The Omnivore’s Curse:
Low Fat versus Low Carb
Sally is a beautiful thirteen-year-old girl, but since the age of eleven she had been gaining 20 pounds per year. She has the lead in her middle school musical and is mortified because she can’t fit into her costume. She comes to my clinic after her family’s attempts at lifestyle intervention are ineffective. An oral glucose tolerance test shows that her pancreas releases too much insulin (see chapter 19), yet she is also insulin resistant and glucose intolerant. We place her on a low-carb diet and prescribe metformin (see chapter 19) to lower her insulin. She loses 20 pounds in the first three months, another 10 pounds after that, and holds steady thereafter. She isn’t abnormally hungry anymore, and her insulin levels have returned to normal. She is a very happy camper.
The “Hunters”
In the beginning there were the hunters. Most hunters killed their food, while some fished. They ate fat and protein, went long stretches between kills, and had to live off their fat stores. Their livers processed dietary fat in one of two ways based on the hunters’ body weight and their current energy supply. If energy was in short supply, the liver would chop up the fatty acids (long carbon chains) systematically into 2-carbon fragments called acetyl-CoA, or ketones. These fragments could then be burned for energy either by the mitochondria (the portion of the cell where energy generation occurs), in the liver, or in other organs. If the energy supply was in excess, the liver would package the fat into particles known as low-density lipoproteins (LDL). These LDL particles would circulate in the bloodstream and eventually take up residence in fat cells to be stored as triglyceride (blobs of fat) for another day, when energy might be needed when food was scarce. In the absence of insulin (as would occur in starvation), this stored triglyceride would break down into free fatty acids. The cycle would then repeat itself—the stored triglyceride would be released into the bloodstream, reenter the liver, and be chopped up into 2-carbon fragments to make acetyl-CoA, or ketones, again. These hunters didn’t know what a carbohydrate was and they didn’t need to, as animal (and human) carcasses were devoid of carbohydrates. Our bodies were, and are, perfectly adapted to burning fat as an energy source.
This is the nature of what has become known as the low-carb diet. Natural examples of this can still be found in cultures around the world, such as the Maasai and Samburu tribes of north-central Kenya (who eat meat, milk, and animal blood) and the Inuit of the Arctic (who eat fish, meat, and whale fat). In the early 1900s, the Arctic explorer Vilhjalmur Stefansson (1879–1962) lived among the Inuit for several years, subsisted primarily on whale blubber, and never felt healthier. He was the first to note that the Inuit, who ate nary a carbohydrate, had an extraordinarily low incidence of cancer, heart disease, diabetes, and other chronic diseases. (This has unfortunately changed in recent years with the introduction of processed foods into their diet.) When he returned to the United States in the late 1920s, Stefansson undertook an experiment. Under medical supervision, he ate only meat for one year and was documented to have no negative health effects from his diet. Stefansson wrote the 1960 book Cancer: Disease of Civilization? about his experiences and observations.
The low-carb diet has achieved mythic status. In the 1970s, Dr. Robert Atkins transformed it into high art—cheeseburgers without the bun, bacon and eggs, and broccoli with cheese sauce. No toast or potatoes, and woe to the beer drinkers. It continues to recruit record numbers of followers, who swear by it for treatment of obesity and promotion of health. The low-carb movement hit its peak in 2002, with the publication of two New England Journal of Medicine articles demonstrating its utility.1 Die-hards still swear by it, mainstream obesity experts have gotten on the bandwagon, and the number of positive testimonials can be documented with one click of your mouse. But in the recent past, the low-carb diet has come under fire, as it is very difficult to stay on it in America. It has also been criticized for having potential negative health impacts.2
The “Gatherers”
Alongside the hunters, there were the gatherers. The gatherers found their food in what came out of the ground. They ate carbohydrates and proteins in the form of fruits and vegetables. If energy was in short supply, the glucose would be completely taken up by the liver. If the gatherers’ energy status was instead replete, the liver would not capture some of the glucose and a rise in the blood glucose and subsequent insulin release would occur. If energy was in great surplus, then the blood glucose would rise even higher and insulin would keep pace, driving energy into fat for storage for a rainy day (e.g., famine).
This is the basis for today’s vegan diet. It is practiced in multiple cultures around the globe, because if you grow your own food, that’s what’s available. Many people in the United States eat this way as a matter of choice and sometimes to an extreme. (For example, fruitarians eat only fruits, nuts, and seeds, and some fruitarians eat only that which has naturally fallen from the tree, to avoid hurting the plant.) This diet can also be perfectly healthy and, when practiced properly, lifesaving.3
The Omnivore’s Curse
The conflict between these two dietary philosophies is touched on in Michael Pollan’s 2006 book The Omnivore’s Dilemma. Evolutionarily, the metabolism of fat and carbohydrates developed separately. The net energy recoupment of each of these processes is minimal. But both metabolic products of these two completely different pathways (fat being broken down serially versus carbohydrates undergoing glycolosis) meet at the mitochondria in the form of the compound acetyl-CoA. As we learned in chapter 9, how much acetyl-CoA the mitochondria have to process has everything to do with how healthy the cell is. It also determines whether the cell will collapse under the weight of processing all that energy.
The hunters ate fat; the liver would beta-oxidize (the process by which fatty acids are broken down by the mitochondria, two carbons at a time) what it needed for its use and would then export any excess LDL to be taken up in adipose tissue. The gatherers ate carbohydrates (glucose); after absorption, the liver would extract what it needed and the insulin would clear the rest out into the bloodstream for muscle and adipose tissue. In the liver, any excess glucose would be converted to glycogen for storage. Our ancestors were rarely exclusively hunters or gatherers, but they likely favored one food type (fat or carbohydrate) over the other depending on where they lived and the time of year. The liver thus developed two separate pop-off valves to protect it from excess energy, one for carbohydrate and one for fat. In both cases, the mitochondria’s exposure to acetyl-CoA was exquisitely regulated so as not to overwhelm their capacity. The mitochondria never had to bite off more than they could chew.
But then, as humans learned to irrigate and farm, we became omnivores. Sally, and with few exceptions, our entire society, eat fat and carbohydrates at the same meal (e.g., steak and potatoes). As food became more plentiful, we began to overload both sides of our metabolic pathways: the 2-carbon breakdown of fat and the glycolysis of carbohydrates. Now the mitochondria are catching hell; they have to deal with an onslaught of acetyl-CoA coming from both directions. One high-fat, high-carbohydrate meal is no big deal. But keep this up for ten thousand meals in a row (about ten years; just in time for your teenage years) and we’re talking about some real damage: an increase in chronic metabolic disease or metabolic syndrome.
Fat or Carbohydrate? Or Fat and Carbohydrate?
Here’s some food for thought. With very few exceptions, every naturally occurring foodstuff contains either fat or carbohydrates, but usually not both. Meat, fish, and poultry have no carbohydrates. Grains, roots, and tubers (e.g., potatoes and yams) have no fat. Those fruits that have fat, such as avocados, olives, and coconut, have minimal carbohydrates. Nuts are an exception, but they are still pretty low in carbohydrates and very high in fiber. (That’s why they’re brown; see chapter 12.) Milk is another exception to the rule, but other than that which came from their mothers, humans were not exposed to other mammals’ milk until the beginnings of agriculture, in the Neolithic period. They didn’t have a USDA Food Pyramid to follow.
It wasn’t until we became gourmets, eating fat and carbohydrates in the same meal, that our cells first felt the wrath of mitochondrial wear and tear. This accounts for the appearance of metabolic disease with the advent of trade in the early seventeenth century; before that, food was still a function of what you killed or you grew yourself. Eventually, we became gourmands, eating fat and carbohydrate in the same food. This is the essence—the blessing and the curse—of processed food. Except for one big item, which has both fat and carbohydrates at the same time. (I’ll give you a hint: it’s really sweet.)
The Battle Royale
The prevalence of heart disease had begun to rise slowly over the early twentieth century when Paul Dudley White wrote his classic treatise Heart Disease in 1931. White was Eisenhower’s cardiologist in 1955 after the president’s heart attack. The move to reduce heart disease through dietary intervention was in full swing by the 1960s, with the U.S. government wanting to take a proactive role. This set the stage for a nutritional “holy war,” played out in kitchens and restaurants across America. The goal was to alter our diet for the better. Instead, we’ve laid waste to every nutritional hypothesis, lost the public’s trust, and killed countless millions in the process. We will be suffering the aftermath of this Battle Royale for generations to come.
The first salvo in the battle emanated from the dental community. Prior to 1960, the known problems associated with sugar were restricted to the development of cavities.4 With the advent of water fluoridation in 1945, cavities were no longer a public health issue. Sugar dropped from the radar.
Enter John Yudkin and Ancel Keys. Yudkin, a British physiologist and nutritionist, researched the nature of chronic disease. In 1957 he postulated that dietary composition was the cornerstone of coronary thrombosis (heart attacks). By 1964 he had determined through natural observation that the consumption of sucrose was most closely associated with heart disease. He was the first to show that sugar uniquely raised serum (blood) triglycerides and insulin levels. In 1972 he published his seminal work on the subject, Pure, White, and Deadly, in the United Kingdom. Yudkin published countless papers on the biochemistry of sucrose, specifically the molecule called fructose, which gives sugar its sweetness. He was the first to warn that excessive consumption could lead to coronary heart disease, diabetes, GI disease, eye disease, and other inflammatory diseases.
Ancel Keys, a Minnesota epidemiologist, was already in the public eye as the inventor of the K-ration during World War II. In 1952 he took a sabbatical in England, where he saw enormous increases in heart disease in the face of the English diet, which consisted of incredibly high fat and high cholesterol items. (Think bangers and mash, fish and chips.) He noted that those who were the best fed in both the United States and the United Kingdom, those able to afford meat, were the ones who suffered most often from heart problems. He returned to the United States on a mission to prove that cholesterol and dietary fat were the direct sources of heart disease.
Keys published many studies in the 1960s and ’70s that demonstrated higher cholesterol levels in patients with heart disease; he also showed that increased consumption of dietary fat led to higher cholesterol. Keys’ seminal “Seven Countries” study (1980) was a 500-page volume dedicated to the concept that, through its cholesterol content, dietary fat was the single cause of heart disease. Unfortunately, based on his own work, there are four problems with his thesis.
1. The Seven Countries study started out as the Twenty-two Countries study. Keys’ seven countries were Japan, Italy, England, Wales (included as a separate country by Keys), Australia, Canada, and the United States. For these seven, the relationship between dietary fat and heart disease looked pretty convincing. But when all twenty-two countries were plotted (add Austria, Ceylon, Chile, Denmark, Finland, France, Germany, Ireland, Israel, Mexico, Netherlands, New Zealand, Norway, Portugal, Sweden, and Switzerland), the correlation became a lot less convincing. He also chose to leave out “indigenous tribes,” such as the Inuit (North America), Tokelau (Oceania), and Maasai and Rendille (both Africa), who ate only animal fat and have among the lowest prevalence of heart disease on the planet.
2. The role of dietary fat in heart disease is complicated by the consumption of trans fats (e.g., margarine), which are a significant factor in the etiology of metabolic syndrome. Trans-fat use peaked in the 1960s with the advent and popularization of margarine—remember Imperial Margarine, “fit for a king”?—just as Keys was starting his epidemiologic research. Could he have been studying an effect of trans fat instead of saturated fat in the developed countries? Since he did not separate the two in his work, we don’t know.
3. The correlation itself is a problem. At one end of the graph are Japan and Italy, as they eat the least amount of saturated fat. But they also eat the least amount of dietary sugar of all the countries included. How can you determine whether it is the fat or the sugar that is driving this relationship when both go together?
4. On page 262 of his mega-opus, Keys wrote, “The fact that the incidence rate of coronary heart disease was significantly correlated with the average percentage of calories from sucrose in the diets is explained by the intercorrelation of sucrose with saturated fat.” In other words, sucrose also correlated with heart disease, but Keys did not think this was an issue. When one does a multivariate correlation analysis (determining whether A causes B regardless of the impact of C, D, and E) one has to do it both ways; in this case, one would need to hold sucrose constant and show that dietary fat still correlates with heart disease. Keys didn’t perform this kind of analysis. We don’t know why. So which was it—the fat or the sugar?
In the midst of the Yudkin-Keys battle came the lipid hypothesis of heart disease. In the 1970s, the Nobel Prize–winning team of Michael Brown and Joseph Goldstein in Dallas discovered how the liver recycled fatty acids.5 From this discovery we learned four important precepts. First, we identified LDL, or low-density lipoproteins (the main export particle of dietary fat), and the liver LDL receptor (which gobbles them up to recycle them). Second, we learned that dietary fat increased blood LDL levels. Third, one rare genetic disease generates massively high LDL levels, and these patients die of heart attacks very early in life. Fourth, in large populations of adults, blood LDL levels correlate with risk for coronary heart disease.
The implications of this work seem quite logical on the surface. Let’s call dietary fat A, LDL B, and cardiovascular disease C. The implication was that “If A leads to B, and B correlates with C, then A must lead to C; therefore, no A, no C.”
This was the debate of the late 1970s, specifically taken up by Senator George McGovern’s bipartisan, nonlegislative Select Committee on Nutrition and Human Needs in 1977, and chronicled by Gary Taubes.6 McGovern appointed a labor reporter named Nick Mottern, who had no scientific background, to research and write the first dietary goals for the United States. Rather than doing extensive research on the subject, Mottern relied almost exclusively on the work of Mark Hegsted, a nutritionist at the Harvard School for Public Health. Hegsted was of the opinion that dietary fat was the ultimate cause of dietary woes in the United States, and that the solution was to limit its intake. Thus, Mottern’s report recommended that the American populace limit its fat intake to 30 percent of their diet and saturated fat to 10 percent. Mottern admitted that not all scientists agreed with his suggestions, but he stated that Americans could only improve their health by following his advice. What did they have to lose?
Although it took seven years and several twists and turns, the USDA, the AHA, and the American Society of Clinical Nutrition all endorsed the document. Mottern’s brainchild, Dietary Goals for the United States, was implemented, and our dietary practices began to change as the food industry retooled itself to deliver low-fat products rushed to meet the new directives.
What Went Wrong?
Seems logical—A to B to C; so no A, no C—i.e., no dietary fat, therefore no LDL, and no heart disease. Not so fast. A can lead to B, but it can also lead to D, E, F, and G, and never make it back to C. And the contrapositive of the statement is, “No C, no A.” This is flawed logic, to be sure.
The implicit assumption was that all LDL was bad. As it turns out, there are two types of LDLs: one is called large buoyant LDL, or type A LDL, and the other is called small dense LDL, or type B LDL. Large buoyant LDL floats in the bloodstream. It’s too big to get underneath the cells lining your blood vessels to start the atherosclerotic (artery wall thickening) process. Eighty percent of blood LDL is large buoyant and is thought to be neutral from a cardiovascular standpoint. However, small dense LDL doesn’t float; it sinks. It’s small enough to get underneath the blood vessel cells and has been specifically implicated in the start of atherosclerotic plaques. True, dietary fat raises LDL, but it’s the large buoyant kind. The small dense variation is raised by carbohydrates.7
Here’s one more fly in the ointment. Dietary fat isn’t one entity. It’s at least seven, listed in table 10.1. Some of these, such as omega-3 fatty acids, are good for you and protective against heart disease. Trans fats are disasters because our mitochondria can’t break them down completely for energy. Because a calorie is not a calorie. The fat remnants precipitate in arterial walls—a great way to get a heart attack. Omega-6 fats are pro-inflammatory and associated with heart disease. Keys’ personal demon was saturated fat, which is in the middle of this spectrum and does neither harm nor good. Indeed, recent studies have exonerated saturated fat from a primary role in the atherogenic process.8
Table 10.1. Dietary Fats and Their Value,
in Descending Order, to Human Health
| Dietary Fat | Dietary Source | Medicinal Value or Danger |
| Omega-3 fatty acids | Wild fish, flaxseed oil | Anti-inflammatory, lowers serum triglycerides, repairs membranes |
| Monounsaturates | Olive and canola oil | Stimulates liver metabolism, reduces atherogenesis |
| Polyunsaturates | Vegetable oils | Anti-inflammatory, but in excess amounts can cause immune dysfunction |
| Saturated fatty acids | Grass-fed animal meats, milk and dairy products | Atherogenic in a specific genetic background (familial hypercholesterolemia, or FH); raises levels of type A LDL very high |
| Medium-chain triglycerides | Palm oil, coconut oil, palm kernel oil | Energy source, some suggestion of stimulation of atherosclerosis |
| Omega-6 fatty acids | Farm-raised animals and fish (fed on corn and soy) | Atherosclerosis, insulin resistance, immune dysfunction, pro-inflammatory |
| Trans fats (partially hydrogenated oils) | Synthetic, found in processed foods only | Atherosclerosis, nonalcoholic fatty liver disease |
But the proof’s in the low-fat pudding, right? Does a low-fat diet prevent heart disease or not? This was put to the test in the Women’s Health Initiative, started in 1993. The study followed nearly fifty thousand postmenopausal women over eight years. Fat (saturated, monounsaturated, and polyunsaturated) was decreased in their diets to 30 percent of their total calories—but there was no change in the incidence of heart attack or stroke. A long-term, prospective, randomized controlled study on a lot of people, and it was a bust.9
Nevertheless, in the early 1980s, none of these concerns about sugar, carbohydrates, and types of fats was known. With the endorsement of the Dietary Guidelines, Keys delivered the knockout punch and won the food fight, while Yudkin was thrown under the bus. We were beseeched to reduce our consumption of dietary fat from 40 to 30 percent. The food industry had to retool its products to meet the demand for low-fat fare. This meant altering its recipes. But when you take the fat out, the food tastes like cardboard. And palatability equals sales. The food industry had to find ways to make this low-fat fare palatable. They therefore upped the carbohydrate content, specifically the sugar. An example is Nabisco SnackWells, which are still stocked on the shelves. For each serving, 2 grams of fat were removed and 13 grams of carbohydrates, 4 of which were sugar, were added.
In the 1990s there was a major shift in the availability of specific foodstuffs. The foods containing fat, such as milk, saw a drop or a stabilization in consumption. Conversely, levels of refined carbohydrates, devoid of their inherent fiber, went through the roof. Remember, refined carbohydrates means lots of insulin, which means more energy storage in fat tissue. And thus the obesity epidemic was born in the aftermath of this seemingly logical and well-meaning, yet tragically flawed, understanding of our biochemistry.
The gradual understanding that dietary fat isn’t always the demon that it was portrayed to be in the Dietary Guidelines, and the work of Dr. Robert Atkins and other pioneers, led to the introduction of the “low-carb diet” into the American lexicon. Restaurants started serving cheeseburgers wrapped in a lettuce leaf instead of a bun (hold the fries). By the early 2000s, the carbohydrate-restricted diet was put to the test; it went head to head against the low-fat diet for the treatment of obesity and type 2 diabetes. From controlled studies, we learned the following five lessons10: First, carbohydrate restriction improves glucose control, the primary target of diabetes therapy. Second, carbohydrate-restricted diets are at least as effective for weight loss as low-fat diets. Third, substitution of fat for carbohydrates is generally beneficial for markers of and incidence of heart disease. Four, carbohydrate restriction improves features of metabolic syndrome. Five, the beneficial effects of carbohydrate restriction are independent of weight loss. (Look at Sally.) Carbohydrate restriction lives on in many guises throughout the food world. Yet so do the vegan, traditional Japanese, and other low-fat, high-carbohydrate diets.
Because the two overlap.
There is one specific foodstuff that is both fat and carbohydrate at the same time. It’s the one item that’s excluded from every successful diet in the world. It the real omnivore’s curse. And it’s the real culprit of the global obesity and metabolic syndrome pandemic.