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How Evolutionary Is The New Evolution Diet?

A Review of The New Evolution Diet: What Our Paleolithic Ancestors Can Teach Us About Weight Loss, Fitness, and Aging

February 2, 2011
Reviewed by Chris Masterjohn

"Fat is poison" — Art De Vany.

Arthur De Vany's new book, The New Evolution Diet: What Our Paleolithic Ancestors Can Teach Us About Weight Loss, Fitness, and Aging is an interesting mix. It's full of excellent nutritional and fitness advice, but introduces a strange mix of carbophobia and lipophobia and quite a number of bizarre theories with lots of "just so stories" presented as fact when they are little more than speculation.

While most of the ideas presented in the book will not be new to those who have been well-steeped in the evolutionary, paleo, ancestral, and traditional foods movements, the book would make an imperfect yet useful introduction to these ideas for those new to them. Nevertheless, I would hesitate to give this book to a beginner, for reasons outlined in the conclusion.

Dr. De Vany is an economics professor by trade, but began his journey towards better health and fitness when his son, and then wife, developed type 1 diabetes. Banning carbohydrate-dense foods from their menus was so effective that one doctor refused to believe his wife was diabetic because she was injecting so little insulin. After speaking with an anthropology graduate student about the diet of a tribe she was studying, De Vany realized that in placing his family on a diet of fresh vegetables, fruits, nuts, seafood, and meat he had reinvented the typical hunter-gatherer diet.

In the early 1990s, De Vany put everything he'd learned about health into an essay entitled "Evolutionary Fitness," and when he retired in 2003 he started a blog with the same theme. Many people owe their initial journey into the world of real food to De Vany, and he is known by many as the "grandfather" of the Paleo movement. De Vany deserves our respect for treating his family with compassion and ingenuity and for sharing his results and ideas with so many people.

Nevertheless, De Vany also introduces some very strange ideas about genetics, evolution, and metabolism, and these ideas, along with his personal experience of diabetes in his family, lead him to condemn both foods rich in carbohydrates and foods rich in fats, and lead him to discard many nutrient-dense fatty foods such as egg yolks.

Good Food — But Not Great

There is no question that some of the advice in The New Evolution Diet is good. But while De Vany advocates fresh, whole foods, he also recommends throwing away egg yolks, using canola oil, eating skinless chicken breast, preferring white meat over red meat, and occasionally consuming cheese made from skim milk.

He allows liver, but you wouldn't know it from his chapter "A Month on the New Evolution Diet." Here we find no organ meats, but rather the occasional indulgence in dairy in the form of skim milk cheese or in the form of butter, which "is OK now and then." Strangely, fattier cuts of meat like pork chops and bacon make it on to the menu alongside skinless chicken breast. A "small yam once in a while" is also allowed, though in general carbohydrate-rich tubers are banned.

De Vany's opposition to fat and carbohydrate sometimes reduces the nutrient-density of his diet in dangerous ways. The clearest case is that of the egg yolk. Most of the nutrition in an egg is contained in the yolk (see my article, "The Incredible, Edible Egg Yolk"). Perhaps the most important of these is choline, which is essential to many processes, including mental health and liver function (see my article, "Meeting the Choline Requirement — Eggs, Organs, and the Wheat Paradox").

The whites, moreover, contain avidin, which inhibits biotin absorption, and is never fully destroyed by cooking. Feeding raw egg whites or administering biotin-deficient total parenteral (intravenous) nutrition are the two clasically understood textbook ways to induce biotin deficiency (for example, see the biotin chapter of Modern Nutrition in Health and Disease). Symptoms arise gradually over weeks to years of raw egg white feeding and include brittle nails, thinning and loss of hair, shedding of eye lashes and eye brows, and red scaly skin around the eyes, nose, mouth, and genitals. Candida can usually be cultured from the skin lesions. Biotin deficiency also leads to depression, lethargy, and tingling of hands and feet. The need for biotin increases during pregnancy, and subclinical biotin deficiency may play a role in birth defects (see my article, Vitamins For Fetal Development: Conception to Birth).

Cooking destroys between one third and two thirds of the avidin in egg whites. Liver and egg yolks are unique in their abundance of biotin, so consuming them along with egg whites seems like an obvious precautionary measure, especially for women with a tendency towards vaginal yeast infections or who hope to have children. While the role of biotin in preventing birth defects in humans is still an open question, I recommended following the precautionary principle on this matter in my 2007 article on pregnancy nutrition, where I suggested the addition of pure egg yolks to smoothies or homemade ice cream as a palatable way to obtain extra biotin.

Throwing away the yolks and keeping the whites achieves the opposite.

Unfortunately, there is so much potentially harmful dietary advice in this book that it could prove to be a step down from the Standard American Diet depending on how it is executed. Many people may begin throwing egg yolks and chicken skin away, rather than cutting out the white bread or starting high-intensity interval training. Some may suffer harm from these changes and others may just find a low-fat, low-carb diet impossible to stay on.

Carbophobia, Lipophobia, And Other Strange Metabolic Ideas

De Vany's opposition to egg yolks seems to derive from his ultimate view that "fat is poison" (p. 10). Although he meant this particular quote to apply to body fat, he has similar views of dietary fat (p.44):

The term "good oils" is somewhat of a misnomer, because the truth is that no fat is partcularly good for you.

Of course, De Vany doesn't like carbohydrates either. He recommends restricting carbohydrate to initiate DNA repair (p. 9, p. 136), stabilize blood sugar (p. 12-17), improve glucose transport into the brain (p. 126), lengthen lifespan (p. 55, p.137), and prevent oxidative stress (p. 85).

The worst option in his view, however, is to combine fats and carbohydrates together (p. 85):

A combined carb-fat load would have been an extremely rare even in the nutritional history of our species. In ancestral times of 100,000 years ago, fat would have accompanied protein — not a simple carb. Our metabolic networks must be stressed by this combination. The carbs prompt our bodies to release insulin, which shuts down fat burning. The resulting high-fat load and high blood sugar becomes a heavy sludge in the bloodstream, bruising the lining of our blood vessels. The release of insulin also opens this lining to the intrusion of fats. These fats are then oxidized, driven by the inflammatory response to high blood glucose. Oxidizing fat on a stream of glucose-mediated free radicals inflames the vasculature, promoting cardiovascular disease.

De Vany thus claims that carbohydrates cause hyperglycemia, which causes oxidative stress. Consuming fats with them will just subject the fats to this oxidative stress. This is a rather strange point of view, considering that fats actually prevent carbohydrates from causing hyperglycemia (see this reference). The following graph shows the effects of 50 grams of potato with or without 50 grams of butter, and compares them to two meals that were free of carbohydrate:

While the potato alone raised blood sugar levels to about 7 mM (125 mg/dL), the potato with butter led to modest blood sugar fluctuations that stayed roughly between 3.5-5 mM (60-90 mg/dL), which is within the range of normal fasting blood sugar. It seems unlikely, then, that the potato would have subjected the butter to oxidative stress by promoting hyperglycemia, when the potato in fact failed to produce hyperglycemia at all in the presence of butter.

These results may have been very different in diabetics, and De Vany's choice to banish carbohydrates from the menus of his diabetic mother and son was likely the best choice he could have made.

Even his bashing of french fries is warranted since french fries are usually fried in modern vegetable oils at very high temperatures, often partially hydrogenated and reused over and over again. Generalizing from the french fry to any combination of carbohydrate and fat, however, is pretty unreasonable.

De Vany promotes a rather simplistic view where carbs stimulate insulin and insulin resistance, and thus lays all of the metabolic abnormalities associated with insulin resistance at the feet of carbs and insulin. I think that people who promote this point of view need to contend with the fact that many groups of natives consume high amounts of carbohydrate with impunity but develop diabetes and obesity only when they switch to modern foods.

For example, De Vany points out that fasting insulin levels are more than twice as high in Americans than in Kitavans, but he fails to point out that the Kitavan diet is almost 70 percent high-glycemic carbohydrate (see Stephan Guyenet's series).

In a lecture at the 2010 Wise Traditions conference (which can be purchased here), Stephan Guyenet discussed traditional health-promoting diets of the Pacific Islands that were over 90% carbohydrate and others that were mostly fat, with a whopping 50% of calories as saturated fat. None of the populations had any meaningful incidence of insulin resistance, diabetes, or cardiovascular disease, and virtually none of the islandsÂ’ inhabitants were fat. In came refined foods, and they became vulnerable to all of these diseases. In a blog post soon after the conference, he pointed out that these populations also have very low fasting and postprandial blood glucose.

These results emphasize variability and flexibility in human responses to diet, topics that get very little coverage in this book — a point that will be discussed in the next two sections on genetics and evolution.

Of course, variability and flexibility may have limits. For example, none of these groups had diets that were mostly protein, the one macronutrient that does not seem to fall into Dr. De Vany's disfavor. And all of them were getting most of their calories from fat and carbohydrate, the two macronutrients Dr. De Vany treats as toxic.

Before we proceed to the sections on genetics and evolution, it may be worth discussing a few other strange metabolic ideas that Dr. De Vany promotes.

De Vany believes that we are genetically programmed to be "lazy overeaters" (p. 3). He also believes that body fat is "poison" because it plays a role in inflammation (p. 10). But body fat is responsible for secreting leptin, which suppresses appetite and increases energy expenditure. One major theory of obesity is the "set point," where leptin is responsible for regulating a specific level of body fat by adjusting food intake and energy expenditure to the appropriate levels. In this view, something has altered the set point during obesity. This is Stephan Guyenet's primary area of research, and he blogs about these emerging theories frequently over at Whole Health Source. De Vany's theory is essentially that the set point is set at infinite adiposity, which seems to contradict everything we know about the set point. His theory, moreover, seems to contradict the common experience of getting full after a meal.

De Vany's ideas about leptin get stranger than this. He states that the gene for leptin is highly conserved across species and is thought to have evolved in primates some four to seven million years ago (p. 46). If leptin evolved in primates four to seven million years ago, it would be difficult to say it is "highly conserved across different species," and indeed leptin studies are commonly done in rodents, who are thought to have diverged from our ancestral lineage some 80 million years ago. De Vany lists leptin among the hormones that cause insulin resistance (p. 129), even though leptin-deficient and leptin-resistant rodents are universally insulin resistant, showing clearly that leptin helps maintain insulin sensitivity. De Vany tells us that "The New Evolution Diet turns down the expression of the obesity gene in four different ways" and that "this gene's job is to 'express' fat — that is, to ramp up metabolic pathways that lead to the production of fat cells" (p. 105), but seems to have missed the memo that the obesity (ob) gene codes for leptin and actually prevents obesity.

Indeed, elsewhere (p. 113) De Vany acknowledges that leptin is "the hormone that would ordinarily tell your body that it has adequate reserves of energy and need not store any more." The views promoted about leptin in this book can be said, at best, to be disorganized and incoherent.

Ultimately, however, De Vany's view that we are genetically programmed to be lazy overeaters is symptomatic of deeper views of genetics and evolution that allow little room for flexibility in human individuals and variability within human populations, which are the topics of the next two sections.

Do We "Take Orders" From Our Genes? Not According to Molecular Biology

Although Dr. De Vany recognizes that "our genes are not the sum total of our destiny" because "we can alter our gene expression for better or worse," (p. 7) his view of how gene expression can be altered is essentially limited to these poles: better, or worse. "For example," he writes, "you can determine what you eat and drink and how you will exercise. But your genes will express themselves as they will" (p. 117). If we eat and live in the correct way, our genes will express themselves for the better, and if we eat and live in the wrong way, they will express themselves for the worse.

De Vany locates so much control at the level of genes that he even states the following:

Your pancreatic cells don't take orders from your brain, your blood, or anything else except the DNA that created them.

These views of genetics are rather bizarre and are completely irreconcilable to what we have learned about molecular biology over the past half century. DNA does not create cells. Cells create cells. Genes do not "express themselves" at all. If you put DNA in a petri dish with a bunch of nutrients it will do nothing. Living cells direct the expression of their genes in response to their own needs and to their environment. Genes act as files within a complex database that the cell accesses and uses as needed. Since our cells must cooperate with each other to form an integrated human being, they constantly take orders from our brain and other organs. These orders are carried in the blood and are called "endocrine hormones."

Let us take a brief look at the very different picture of gene expression presented in chapter seven of Molecular Biology of the Cell, the definitive guide to mainstream molecular biology.

The chapter begins by discussing experiments showing that although our liver cells, brain cells, skin cells, and many other types of cells all look and function very differently, they all contain the same DNA. If the nucleus of a frog's skin cell is taken out and put into a frog's egg, the egg will form a normal tadpole, not a skin cell. Thus, when a cell becomes a pancreatic cell, it does so not because its DNA "created" it that way, but because it computed information about its environment and accessed its DNA in the appropriate way.

A gene is completely impotent to express itself. The cell must access a gene's information and use it to make a protein in order for that gene to be expressed. The cell regulates the expression of genes for its own needs and for the needs of the organism in many different ways. First, the cell determines whether it makes an RNA transcript, and if so, how much of this RNA transcript it will make. Then the cell processes the RNA transcript, often by editing it, and regulates the export from the nucelus to another part of the cell. Still no protein is made from that RNA transcript unless the cell summons its enzymes to do so. It controls both the activity of these enzymes and the degradation of the transcript itself in order to regulate the production of the protein. Finally, the cell can modify the activity of that protein once it is made in a whole host of ways. Each one of these steps allows an opportunity for the cell to respond to its needs and to the needs of the organism.

Molecular biologists estimate that cells use about two thousand different proteins just to regulate the production of RNA transcripts from genes. These comprise an estimated eight percent of human genes. Consider the comments made by the authors of Molecular Biology of the Cell:

This large number of genes reflects the exceedingly complex network of controls governing expression of mammalian genes. Each gene is regulated by a set of gene regulatory proteins; each of those proteins is the product of a gene that is in turn regulated by a whole set of other proteins, and so on. Moreover, the regulatory protein molecules are themsleves influenced by signals from outside the cell, which can make them active or inactive in a whole variety of ways. Thus, we can view the pattern of gene expression in a cell as the result of a complicated molecular computation that the intracellular gene control network performs in response to information from the cell's surroundings.

They go on to describe how enormously complex the computational information networks are that the cell uses to regulate the expression of its genes, and ultimately conclude that, despite having written just under 90 pages on the matter, scientists understand very little of it. They describe experiments where scientists isolate components of the control networks, combine them in new ways, and attempt to predict the resulting system's behavior:

Scientists use this approach to test whether they truly understand the properties of the component parts; if so, they should be able to combine these parts in novel ways and accurately predict the characteristics of the new device. The fact that these predictions usually fail illustrates how far we are from truly understanding the detailed workings of the cell.

The New Evolution Diet presents a view of genetics that is very static and inflexible. If we do not give our genes the appropriate macronutrient ratio that approximates what they received 100,000 or 40,000 years ago, they will express themselves poorly; if we do give our genes that macronutrient ratio, they will express themselves well. This ignores the possibility that we are genetically programmed to flexibly respond to our environment.

Flexibility is not the only principle that is conspicuously absent from this book. The principle of variability is also quite absent, which is surprising, given the title of the book and the central role that the principle plays in evolutionary theory.

How Evolutionary is the New Evolution Diet?

Ordinarily, I do not evaluate books based on their agreement with evolutionary theory, but in the case of a book entitled "The New Evolution Diet," it seems appropriate.

The principle claim of Darwinian evolutionary theory is that all life is descended from a common ancestor and that the diversity of life can be accounted for by six basic principles (my six-fold division is somewhat arbitrary):

  • There is variation among organisms.
  • A portion of this variation is inherited.
  • Organisms produce too many offspring to all have maximal reproductive success.
  • In the struggle for survival and reproductive success, those organisms that are best adapted to their environments will be most reproductively successful.
  • As a result, the characteristics of organisms change over time.

It seems, then, that a diet and lifestyle plan based on evolutionary principles must consider the following topics:

  • What can other animals with whom we share a common ancestor teach us about ourselves?
  • How do humans vary in their response to diet and lifestyle between and within populations?
  • How has the human response to diet and lifestyle changed over time?
Ironically, The New Evolution Diet does not seem to tackle any of these questions.

Katherine Milton, by contrast, researches what the diets of other primates might teach us. Her contention that "Foods of Wild Primates Have Relevance for Modern Human Health" is very dependent on evolutionary theory because her contention depends on our common ancestry with other primates. Strangely enough, De Vany cites this article (p. 159) as evidence of our similarity to Cro-Magnon men who lived between 100,000 and 40,000 BC, but within the article Milton states the following:

Regardless of what paleolithic hunter-gatherers were eating, there is little evidence to suggest that human nutrient needs or digestive physiology were significantly affected by such diets at any point in human evolution.

How we are similar with and different from great apes would be an appropriate topic for a book claiming to be about evolution. Without any emphasis on common ancestry with other species, the term ancestral diet would be much more appropriate than evolutionary diet.

The principle of variability seems conspicuously absent from the book, even in the notes. Are Asians, Africans, and Europeans, all adapted to the same diet? Have microevolutionary principles fine-tuned the dietary requirements of different populations as they have become somewhat segregated over time? Again, there is almost no discussion of this topic in the book.

Finally, what does this book have to say on the subject of genomic change? De Vany acknowledges in the notes (p. 158-9) that some change has continued to occur, but in the main text dismisses these changes as minimal. Indeed, he not only tells us that "nothing much has changed" since the Stone Age (p. 2), but even tells us that corn and other grains "did not exist when our genes stopped evolving" (p. 38) and that "thanks to civilization, the world has changed a great deal since our genes stopped evolving" (p. 92). If De Vany's thesis is that genomic change has not occurred over the last 100,000 years, he is essentially excluding not only macroevolutionary principles but even microevolutionary principles from consideration. Again, this approach would be much more appropriately designated ancestral than evolutionary.

Of course, De Vany's conceptions about what is and isn't ancestral are occasionally contradictory to direct evidence and usually very speculative. Grains not only existed in the Paleolithic era but have been found in the teeth of Neanderthals, providing what most of us would consider pretty strong evidence that they were eating them. Perhaps grains killed off the Neanderthals (I emphasize "perhaps"), but they certainly existed.

De Vany estimates the waist-to-hip ratios of early humans based on the waist-to-hip ratios of modern athletes (p. 27), which is pretty speculative, to put it politely and diplomatically. De Vany argues that it is not entirely our fault we are fat, because we are genetically programmed to be lazy overeaters (p. 92), but also suggests that, though the stigma currently is maladaptive, our propensity to judge obese people too harshly probably evolved as an adaptation "during evolutionary times, when obesity was rare and almost surely indicated that that person was taking more from the group than they were contributing to it" (p. 179). In the absence of any attempt to identify the genes and biochemical pathways that are responsible for the obesity stigma, I'm afraid this speculation is what Stephan Jay Gould and others would have referred to as a "just so story" rather than science.

In any case, the argument that we have ceased to evolve over the last 40,000 to 100,000 years is somewhat questionable. Some scientists argue that evolution has accelerated 100-fold in the last 10,000 years or so (see here for an overview). Although I think the methods of dating mutations involve some problematic assumptions, I do think this research makes it highly questionable to assume that little change has occurred over time in the human genome. More importantly, small changes in DNA that are not even located in genes can cause large changes in function, and we have trillions of microorganisms that contribute to our digestive and metabolic phenotype who evolve with us, not only over grand scales of time, but even within our own lifetimes.

I am thus left wondering why The New Evolution Diet incorporates "evolution" into its title when it has so little to do with evolutionary theory. Indeed, had humans been specially created with a fixed genome 100,000 years ago, I do not think it would change the principles of this diet very much.

Ultimately, this book has many good insights, but none that haven't been offered elsewhere. It opens up the potential for a beginner to try a low-fat, low-carb diet, and give up on getting healthy after always being hungry. It opens up the opportunity for the dieter with pre-conceived notions — you know, the kind who tries to do the Atkins diet "low-fat" style — to institute the worst recommendations at the expense of the best.

I would recommend reading this book if you have a personal connection to Dr. De Vany and you'd like to help him out — but I would think twice about recommending it to a friend or family member.

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