.

This entire rebuttal of Dr. Bray’s reminds me of my own favorite lines from Good Calories, Bad Calories.  They are my favorite because I’ve seen first hand what they describe.

The institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades.  For this reason, it is difficult to use the term “scientist” to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book.  It’s simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created, as a result, can reasonably be described as science, as most working scientist or philosophers of science would typically characterize it.  Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but “the results of their enterprise,” as Thomas Kuhn, author of The Structure of Scientific Revolutions, might have put it, “do not add up to science as we know it.”

The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of all, that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.

Is it any wonder that Dr. Bray didn’t enjoy the book?

Skulls in our library. See bottom of post for description.

In 1981 MD and I read a book that changed our lives.  I don’t know why because I didn’t have a particular interest in paleontology or anthropology at the time, but I picked up a copy of Lucy: the Beginnings of Humankind by Donald Johanson.  The book sat around the house for awhile before I found the time to read it, but when I started reading, I couldn’t quit.  It was an absolutely riveting read.

I carried the book with me and read it everywhere.  At the time, I was doing a lot of emergency room medicine, so I took the book along on one of my 24 hour shifts.  As luck would have it, I had a slow night, so instead of sacking out as I would have usually done, making sure I got some shut eye before the inevitable car wreck or gunshot wound showed up to shatter my peace, I read Lucy.  I finished it sometime during the middle of the night and the couldn’t get back to sleep for thinking about it.  I couldn’t wait to get home to MD and tell her about it and force her – at gunpoint, if necessary – to read it.  I couldn’t live with myself if I were this enthusiastic about something and had no one to discuss it with.

She started reading it, and before I knew it, she was as fired up about it as I was.  She read a lot of it in bed before we went to sleep, and our conversations went much like this:

Me: What part are you reading?

MD: I’m at the part about the ‘R’ and ‘K’ factors.

Me: Isn’t that cool.  Then on to a general conversation between us about R and K.

MD: (Exasperated) Let me get back to the book.

Ten minutes later.

Me: What part are you reading now?

When she finally finished, it seemed that Lucy was all we could talk about for about a month.  Just around the time we finished the book, the Little Rock public library had its big, once-a-year, friends of the library sale.  People donate old books, new books, magazines, and any and all kinds of reading matter to this fundraising event.  I knew that there were usually a lot of old medical and scientific journals there, so MD and I headed on down.  When we got there, we hit pay dirt.  We found EVERY one of the original journals that contained all the papers written on the discovery of Lucy and the anthropological and paleontological work to figure out what she actually was.

It has just occurred to me in my stream of consciousness writing, driven by my excitement from just thinking about those days, that, for those who don’t know, I haven’t explained who Lucy is.  Lucy was a little upright walking creature who lived about 3.2 million years ago in what is now

Ethiopia.  Anthropologist Donald Johanson and is team found her almost complete fossilized skeleton while on a dig there about 30 years ago.  Although her skeleton (seen at right) might not look like it’s almost complete, it represents a huge find paleontologically.  When you consider that many paleontologists go their whole careers and find only a small bone or two.  Over a career.  Lucy has most of her parts.  And those she doesn’t have on one side, she has on the other, so it’s relatively easy to reconstruct her entire skeleton.

The book Lucy details not only Lucy’s discovery, but the history of paleontology until that point (that part probably sounds dreadful, but it’s truly a wonderful read), and all the work to figure out what Lucy really was and where she fit into the hominid spectrum.  At the time she didn’t fit into any of the categories of hominids that were known, so Johanson and team ended up calling her Australopithicus afarenses, the forerunner to Australopithicus africanus.  The descriptions of how tooth and jaw structure were used to place her where she belongs sound like boring reading, but they aren’t at all.  That part of the book was where I got my first notions of the idea that there might be a diet we had evolved to eat.

MD and I swore to one another that somehow, someway we were going to by God see Lucy’s actual skeleton (it wasn’t really her actual skeleton, it was a fossil of her skeleton), even if we had to go to Ethiopia to do it.  Not long after we made this vow, we learned that an entire Lucy exhibit was going to be presented at the Museum of Natural History in New York.  Neither of us had ever been to New York at that time, but we made plans to go.  When the exhibit opened, we were there.  And a fabulous exhibit it was.  It had the Taung child skull, which figures prominently in the history of man, and many of the other famous fossils we had read about.  When we finally got to Lucy and read the little plate on the display case with her skeleton, we were devastated to learn that it wasn’t really Lucy’s skeleton we were seeing, but a reproduction of Lucy’s skeleton.  The real Lucy’s skeleton was still in Ethiopia where it had been repatriated.  And the Ethiopian authorities weren’t about to let her go on tour.

We were mightily disappointed and figured we would probably have to go to Ethiopia to see Lucy if we were ever going to see her in the flesh, so to speak.

But a couple of days ago we were driving along in Seattle and I noticed a sign advertising a Lucy exhibit at the Pacific Science Center.  I found out that the exhibit was called Lucy’s Legacy: The Hidden Treasures of Ethiopia.  The brochure promised that the exhibit

provides visitors with an extraordinary opportunity to come face to face with Lucy, the oldest, most complete, and best preserved adult fossil of any erect-walking human ancestor.

Hmmm, thinks I.  Could it really be?  I worried about the styling of the exhibit.  Lucy’s Legacy?  What does that really mean.  Hidded treasures of Ethiopia?  What hidden treasures?  We were in the midst of an extremely busy few days, but we didn’t want to miss out if this truly was an opportunity to see the real Lucy.  We got tickets and showed up at the appointed time (they were letting people in in 15-minute increments).

When we got in, we walked through exhibit after exhibit of Ethiopian history, Ethiopian languages, Ethiopian religion, Ethiopian writing, Ethiopian art, Ethiopian everything, but no sign of Lucy.  As I was beginning to despair, we finally rounded a corner and there was at least an exhibit on hominid fossils.  We went through that part of it and finally came to the same reproduction of Lucy (or at least one that looked the same) as we had seen in New York.  Then we found, in a case in a darkened room, the actual, real, honest-to-God fossil of Lucy.  It was the same size and shape as the model we had seen, but was a different color.  Whereas the model looked kind of yellowish, the way old bones look, Lucy’s fossil was a greyish white.  It looked like, well, rock.  Which it is.

At any rate, now we don’t have to go to Ethiopia because the Ethiopian authorities made Lucy available to us.  Despite the fact that these authorities used Lucy to pimp for Ethiopia, we were damned glad to see her.

I can’t recommend the book Lucy enough.  It should be a part of every low-carbers library.  Once you read it, you will know what it means when you read that Australopithicus africanus had elevated levels of Carbon-13.  You will realize how far back in our lineage we were meat eaters.  And you will find out what happened to the branch of pre-humans who evolved down the plant-eating road.

The photo at the top of this post are of skulls and skull models in my library.  The one on the left is Australopithicus robustus, a branch that came to a bad end.  The skull next to that one is a mountain lion, the next is Homo habilis (a descandant of Lucy’s), and the one on the far right is a black bear.  Looming behind them all is the cave bear skull we wrote about in the Protein Power LifePlan.

Paleolithic paintings from Lascaux cave in southern France

I imagine most readers of this blog would expect a group of subjects to do better on a Paleolithic diet as compared to a standard American diet, but there are few studies actually making the comparison. One was posted yesterday in the Advance-0nline-Publication section of the European Journal of Clinical Nutrition that shows subjects following a Paleolithic diet made major metabolic changes, and made them rapidly.

Before we get into the study, let’s make sure we’re all on the same page when we discuss the Paleolithic diet. We we say Paleolithic diet, what are we really talking about?

The Paleolithic era refers to that period of history of the genus Homo, which began more than 2 million years ago and ran until the Neolithic period started circa 10,000 years ago. The Neolithic era dates to the time when early man set down roots both literally and figuratively when he started to cultivate plants for food and domesticate animals. The Paleolithic era ends and the Neolithic era begins with the advent of agriculture.

So what did Paleolithic man eat? We don’t know precisely because Paleolithic man didn’t leave any written records, menus, cookbooks, etc. The only records Paleolithic man left are the cave paintings, of which Lascaux in France is the most famous. Virtually all of these paintings feature animals prominently, which would lead one to believe that animals figured greatly in the lives of Paleolithic people. Since they didn’t domesticate these animals, and since it seems unlikely that they kept zoos, the most obvious reason these early people focused so much artistic effort on these animals is that they ate them. Carbon-13 isotope studies bear out that idea as the same carbon isotopes found in grass are also found heavily concentrated in the bones of Paleolithic man and other known carnivores, which leads to one of two conclusions: either Paleolithic man spent his days grazing or he ate animals that grazed. I would opt for the latter interpretation.

Keep this idea of Paleolithic man as a meat eater along with the idea of the cave pictures in your mind. We’ll return to them later, but first, let’s look at this study.

Nine healthy, sedentary, non-obese subjects (6 men; 3 women) over the age of 18 recruited from the San Francisco Bay area completed the study. These subjects had their starting diets analyzed – all were on their own version of the standard American diet – and a battery of tests done on them to evaluate multiple metabolic parameters.

Once the beginning data was in hand, the researchers started the subjects on a ramp up to the full Paleolithic diet by giving them daily increases of fiber and potassium.

For the intervention phase, beginning day 1, for adaptation purposes, a series of 1-day cycle diets with gradually increasing levels of potassium and fiber were developed by the research dietitians. This was to allow the subjects’ intestinal tract and potassium handling systems to adjust to the markedly higher dietary content of fiber and potassium. ‘Ramp 1′ diet was given for 1 day, ‘Ramp 2′ diet for 3 days, ‘Ramp 3′ diet for 3 days and finally the ‘Paleo diet’ for the remainder of the study.

Once ramped up, the subjects went on the full Paleo diet for 10 days.  An interesting twist to this study was that the subjects were monitored carefully for any signs of weight loss over the course of the study, and any subjects losing even small amounts of weight were encouraged to eat more of the Paleo foods in an effort to maintain their starting weights.  Since weight loss itself can bring about metabolic changes, the researchers wanted to make sure that any changes came about as a result of the diet composition and not as a side effect of weight loss.

What did they eat?

Meat, fish, poultry, eggs, fruits, vegetables, tree nuts, canola oil, mayonnaise and honey were included in the Ramp and Paleo phases of the diet. We excluded dairy products, legumes, cereals, grains, potatoes and products containing potassium chloride (some foods, such as mayonnaise, carrot juice and domestic meat were not consumed by hunter-gatherers, but contain the general nutritional characteristics of preagricultural foods).

Hmmm. More about which later. For now, here is a layout of the specific foods the subjects ate during the ramp and the full Paleo diet.

Table 2

The macronutrient composition of the regular diets of these subjects was 18% protein, 44 % carbohydrate and 38% fat.  The Paleo diet was 30% protein, 38% carbohydrate and 32% fat, mostly unsaturated, as the authors were quick to point out.
After the 7 day ramp period and the 10 days of Paleo dieting, subjects experienced large changes in most parameters measured.  Lipid changes are shown in the table below.

Derived from Table 3

As you can see, there were significant decreases in triglycerides, total and LDL-cholesterol with no change in HDL-cholesterol.

The body of the paper reports an insignificant decrease in blood sugar after the Paleo diet, but the units listed in the paper are incorrect, which is one of the hazards of dealing with a pre-publication paper.  All the kinks haven’t been worked out.

Fasting insulin levels plummeted by more than two thirds in (11.5 to 3.6 µU/ml) and the total area under the insulin curve was lowered by almost half.  What these figures tell us is that the diet made these subjects much, much more sensitive to their own insulin.  In other words, they required substantially less insulin to keep their blood sugars in the normal range.  Since they were producing less insulin, they had less circulating insulin, which meant less fat storage, less arterial stiffening and less of all the things that too much insulin causes.

Along with the improvements in lipids and insulin sensitivity, the subjects experienced a significant drop in diastolic blood pressure and a decrease in mean arterial pressure.  These improvements likely occurred in part because these subjects had substantially increased brachial artery diameter, a measure of arterial distensibility.  There arteries had become less stiff and more pliable over a mere 17 days of dietary change.

Urinary potassium loss increased, indicating an increased potassium intake by the subjects.  And urinary calcium excretion decreased.

Another interesting aspect of this study is that these findings were pretty much across the board.  Instead of a couple of hyper responders raising the average, either all nine or in a couple of cases, eight of the nine subjects demonstrated pretty much the same changes, indicating

consistently improved metabolic and physiological status with respect to circulatory, carbohydrate and lipid metabolism/physiology.

The authors of this paper found

in a small group of sedentary, slightly overweight, but not obese adult humans, that switching from their usual diet to a paleolithic-type diet, which contained no cereal grains, dairy [or] legumes, resulted, after only a short period of time [17 days] and without weight loss or increase in activity levels

significant positive changes in all the parameters discussed above.

I was fascinated by this study because the changes were so rapid, but I was a little put off because it could have been so much better.  I mean why didn’t they test a real Paleolithic diet?  Probably because of nutritional correctness, i.e., fear of saturated fat.

During Paleolithic times, man primarily subsisted by hunting.  The preferred food was large game animals, and Paleolithic man, a skilled hunter, wiped most of them out.   And not just the large grazing animals.  Paleolithic man completely decimated the Cave bear.  As you can see from the photo of my Cave bear skull below (from a slide I use in presentations), these were enormous animals that didn’t go down easily.  Cave bear, like all bears, had high levels of body fat, which must have been highly desired because these ferocious animals were hunted to extinction about 15,000 years ago by people wielding little more than pointed sticks.  I would have to value fat a whole lot more than I do to tackle one of these guys.  The largest bears that I could find the fatty acid composition for were polar bears, which should be appropriate since cave bear lived in northern latitudes.  Polar bears have on average 30 percent saturated fat, 50 percent monounsaturated fat and 15 percent polyunsaturated fat.  (I know these figures don’t add up to 100 percent, but they are the figures as presented in the article.)

The majority of the large animals that roamed the world are gone thanks to the depredations of Paleolithic man.  If you ever get the chance to go to the American Museum of Natural History in New York, take a stroll through the many large halls filled with the enormous skeletons of these animals that used to roam what is now the United States.  Experts estimate that it took Paleolithic man only about a thousand years to range from northern North America were he crossed the Bering strait to the southern tip of South America wiping out all the large game that existed at the time.

These large mammals that Paleolithic man decimated are now only present in skeletal form so we don’t know for sure what their fatty acid composition was.  But we do know that of those left, the larger the animals, the larger the percent body fat.  And the larger the percent body fat, the greater the percentage of saturated fat.  Given those two facts, one has to conclude that Paleolithic man consumed a large percentage of his energy as saturated fat.  We can’t look at the fat content of deer, for example, and use that to estimate the saturated-fat content of the Paleolithic diet.  Deer, as we know them today, were tiny animals as compared to those Paleo man typically dined on.

If you look at the fatty acid breakdown of the horse, a large animal (not grain fed) that we are all familiar with that is comparable in size to many of the animals Paleolithic man hunted to extinction, you find a large proportion of saturated fats.  Horse fat is about 36 percent saturated fat, 34 percent monounsaturated fat, and the rest polyunsaturated fat.  Even rabbits carry over 40 percent of their fat as saturated fat, but rabbits have much less fat per weight than the larger animals.

It seems pretty obvious that Paleolithic man would have eaten considerable saturated fat.  Which begs the question: Why always cut the saturated fat in experimental diets testing the hypothesis that the Paleolithic diet is more healthful?

I don’t know the answer for sure, but I expect that it’s due to the nutritional equivalent of political correctness, which I call nutritional correctness.

Researchers are simply afraid to imply that saturated fats might actually be harmless, so they go through all kinds of contortions to present their data in such a way that it couldn’t possibly present saturated fats in a positive light.  And much good research and reporting has suffered as a consequence.

A case in point is a otherwise wonderful book published 20+ years ago titled The Paleolithic Prescription.  This fascinating book goes into great detail describing the physical exploits of our ancient ancestors based in large part of reports by European explorers encountering ‘primitive’ peoples untouched by the forces of ‘civilization.’  The authors, based on the anthropological literature, describe the size of our Paleolithic forebears as being similar to our own, but their strength was significantly greater:

These people were strong – stronger by all estimates than most agricultural and industrial people (including ourselves) who lived after them.  Skeletal remains reflect strength and muscularity: the size of joints and the sites where muscles are inserted into bones indicate both the mass of the muscles and the magnitude of the force they were able to exert.  Average Cro-Magnons, for example, were apparently as strong as today’s superior male and female athletes.  Strange as it may seem, Cro-Magnons and other hunters and gatherers may have worked fewer hours per week than did the agriculturalists who followed, yet they were significantly more robust.

Think about this last sentence for a minute.  Strong, robust Cro-Magnons who settled into a life of agriculture circa 10,000 years ago, and who worked harder than their pastoral predecessors, showed a decline in strength and muscle mass.  Why?  What The Paleolithic Prescription says about energy expended is true.  The skeletal remains of agriculturalists show much more arthritic changes and incidence of joint wear implying much more regular physical activity than hunters.  So why did agriculturalists develop less muscle mass and strength?  Could it be because of a switch from diets high in fat and protein to diets low in fat and protein and high in carbohydrates?  Makes sense to me.  Same genetic material, greater exercise, different diet, yet weaker and less robust.

Getting back to my original point about this book, the authors presented a mass of data showing our Paleolithic ancestors to be more robust, healthier and able to routinely perform feats of strength that are almost unbelievable to us today.  And they dwelt on the massive amount of hunting that sustained these ancient peoples.  Then, when it came time to apply these dietary lessons to people of today, the authors tried to shoehorn their findings in a nutritionally correct regimen that followed the low-fat diet precepts that academicians are so attached to.  It’s really a shame because this could have been a wonderful book.  It’s still well worth reading, but simply ignore the dietary advice.

It would have been great had the authors of the paper above used a real Paleolithic diet for their study instead of an imaginary Paleolithic diet that conformed to the tenets of nutritional correctness.

Based on my own experience with thousands of patients, I can predict what the findings would have been.  Lipid parameters would have been improved, but with LDL staying about the same or maybe going up a little.  HDL would have gone up significantly.  Triglycerides would have fallen maybe more.  The all-important triglyceride/HDL ratio would have plummeted much more than with the faux Paleo diet.  Fasting insulin would have dropped like a rock and the area under the insulin curve would have fallen at least as much, if not further.  Blood pressure would have decreased and all the measures of vascular pliability would have improved.  All in all, my prediction is that the outcome of the study would have been better than the outcome of the study as it currently exists.

The Paleolithic diet data indicates that early man ate more saturated fat than he did carbohydrates.  And he was molded by the processes of natural selection to thrive on such a diet.  When he bolted from that meat-based diet, as he did when he settled in to life as an agriculturalist, he paid dearly for it with a devolution in health.  Since the evidence is so obvious that a diet higher in saturated fat worked wonders for Paleolithic man, it seems like some academicians somewhere would ranger up and test such a diet.  But it appears that the pox on saturated fat is so virulent that no one wants to risk it.

If such a study were done and the results tally with what I’m positive the results would be, the authors would find themselves in the untenable position of having to at least tacitly imply that saturated fats aren’t harmful.  And that could ruin an academic career.  No more invitations to present at meetings. Expulsion from the club.  People tsk tsking behind their hands.  It just couldn’t be done.