The science on low-carb vs. high-carb diets

1 The science on low-carb vs. high-carb diets: Journal-notes on a magisterial book By Chris Wright (For more summaries of great scholarship, see this document) I’m reading Gary Taubes’ brilliant, albeit controversial, book Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease (2007). It argues against the widespread idea that diets high in saturated fats and cholesterol are bad for your heart and your weight, instead insisting that high-carbohydrate diets are, more often, what lead to obesity and heart disease. For decades, until very recently, the Establishment declared that carbs are rather good for the heart and for weight control, while fats are bad, but it seems that the opposite is the truth. Actually, it’s pretty common now, finally, to hear about the downsides of high-carb diets—and even in the late nineteenth and early twentieth centuries, as Taubes describes, it was widely known that high-carb diets can lead to excessive weight gain. (This is also a premise of the famous Atkins diet from the 1970s to the present, along with other diets and many bestselling books from the 1940s on.) But things went awry in the middle and late twentieth century, when influential scientists starting with Ancel Keys got things backward. Doubtless one reason the “good carbs” dogma conquered the culture was that it benefited agribusiness and other corporate interests, which promoted it. (The dairy, egg, and meat industries, on the other hand, certainly opposed it.) The dogma wasn’t totally absurd, at least prima facie. For it was thought that consuming too many calories was what led to obesity, and since fat has more than twice as many calories per gram as protein and carbs, cutting down on fat should lead to losing weight. So should exercise: burn more calories than you consume. But Taubes argues—on the basis of prodigious evidence— that it isn’t the quantity of calories that matters but the quality. Let’s look at some of the basics first. [Coronary heart disease] is a condition in which the arteries that supply blood and oxygen to the heart—known as coronary arteries because they descend on the heart like a crown— are no longer able to do so. If they’re blocked entirely, the result is a heart attack. Partial blocks will starve the heart of oxygen, a condition known as ischemia. In atherosclerosis, the coronary arteries are lined by plaques or lesions, known as atheromas, the root of which 2 comes from a Greek word meaning “porridge”—what they vaguely look like. A heart attack is caused most often by a blood clot—a thrombosis—typically where the arteries are already narrowed by atherosclerosis. Cholesterol, on the other hand, “is a pearly-white fatty substance [a lipid] that can be found in all body tissues, an essential component of cell membranes and a constituent of a range of physiologic processes, including the metabolism of human sex hormones. Cholesterol is also a primary component of atherosclerotic plaques, so it was a natural assumption that the disease might begin with the abnormal accumulation of cholesterol…” Actually, in the 1940s even Ancel Keys insisted that dietary cholesterol (the cholesterol we consume in our diets) had little relevance to heart disease. Like other researchers, he observed, correctly, that eating foods high in cholesterol usually had almost no effect on the cholesterol levels in our blood. A few years later, however, he decided that dietary fat is what elevates cholesterol levels. (Hence the still-widespread belief that a low-fat diet is a low-cholesterol diet.) But he had oversimplified. It turns out it isn’t the total amount of dietary fat that increases cholesterol but rather the fat’s degree of “saturation,” as well as what’s called the chain length of the fats. “This saturation factor is a measure of whether or not the molecules of fat—known as triglycerides— contain what can be considered a full quotient of hydrogen atoms, as they do in saturated fats, which tend to raise cholesterol, or whether one or more are absent, as is the case with unsaturated fats, which tend, in comparison, to lower it.” Hence the common notion for many decades that saturated fats are where the real danger is. The problem is that a lot of research has failed to show that people with high cholesterol have unusually clogged arteries. Besides, “even if high cholesterol was associated with an increased incidence of heart disease, this begged the question of why so many people…suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease.” Nevertheless, in 1960 the American Heart Association endorsed Keys’ idea that high cholesterol is the leading heart-disease risk and therefore that Americans should reduce the fat in their diets, especially saturated fat. (Strangely, this endorsement was less than four years after the AHA had firmly rejected Keys’ hypothesis. The evidence hadn’t changed, so maybe some corporate lobbying had made a difference? Less dietary fat = more carbs, more sugar, more profits for certain industries, etc.) 3 Through shoddy science, the fat-cholesterol hypothesis gained popularity in the following decades. For example, it was observed that Japanese men who lived in Japan had low bloodcholesterol levels and low levels of heart disease, while Japanese men in California had higher cholesterol levels and higher rates of heart disease. It was considered largely irrelevant that Japanese men in California who had very low cholesterol levels still had higher rates of heart disease than men in Japan. There are plenty of other examples of such flawed research. Keys and scientists who agreed with him saw in research what they wanted to see, and the press reported their conclusions. Sometimes studies coming to opposite conclusions wouldn’t even be published. More often, though, they were just dismissed or ignored. In passing, Taubes mentions the “French paradox”: “a nation that consumes copious saturated fat but has comparatively little heart disease.” One of the many pieces of evidence against the fat-cholesterol hypothesis. (In fairness, I should note that one study in the 1990s concluded that a man who avoided saturated fat his entire adult life until the age of 90 could expect to live…an extra four months.) The climate of opinion turned decisively in favor of Keys’ hypothesis in 1977, when Senator George McGovern’s Select Committee on Nutrition and Human Needs published the first Dietary Goals for the United States. It basically endorsed Keys’ ideas, despite acknowledging that they were scientifically controversial. “Eat less fat and more carbs!” There was a lot of dissent among the scientific and medical communities, not to mention the livestock industry, but it didn’t much change the thinking of the committee. A few years later, the Department of Agriculture published its Dietary Guideliness for Americans, which echoed McGovern’s report. From then on, more and more scientists (whose funding often depended on government priorities) began to fall in line. Soon the National Institutes of Health, the Surgeon General, the National Academy of Sciences, etc. were enforcing the new “consensus”—which was still based on astonishingly little science. Even international bodies like the World Health Organization have tended to accept it. Meanwhile, a number of studies have suggested the opposite of the fat-cholesterol hypothesis. In some cases in Japan, Spain, and Italy, increases in fat consumption over decades have correlated with declines in heart disease and strokes. Studies of Mediterranean immigrants to Australia suggest that the initially low heart disease rates of these people fall even lower after they’ve immigrated, despite a considerable increase in their meat consumption. In fact, by the late 1980s Ancel Keys himself told the New York Times, “I’ve come to think that cholesterol is not as 4 important as we used to think it was”! That’s a pretty big “whoops,” considering the impact of his earlier hypotheses. Okay, let’s shift now to evaluating what Taubes calls the carbohydrate hypothesis. He starts out by noting that “diseases of civilization” have invariably appeared among “traditional” populations that began to be exposed to Western diets: …The new diet inevitably included carbohydrate foods that could be transported around the world without spoiling or being devoured by rodents on the way: sugar, molasses, white flour, and white rice. Then diseases of civilization, or Western diseases, would appear: obesity, diabetes mellitus, cardiovascular disease, hypertension and stroke, various forms of cancer, cavities, periodontal disease, appendicitis, peptic ulcers, diverticulitis, gallstones, hemorrhoids, varicose veins, and constipation. When any diseases of civilization appeared, all of them would eventually appear. This led investigators [in the 1920s and later] to propose that all these diseases had a single common cause—the consumption of easily digestible, refined carbohydrates. The hypothesis was rejected in the early 1970s, when it could not be reconciled with Keys’s hypothesis that fat was the problem, an attendant implication of which was that carbohydrates were part of the solution… It’s not easy to summarize Taubes’ very rich and long description of the history and the science. As with the fat-cholesterol story, there’s a shameful amount of bad science and lack of common sense on the part of authorities. For half a century, diabetologists rejected convincing evidence that sugar and refined carbohydrates were responsible for diabetes, believing instead that fatty diets caused the disease. Some influential researchers also attributed far too much importance to dietary fiber in preventing “diseases of civilization,” believing wrongly that a fiber-deficient diet was responsible for colon cancer, polyps, diverticulitis, and so on. (You’ll still see claims like this on “respectable” websites, for example.) Following a remarkable and far-seeing British scientist named Thomas Latimer Cleave (and his collaborator George Campbell), Taubes argues that these modern chronic diseases are largely caused by the most radical change to the internal environment of human bodies in two million years: the introduction of diets high in sugar and refined carbohydrates. Excessive consumption of these can lead to a constellation of conditions now called insulin resistance 5 syndrome or, more often, metabolic syndrome. These conditions are common to diabetes, obesity, and heart disease. They include, for instance, elevated levels of blood fats known as triglycerides, low levels of HDL cholesterol (now known as the “good cholesterol”), hypertension, chronically high levels of insulin (called insulinemia or hyperinsulinemia), the increased presence of LDL particles (“bad cholesterol”), a relative insensitivity of cells to insulin (called insulin resistance), and high levels of a protein called fibrinogen that increases the likelihood of blood clots in arteries. The introduction of refined carbs in modern diets has massively compromised the incredibly complex homeostatic mechanisms in the human body that evolved over millions of years. I have to include a long quotation here: This whole-body homeostasis is orchestrated by a single, evolutionarily ancient region of the brain known as the hypothalamus, which sits at the base of the brain. It accomplishes this orchestral task through modulation of the nervous system—specifically, the autonomic nervous system, which controls involuntary functions—and the endocrine system, which is the system of hormones. The hormones control reproduction, regulate growth and development, maintain the internal environment—i.e., homeostasis—and regulate energy production, utilization, and storage. All four functions are interdependent, and the last one is fundamental to the success of the other three… All other hormones, however, are secondary to the role of insulin in energy production, utilization, and storage. Historically, physicians have viewed insulin as though it has a single primary function: to remove and store away sugar from the blood after a meal. This is the most conspicuous function impaired in diabetes. But the roles of insulin are many and diverse. It is the primary regulator of fat, carbohydrate, and protein metabolism; it regulates the synthesis of a molecule called glycogen, the form in which glucose is stored in muscle tissue and the liver; it stimulates the synthesis and storage of fats in fat depots and in the liver, and it inhibits the release of that fat. Insulin also stimulates the synthesis of proteins and of molecules involved in the function, repair, and growth of cells, and even of RNA and DNA molecules, as well. Insulin, in short, is the one hormone that serves to coordinate and regulate everything having to do with the storage and use of nutrients and thus the maintenance of homeostasis and, in a word, life. It’s all these aspects of homeostatic regulatory systems— in particular, carbohydrate and fat metabolism, and kidney and liver functions—that are 6 malfunctioning in the cluster of metabolic abnormalities associated with metabolic syndrome and with the chronic diseases of civilization. I had no idea insulin is so important for so many functions. In six very dense chapters, Taubes discusses the history of the science of “the carbohydrate hypothesis.” I’ll try to summarize the main points. Most of the fat in the body consists of triglycerides, though cholesterol is a type of fat too. Both types are shuttled through the blood in particles called lipoproteins, and the amount of cholesterol and triglycerides varies in each type of lipoprotein. The types include low-density lipoproteins (LDL), high-density ones (HDL), and very low-density ones (VLDL). Most of the triglycerides in the blood are carried in VLDL, while much of the cholesterol is found in LDL. (Some is also found in VLDL.) LDL and, much more so, VLDL are implicated in heart disease and other conditions. Measuring total cholesterol in the blood doesn’t tell you how much of it is carried by the bad low-density or very low-density particles and how much by the good highdensity particles, so it isn’t a particularly useful measurement. (One reason HDL particles are “good,” apparently, is that they transport cholesterol back to the liver, either for excretion or to be used by other tissues that synthesize hormones.) The amount of (slightly bad) LDL in the blood can be raised by consuming saturated fats, but levels of the more damaging VLDL are raised by consuming carbohydrates. (Moreover, saturated fats also raise the good HDL cholesterol.) So, to paraphrase a pioneering researcher in the 1950s-60s named John Gofman, If a physician put a patient with high cholesterol on a low-fat diet, that might lower the patient’s LDL, but it would raise VLDL. If LDL was abnormally elevated, then this lowfat diet might help, but what Gofman called the “carbohydrate factor” in these low-fat diets might raise VLDL so much that the diet would do more harm than good. Indeed, in Gofman’s experience, when LDL decreased, VLDL tended to rise disproportionately. And if VLDL was abnormally elevated to begin with, then prescribing a low-fat, highcarbohydrate diet would certainly increase the patient’s risk of heart disease. It's worth noting that not only a low-carb diet but also a low-calorie diet can reduce the level of triglycerides in the blood, although for other reasons such a diet might not be very healthy. 7 Meanwhile, other researchers found (in 1960) that high triglyceride levels were far more common than high cholesterol in coronary-heart-disease patients. “Only 5 percent of healthy young men had elevated triglycerides, compared with 38 percent of healthy middle-aged men and 82 percent of coronary patients.” So, again, since a high-carb diet increases triglycerides (carried by VLDL), it’s a good idea to avoid such a diet. Another interesting finding, from 1977, was that the higher the HDL cholesterol, the lower the triglycerides and risk of heart disease. (And vice versa: the more triglycerides, the less HDL.) Evidently there was some mechanism that inversely linked HDL to triglycerides. Unfortunately, the medical and political establishment chose to ignore the implication that, to prevent heart disease (and obesity and diabetes), raising HDL is much more important than lowering either LDL or total cholesterol. For decades, the country would remain in the grip of Keys’ simplistic “cholesterol is bad” hypothesis. In fact, even today we’re regularly told that LDL cholesterol is a significant predictor of heart disease, when the truth, according to Taubes, is that high levels of triglycerides are far more dangerous. LDL is a relatively marginal risk. I’ve noted that consuming saturated fat, contrary to over fifty years of dogma, isn’t very bad, since it increases the good HDL (and the potentially slightly bad LDL). Carbohydrates, on the other hand, lower both LDL and HDL, as they raise triglycerides. But another noteworthy fact is that monounsaturated fat is good, because it both lowers LDL cholesterol and raises HDL. The reason this is noteworthy is that the principal fat in red meat, eggs, and bacon—foods we’ve been told are unhealthy—is monounsaturated fat. With a porterhouse steak, for instance, about 70 percent of the fat might improve the relative levels of LDL and HDL, compared with what they would be if carbohydrates like bread, potatoes, and pasta were consumed. Thus, “eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.” I’ve ignored some complications in this summary. In particular, it turns out that LDL particles actually come in seven different types! The smallest and densest of these types are what correlate negatively with HDL and positively with heart disease. So it’s too simplistic to say “LDL is bad,” as we usually hear. Rather, only the small and dense LDL is bad. Some people have mostly large, fluffy LDL particles, which are harmless, while others have mostly small, dense LDL, which are more likely to cause atherosclerosis. “Small, dense LDL can squeeze more easily through 8 damaged areas of the artery wall to form incipient atherosclerotic plaques.” The proliferation of small, dense LDL in the blood goes together with high triglycerides and low HDL. And once again, research shows that the less fat in the diet and the more carbohydrates, the smaller and denser the LDL (and therefore the greater the risk of heart disease). At the same time, the more saturated fat in the diet, the larger and fluffier the LDL—which is a beneficial effect. So what are the actual mechanisms that explain all this stuff? Here’s a simplified summary of some of them: After we eat a carbohydrate-rich meal, the bloodstream is flooded with glucose, and the liver takes some of this glucose and transforms it into fat—i.e., triglycerides—for temporary storage. These triglycerides are no more than droplets of oil. In the liver, the oil droplets are fused to [lipoproteins]. The triglycerides constitute the cargo that the lipoproteins drop off at tissues throughout the body… This lipoprotein has a very low density, and so is a VLDL particle… The liver then secretes this triglyceride-rich VLDL into the blood, and the VLDL sets about delivering its cargo of triglycerides around the body. Throughout this process, the lipoprotein gets progressively smaller and denser until it ends its life as a low-density lipoprotein—LDL… If the liver has to dispose of copious triglycerides [because of a high-carb diet], then the oil droplets are large, and the resulting lipoproteins put into the circulation will be triglyceride-rich and very low-density. These then progressively give up their triglycerides, eventually ending up, after a particularly extended life in the circulation, as the atherogenic [i.e., bad] small, dense LDL. This triglyceride-rich scenario would take place whenever carbohydrates are consumed in abundance… Lipoproteins that cling to artery walls “begin the accumulation of fat and cholesterol that is characteristic of atherosclerotic plaques,” which cause heart disease. What does insulin have to do with all this? Taubes’ discussion isn’t ideal, so I’ve had to do some investigating online. Insulin, produced in the pancreas, is released in response to increased blood glucose (sugar) levels. It transports the glucose to cells and tissues that use it for energy, and in doing so, it lowers blood sugar levels. It also takes the glucose to the liver, which uses it to synthesize and secrete triglycerides for storage in fat tissue. Problems arise if the conditions of 9 insulin resistance and/or hyperinsulinemia (chronically elevated levels of insulin in the blood) are present. Insulin resistance is when cells don’t respond normally to insulin, with the result that glucose doesn’t get into the cells and instead builds up in the blood. If someone who is insulinresistant eats a carbohydrate-rich diet, his pancreas will have to secrete even more insulin to try to get the glucose into cells; the higher insulin levels will prompt even greater production of triglycerides by the liver, and thus will raise triglyceride levels in the blood. Which increases the risk of heart disease. Diabetes is a condition of chronically high blood sugar, but not everyone with insulin resistance or hyperinsulinemia becomes diabetic. Some people continue to secrete sufficient insulin to overcome their insulin resistance—but this hyperinsulinemia still causes problems by elevating triglyceride levels in the blood. I’ve never known much about diabetes, so I’ll describe it briefly. Type 1 diabetes is a lifelong condition in which the pancreas makes little or no insulin, which means cells can’t absorb glucose. It thus builds up in the blood. Type 2 diabetes, which is much more common, is characterized by cells’ insulin resistance rather than the pancreas’s insufficient production of insulin. Ironically, diabetics can sometimes suffer from low blood sugar—but this often happens because they’ve taken too much insulin in their therapy or some other medication, or they’ve increased physical activity without eating more or adjusting their insulin dose, etc. Why is chronically high blood sugar bad anyway? For one thing, it raises insulin levels, which themselves raise triglyceride levels. But there are other problems. Raising blood sugar increases the production of what are called reactive oxygen species (ROS) and advanced glycation end-products (AGEs), both of which are potentially toxic. The former [ROS] are generated primarily by the burning of glucose (blood sugar) for fuel in the cells, in a process that attaches electrons to oxygen atoms, transforming the oxygen from a relatively inert molecule into one that is avid to react chemically with other molecules. One form of these reactive oxygen species are free radicals, and all of them are together known as oxidants, because what they do is oxidize other molecules… The object of oxidation slowly deteriorates. Biologists refer to this deterioration as oxidative stress. Antioxidants neutralize reactive oxygen species, which is why antioxidants have become a popular buzzword in nutrition discussions. 10 Oxidative stress is an important cause of cancer, arthritis, aging, autoimmune disorders, and cardiovascular and neurodegenerative diseases. So high blood sugar can be very bad indeed! What about AGEs? These can be just as bad as ROS. Glycation is when a sugar molecule, like glucose, attaches to a protein (or a lipid or nucleic acid) without the benefit of an enzyme to control the reaction. Since no enzyme is overseeing the process, “the sugar sticks to the protein haphazardly and sets the stage for yet more unintended and unregulated chemical reactions.” If blood sugar levels are fairly low, the sugar and protein will disengage and that’ll be the end of it. But if blood sugar is elevated, the process of forming AGEs will move forward, until a lot of AGEs will bind together and to other proteins, such that proteins that should have nothing to do with each other will be inexorably joined. Since 1980, AGEs have been linked directly to both diabetic complications and aging itself (hence the acronym). AGEs accumulate in the lens, cornea, and retina of the eye, where they appear to cause the browning and opacity of the lens characteristic of senile cataracts. AGEs accumulate in the membranes of the kidney, in nerve endings, and in the lining of arteries, all tissues typically damaged in diabetic complications. Because AGE accumulation appears to be a naturally occurring process, although it is exacerbated and accelerated by high blood sugar, we have evolved sophisticated defense mechanisms to recognize, capture, and dispose of AGEs. But AGEs still manage to accumulate in tissues with the passing years, and especially so in diabetics, in whom AGE accumulation correlates with the severity of complications. One protein that seems particularly susceptible to glycation and cross-linking is collagen, which is a fundamental component of bones, cartilage, tendons, and skin. The collagen version of an AGE accumulates in the skin with age and, again, does so excessively in diabetics. This is why the skin of young diabetics will appear prematurely old, and why…diabetes can be thought of as a form of accelerated aging, a notion that is slowly gaining acceptance. It’s the accumulation and cross-linking of this collagen version of AGEs that causes the loss of elasticity in the skin with age, as well as in joints, arteries, and the heart and lungs. As one scientist says, “Part of the problem with diabetes, and aging in general [is that] you end up with stiff tissue: stiffness of hearts, lungs, lenses, joints… That’s all caused by sugars reacting with 11 proteins.” Wow. It’s amazing what a panoply of negative outcomes—including aging itself!—can be caused by a high-carb diet. But there is no reason to believe that glucose-induced damage is limited only to diabetics, or to those with metabolic syndrome, in whom blood sugar is also chronically elevated. Glycation and oxidation accompany every fundamental process of cellular metabolism. They proceed continuously in all of us. Anything that raises blood sugar—in particular, the consumption of refined and easily digestible carbohydrates—will increase the generation of oxidants and free radicals; it will increase the rate of oxidative stress and glycation, and the formation and accumulation of advanced glycation end-products. This means that anything that raises blood sugar, by the logic of the carbohydrate hypothesis, will lead to more atherosclerosis and heart disease, more vascular disorders, and an accelerated pace of physical degeneration, even in those of us who never become diabetic. The reason that refined and simple carbohydrates like sugar and flour are especially bad is that, because they’re easier to digest, they produce a greater and faster rise in blood sugar and insulin after a meal. Complex carbohydrates such as starch take longer to digest, especially if they’re bound up with fiber (indigestible carbohydrates). They still aren’t great, though. But it isn’t quite that simple, because the sugar we typically eat (sucrose), in addition to having glucose that goes straight into the bloodstream, also has fructose, which instead goes straight to the liver and therefore doesn’t elevate blood sugar. So for a long time it was thought that there’s nothing wrong with consuming a lot of fructose or even sucrose. In 1986, the FDA actually said sugar (sucrose) probably isn’t a dietary evil! A couple years later, so did the Surgeon General and the National Academy of Sciences. As late as 2002, the Institute of Medicine of the National Academies of Science concluded there was still “insufficient evidence” to warn against consuming too much sugar! But the point is that when fructose goes to the liver, it’s converted into triglycerides—fat— and then shipped out on lipoproteins for storage. Therefore, the more fructose in the diet, the more fat in the blood. The high-fructose corn syrup flooding the market in these decades (with the blessing of the FDA) thus contributed to the obesity epidemic and the diabetes epidemic. And the increase in heart disease. Fructose also is more prone to forming AGEs than glucose. And it helps cause insulin resistance. As well as hypertension. 12 –That’s something I haven’t mentioned, by the way: what causes insulin resistance? Later in the book, Taubes gives his answer: chronically high levels of insulin themselves cause it. When cells are having too much glucose constantly being pushed on them because of excessive glucose and therefore insulin in the blood, they get fed up and say “No more!” Websites, whether rightly or wrongly, mention other causal factors too: excess body fat (frequently a result, as we’ve seen, of consuming carbohydrates, which can be converted into fat), physical inactivity, stress, insufficient sleep, certain medications (like statins), etc. In short, the modern lifestyle and diet tends to lead to insulin resistance, metabolic syndrome, and diabetes. These conditions are also associated with Alzheimer’s disease and cancer. Taubes’ discussion of the former is pretty complicated, but the upshot is that mechanisms have now been identified to make it plausible that eating excessive carbs and increasing insulin levels is a cause of Alzheimer’s. As for cancer, for a long time it was thought that fat and red meat were a significant cause. But by the end of the 1990s, according to Taubes, studies had largely refuted this “fatcholesterol hypothesis.” Some research, on the other hand, had found that sugar intake was positively correlated with both the incidence of and mortality from colon, rectal, breast, ovarian, prostate, kidney, nervous-system, and testicular cancer. This fact isn’t surprising, because many studies have shown that insulin provides fuel and growth signals to cancer cells. Already in the 1970s, researchers reported that malignant breast tumors had more receptors for insulin than did healthy tissue (implying that hyperinsulinemia would favor the growth of tumor cells). Also relevant is the insulin-like growth factor (IGF) secreted by the liver and other tissues. IGF sends growth and proliferation signals to cells, including to cancerous cells. But if insulin levels are high enough, insulin itself can stimulate cells’ IGF receptors—and can even make more IGF available to cells. What’s even worse is that tumor cells have more IGF receptors than healthy cells, just like they have more insulin receptors (to get the glucose they need to grow). So the chronically high levels of insulin and IGF induced by modern diets are great for cancerous cells. In general, then, it seems that people will tend to live longer if they have low levels of insulin and IGF and low blood sugar. Experiments on mice, worms, and fruit flies have supported this hypothesis. When scientists have induced mutations in the genes that control both insulin and IGF signaling, the organisms have lived much longer than usual. For example, in 2003 researchers in Paris reported that mice with only one copy of the gene for the IGF receptor (which meant that 13 cells would be relatively unresponsive to any IGF available in the blood) lived 25 percent longer than mice that had both copies of the gene. The last part of the book is devoted to the science of obesity and the regulation of weight, which so far Taubes hasn’t said much about. He introduces his discussion this way: The trouble with the science of obesity as it has been practiced for the last sixty years is that it begins with a hypothesis—that “overweight and obesity result from excess calorie consumption and/or inadequate physical activity,” as the Surgeon General’s Office recently phrased it—and then tries and fails to explain the evidence and the observations. The hypothesis nonetheless has come to be perceived as indisputable, a fact of life or perhaps the laws of physics, and its copious contradictions with the actual observations are considered irrelevant to the question of its validity. Fat people are fat because they eat too much or exercise too little, and nothing more ultimately need be said. A National Academy of Sciences report years ago contradicted this idea when it concluded that “Most studies comparing normal and overweight people suggest that those who are overweight eat fewer calories than those of normal weight.” It’s also noteworthy that percentage of fat in the diet decreased from the 1970s on, when the population’s weight was increasing. Presumably, then, low-fat diets aren’t a good way to lose weight. (Studies have confirmed this. For instance a Cochrane Collaboration study in 2002 and a USDA analysis in 2001. Semi-starvation diets are typically ineffective as a treatment of obesity.) Regarding the “sedentary behavior is responsible!” hypothesis, evidence accumulated by the CDC and other agencies suggested that in the 1990s, for example, Americans were no less physically active at the end of the decade than at the beginning, despite the continued rise in weight and obesity in those years. Besides, while low-income people tend to be more overweight, they are often the hardest-working people in society. They frequently work at more physically demanding jobs, or they work several jobs to make ends meet. Or think of the women among the Pima Indians in southwestern Arizona over a century ago. They were usually more obese than the men despite working much harder, spending their days harvesting crops and grinding corn, wheat, and mesquite beans. It’s more likely that their relatively new Western diets full of sugar and flour were to blame. 14 Exercise just isn’t a good way to lose weight. It rarely works well, especially in the long term. Study after study has confirmed this, not to mention a ton of anecdotal evidence. And it’s hardly surprising: as one physician calculated in 1942, “a 250-pound man will have to climb twenty flights of stairs to rid himself of the energy contained in one slice of bread!” Besides, when you’re physically active, you work up an appetite, so you tend to eat more. Obesity epidemics, by the way, are hardly a phenomenon unique to the contemporary world. Taubes gives paragraph after paragraph of examples of extreme weight gain among poor populations in non-industrialized or semi-industrialized societies. Here’s a sample: In a 1959 study of African Americans living in Charleston, South Carolina, nearly 30 percent of the adult women and 20 percent of the adult men were obese although living on family incomes of from $9 to $53 a week. In Chile in the early 1960s, a study of factory workers, most of whom were engaged in “heavy labor,” revealed that 30 percent were obese and 10 percent suffered from “undernourishment.” Nearly half the women over forty-five were obese. In Trinidad, a team of nutritionists from the United States reported in 1966 that one-third of the women older than twenty-five were obese, and they achieved this condition eating fewer than two thousand calories a day—an amount lower than the United Nations’ Food and Agriculture Organization recommendation to avoid malnutrition. Only 21 percent of the calories in the diet came from fat, compared with 65 percent from carbohydrates. Taubes spends many, many pages arguing against the still-common idea that obese people simply eat too much and/or aren’t physically active enough. The upshot of his discussion is that genetic, hormonal, and metabolic processes are why some people get fat when others don’t despite having comparable diets. “Some of us simply seem predisposed, if not fated, to put on weight from infancy onward.” Rather than someone’s getting fat being driven by hunger and sedentary behavior, hunger and sedentary behavior can be driven by a hormonal disposition to be overweight—“just as a lack of hunger and the impulse to engage in physical activity can be driven by a metabolic-hormonal disposition to burn calories rather than store them.” Some bodies are predisposed to burn up excess calories in cellular metabolism and increased physical activity, 15 whereas other bodies are predisposed to store excess calories. “The ability to burn up small excesses…on the order of a few hundred calories [consumed in excess] a day, is ‘well within the capacity of the ordinary person, but in the obese individual the power of flexibility is much less evident.’” Thus, “a critical variable in the facility with which we gain weight is whether we respond to superfluous calories by storing them away as fat and/or muscle or by converting them to heat and physical activity.” The body’s internal regulation to maintain a homeostatic equilibrium is a major reason why dieting often doesn’t result in a significant loss of weight. Restricting calories induces a slowing of metabolic rate, i.e., a reduction of energy expenditure in the body (less energy going to cells) to compensate for the loss of calories. People also get lethargic and less physically active because the body has slowed down the metabolism to compensate for the fewer calories coming in. Even semistarvation diets might not accomplish much, especially in the long term. Low-carb diets are a different story. By now, it’s widely known that people can lose a lot of weight on such a diet, so I needn’t go through the many studies Taubes describes. (You can lose weight by consuming as many calories as usual, as long as those calories don’t include carbs.) I should mention a few points, though, such as the common objection that one has to consume enough carbs for the brain and nervous system to get their necessary fuel from glucose. Here’s a useful paragraph: Though glucose is a primary fuel for the brain, it is not the only fuel, and dietary carbohydrates are not the only source of that glucose. If the diet includes less than 130 grams of carbohydrates, the liver increases its synthesis of molecules called ketone bodies, and these supply the necessary fuel for the brain and central nervous system. If the diet includes no carbohydrates at all, ketone bodies supply three-quarters of the energy to the brain. The rest comes from glucose synthesized from the amino acids in protein, either from the diet or from the breakdown of muscle, and from a compound called glycerol that is released when triglycerides in the fat tissue are broken down into their component fatty acids. In these cases, the body is technically in a state called ketosis, and the diet is often referred to as a ketogenic diet. 16 This keto diet, you may know, has become popular for losing weight. And it works: ketosis is when the body burns stored fat for energy instead of glucose, so of course if you stay on the diet long enough, you’ll probably lose fat. But how healthy is a keto diet if you stay on it for years? It seems to be perfectly healthy, despite what nutritionists and authorities may say. In fact, even an all-meat diet can be healthy! To give one example, in the early twentieth century the Harvard anthropologist Vilhjalmur Stefansson spent a decade eating nothing but meat among the Inuit in northern Canada, whom he insisted were completely healthy and vigorous. We still constantly hear that a varied diet is necessary for good health, but this appears to be false. You don’t really have to eat fruits and vegetables. Animal products contain all the essential amino acids and also twelve of the thirteen essential vitamins in large quantities. Only vitamin C is present in small quantities in animal foods. This is why nutritionists think that to avoid scurvy you have to eat fruits and vegetables. But, well, evidently that wasn’t true of the Inuit. Nor of other traders and explorers, such as Richard Henry Dana and his sailing crew in the midnineteenth century, who ate nothing but meat for sixteen months with no adverse consequences. Nor of Stefansson and another guy when they participated in a yearlong experiment (in 1929) overseen by scientists from Cornell and the Russell Sage Institute of Pathology. They ate nothing but meat, and were continually monitored and tested to make sure they weren’t cheating. By the end of the year they were in perfect health: had lost a few pounds of fat, had low blood pressure, no kidney damage or diminished function (as is thought to be a consequence of a high-protein diet), no scurvy, and Stefansson’s gingivitis had cleared up. So why didn’t they suffer from scurvy? Because a vitamin-C deficiency is yet another effect of consuming a lot of sugar and refined carbohydrates! (Same with the B vitamins.) So if you cut out the carbs, you don’t need a ton of vitamin C. The reason is that glucose and vitamin C use the same insulin-dependent transport system to get into cells, meaning they effectively compete against one another. If you increase blood-sugar levels, the cellular uptake of vitamin C drops. To overcome this adverse effect of sugar, it helps to eat fruits and vegetables. Another interesting conclusion from scores of experiments is that people can eat fewer calories in the form of fats and proteins and they won’t feel hungry, whereas they can eat far more calories in the form of carbohydrates and will still feel hungry. The medical-research establishment is apparently unable to explain this stubborn fact, but it cries out for an explanation. Just as the 17 idea that you can lose weight while eating unrestricted amounts of fat and protein demands an explanation. But I want to note, first, how contemptible, destructive, and arrogant the “experts” have always been on these issues. (As on so many others relating to politics, economics, history, and everything else.) “Claims that weight loss occurs even with high-caloric intake, but no carbohydrates, are absurd,” the American Medical Association declared in 1974 and insisted for a long time, dismissing studies, a ton of anecdotal evidence, and the testimony of physicians and patients. Even today you still constantly see false claims and bad recommendations on the websites of organizations like the AMA and the American Heart Association. You simply cannot ever trust what “the experts” say, on any given topic. Experts are nothing but embodiments of political institutions and interests. Millions upon millions of lives have been ruined and ended by the perverse medical advice of so-called experts. When good science contradicts their politically approved dogmas, they’ll do everything they can to suppress it and ignore it. For a long time, experts have thought that overeating and sedentary behavior are the causes of obesity, and the cure is to create a caloric deficit by eating less and/or expending more. But the truth is that overeating and inactivity are typically side effects of a metabolic and hormonal defect that prevents cells from getting the energy they need because calories, instead of going to the cells that need them, are being excessively deposited into fat tissue. “We overeat because we’re getting fat, not vice versa.” The body is trying to compensate for the inadequate energy it’s getting—as a result of the metabolic/hormonal defect that causes too much food to be deposited in adipose (fat) tissue—by inducing overeating…which itself then contributes to the obesity and still doesn’t allow cells to get enough energy! In a sense, the body is being internally starved even as it’s growing larger and larger. The hormonal defect is determined primarily by genetic inheritance, but in order for the defect to actually show up it has to be triggered by environmental factors, namely diet. “Since insulin is the hormone responsible for promoting the incorporation of fat into our adipose tissue and the conversion of carbohydrates into fat, the obvious [dietary] suspects are refined carbohydrates and easily digestible starches, which have well-documented effects on insulin.” In this hypothesis, obesity is another variation on the theme of insulin dysfunction and diabetes. In Type 1 diabetes, the cause is a lack of insulin. The result is an inability to use 18 glucose for fuel and to retain fat in the fat tissue, leading to internal starvation, excessive hunger, and weight loss. In obesity, the cause is an excess of insulin or an inordinate sensitivity to insulin by the fat cells; the result is an overstock of fuel in the adipose tissue and so, once again, internal starvation. But now the symptoms are weight gain and hunger. In obesity, the weight gain occurs with or without satisfying the hunger; in Type 1 diabetes, the weight loss occurs irrespective of the food consumed. As a brilliant physician named Alfred Pennington wrote in the 1940s-50s, “What happens when low-calorie diets are applied is that the starved tissues of the obese are starved further.” A more rational treatment would be one that makes fat flow readily out of the fat cells, that directs “measures primarily toward an increased mobilization and utilization of fuel” by the muscles and organs. He argued that this is what carbohydrate restriction accomplished. As Taubes says, “the cells would respond to this increased supply of fuel by accelerating the rate of metabolism— utilizing the fuel.” Meanwhile, the person’s appetite would decrease because of the accelerated flow of fat out of the adipose tissue, which itself, again, is a result of the faster metabolism, the heightened burning of energy in cells, triggered by a low-carb diet. The person would eat less because his fat tissue was shrinking, rather than—according to the conventional mainstream hypothesis—his fat tissue shrinking because he was eating less. Of course, obesity is more complex than just carbs, insulin, and genes. For one thing, regarding any particular individual, where he gains weight is determined by the lipophilia (“love of fat”) of that region. He or she might have a double chin or fat thighs or buttocks or ankles or a “beer belly”—and in many cases, it wasn’t by eating too much or because of a general metabolic defect. It’s more local than that. As a German endocrinologist named Julius Bauer said in the early twentieth century, “the genes responsible for obesity act upon the local tendency of the adipose tissue to accumulate fat (lipophilia) as well as upon the endocrine glands and those nervous centers which regulate lipophilia and dominate metabolic functions and the general feelings ruling the intake of food and the expenditure of energy. Only a broader conception such as this can satisfactorily explain the facts.” Taubes elaborates: Those of us who seem constitutionally predisposed to fatten simply have adipose tissue that is generally more lipophilic than that of lean individuals; our adipose tissue may be more apt to store fat or less willing to give it up when the body needs it. And if our adipose 19 tissue is so predisposed to accumulate excessive calories as fat, this will deprive other organs and cells of nutrients, and will lead to excessive hunger or lethargy. Even in cases of undernutrition, the abnormal lipophilic tissue might seize on foods and increase its stock at the expense of the whole organism, which could put the energy to better use. Bauer also suggested that insulin enhanced the deposition of glucose in the adipose tissue, exacerbating the problem of lipophilic tissue. American “experts” ignored Bauer’s ideas, but research on laboratory animals has supported them. Genetically obese mice will fatten regardless of how much they eat. Even if they’re starved, their bodies will prefer to consume the protein in their muscles and organs rather than the fat in their adipose tissue. They’ll even starve to death while they still have fat in them, far more fat than lean mice that are allowed to eat as much as they want! Here’s an interesting piece of trivia, by the way. We’re all familiar with squirrels that double their body weight in late summer to prepare for hibernation during the winter. We assume the way they double their weight is by eating much more. It turns out that’s not true. Even if they’re forced in laboratories to eat only as much as they ate in April, they’ll still gain the weight they need. “The seasonal fat deposition is genetically programmed—the animals will accomplish their task whether food is abundant or not. If they didn’t, a single bad summer could wipe out the species.” Let’s go into more depth about insulin. One of its functions, as I’ve said, is to lower blood sugar by facilitating the entry of glucose into cells—which is why diabetics, who have high blood sugar, take insulin therapy. In 1905, a German physician named Carl von Noorden argued that diabetes and obesity are consequences of the same defects in the mechanisms that regulate carbohydrate and fat metabolism. Updating his ideas to take account of the role of insulin, we can say that Type 1 diabetics, who can’t produce insulin, are unable either to use blood sugar as a source of energy or to convert it into fat (triglycerides) and store it—because insulin is crucial to this process too. So the body allows glucose to overflow into the urine, resulting in glycosuria, a primary symptom of diabetes. In the era before the discovery of insulin and insulin therapy, these diabetics became emaciated and wasted away because they couldn’t store fat. In obese people, on the other hand, the ability to get glucose into cells for energy is impaired, but not the ability to convert it to fat and store it. So instead of excreting glucose into 20 the urine, they transfer it to fat tissue. Von Noorden argued that over time, as the ability to burn glucose for energy further deteriorates and “the storage of the carbohydrates in the fat tissues also suffers a moderate and gradually progressing impairment” (perhaps there’s less room in the tissue for as much deposition of fat as before?), glucose chronically builds up in the blood, appears in the urine, and the person becomes diabetic. This is the transition from obesity to Type 2 diabetes. After insulin was discovered in 1921, it began to be used as a fattening hormone for chronically underweight patients. Insulin therapy increased their appetite for carbohydrates, and the latter in turn stimulated their insulin production (to deposit glucose both in cells that burned it as energy and in adipose tissue as fat), in a cycle that eventually brought them to a normal weight. Unfortunately for diabetics, this cycle makes them fatter, even when they’re obese to begin with. So insulin therapy for diabetics is very much a mixed bag, especially because the weight gain increases the risk of heart disease. (It also causes greater insulin resistance in cells, which leads to the need for even more insulin therapy, causing greater weight gain, etc.) But why, on a molecular level, do we get fat? What are the actual mechanisms going on? Taubes’ summary of the science of fat metabolism is fascinating and lengthy, but I can only describe some of the highlights. It was all understood by the 1970s, but somehow it still hasn’t been fully absorbed by mainstream thinking about human obesity. Scientists used to think that fat tissue (all over the body—under the skin, between organs, even in bones) is relatively inert, like a garbage can into which fat is deposited, but nothing could be farther from the truth. The triglyceride in the cells of adipose tissue is in a continuous state of flux, going in and out of cells according to the body’s momentary needs, all of it regulated by hormones and nerves that profusely crisscross the tissue. A triglyceride molecule is composed of three fatty acids linked together on a backbone of glycerol. Some of the triglycerides in fat tissue come from fat in our diet, while the rest come from carbohydrates. Fat is stored in fat cells in the form of triglycerides, but it enters and exists the cell in the form of free fatty acids (triglycerides are too big to slip through the cell membrane). It’s these fatty acids that, along with glucose, are burned as fuel in cells. As soon as free fatty acids pass into a fat cell, they’re immediately repackaged with glycerol into triglycerides, which themselves are continuously broken down (inside the cell) into free fatty acids. Back and forth, assembly and disassembly are constantly going on inside these fat cells. Fatty acids that aren’t immediately assembled into triglycerides slip back out of the cell and into the blood circulation 21 again, where many of them will be taken up by tissues and organs to be used as fuel. Those that aren’t—maybe about half—will go into the liver and be turned again into triglycerides, where they’ll be loaded onto lipoproteins (VLDL particles) and shipped back to the fat tissue for storage. This incredibly dynamic and repetitive process, this continuous flow of fatty acids out of fat cells and into the circulation, depends on the level of glucose in the blood. A single molecule, called glycerol phosphate, is pivotal to the whole system. This molecule is produced from glucose when it’s used for fuel in fat cells and the liver, and it (glycerol phosphate) is essential to the binding of three fatty acids into a triglyceride because it provides the glycerol molecule that links the three acids together. In fact, the rate at which fatty acids are assembled into triglycerides, and so the rate at which fat accumulates in the fat tissue, depend primarily on the availability of glycerol phosphate. The more glucose that is transported into the fat cells and used to generate energy, the more glycerol phosphate will be produced [as a byproduct of the burning of glucose]. And the more glycerol phosphate produced, the more fatty acids will be assembled into triglycerides. Thus, anything that works to transport more glucose into the fat cells—insulin, for example, or rising blood sugar—will lead to the conversion of more fatty acids into triglycerides, and the storage of more calories as fat. So you can already see why a high-carb diet can lead to weight gain: you need glucose to form triglycerides, and the more glucose there is in the blood, the more triglycerides. With low blood sugar, fewer fatty acids are bound up into triglycerides and more can escape into the blood, where they can be burned up as fuel in tissues and organs. With high blood sugar, more glycerol phosphate is produced (by cells’ use of glucose as fuel), which in turn increases the conversion of fatty acids into triglycerides, “so that they’re unable to escape into the bloodstream at a time when they’re not needed” (since the glucose that’s circulating can be used for cells’ energy needs). In fact, without at least some carbohydrates in the diet, it may be impossible to accumulate any excess body fat at all. For there won’t be any glycerol phosphate to create triglycerides (fat molecules). As an endocrinologist named Edgar Gordon wrote in 1963, “It may be stated categorically that the storage of fat, and therefore the production and maintenance of obesity, cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it also may be stated categorically that obesity is impossible 22 in the absence of adequate tissue concentrations of insulin.” Lower concentrations of insulin in the blood will therefore allow more fatty acids to flow out of adipose tissue, thus facilitating the body’s weight reduction. It should also be clear now why a kind of “internal starvation” can take place in the presence of high blood sugar, insulin, and obesity. For as more and more fatty acids are fixed in the fat tissue (due to the abundance of glycerol phosphate), energy available to cells all over the body is reduced by the “relative unavailability of fatty acids for fuel.” Another important point is that fructose is converted into glycerol phosphate more efficiently than is glucose. This is why fructose is considered the most lipogenic (fat-producing) carbohydrate. However, glucose is still needed to stimulate the pancreas to secrete insulin. What this suggests is that the combination of glucose and fructose—either in sucrose (table sugar) or in high-fructose corn syrup—is the best formula for stimulating fat synthesis and storing fat in the body’s tissues. No wonder obesity rates have climbed as high-fructose corn syrup has conquered American diets since the 1970s. What about lipophilia? Why do some parts of the body accumulate more fat than others? Insulin is relevant here, too. It has to do with an enzyme called lipoprotein lipase. A critical enzyme in this fat-distribution process is known technically as lipoprotein lipase, LPL, and any cell that uses fatty acids for fuel or stores fatty acids uses LPL to make this possible. When a triglyceride-rich lipoprotein passes by in the circulation, the LPL will grab on, and then break down the triglycerides inside into their component fatty acids. This increases the local concentration of free fatty acids, which flow into the cells—either to be fixed as triglycerides if these cells are fat cells, or oxidized for fuel if they’re not. The more LPL activity on a particular cell type, the more fatty acids it will absorb, which is why LPL is known as the “gatekeeper” for fat accumulation. Insulin is the main regulator of LPL activity, and the regulation functions differently between tissues and sites in the body. “In fat tissue, insulin increases LPL activity; in muscle tissue, it decreases activity. As a result, when insulin is secreted [because of the consumption of carbohydrates], fat is deposited in the fat tissue, and the muscles have to burn glucose for energy. When insulin levels drop [as with high-fat diets], the LPL activity on the fat cells decreases and the LPL activity on the muscle cells increases—the fat cells release fatty acids, and the muscle 23 cells take them up and burn them.” So this is another reason the body tends to lose fat on fatty diets. LPL activity is also affected by sex hormones, age, weight, and other factors. Women have greater LPL activity in their adipose tissue than men, which “may be one reason why obesity and overweight are now more common in women than in men.” Testosterone suppresses LPL activity in abdominal fat but has no effect on LPL in the hips and buttocks. So increasing fat accumulation in the abdomen as men age may be a result of both increasing insulin and decreasing testosterone. The obese have increased LPL activity in their fat tissue, so they gain more weight. As for diet, it seems that LPL activity in fat tissue increases with weight loss on a calorie-restricted diet and decreases in muscle tissue, causing fat to remain in fat tissue rather than being burned up by muscles. So this is another reason why low-calorie diets, unless they’re extreme, might not be very effective in losing weight. The science of fat metabolism, in short, is pretty unequivocal about the evils of carbohydrates (especially carbohydrate-dense starches and refined carbohydrates) and the benefits of dietary fat. And this science was thoroughly understood by the 1970s. Nevertheless, it’s precisely in the 1970s and 1980s that most authorities began saying high-carb diets weren’t the main problem! An enormous amount of evidence, presented at numerous conferences and in journal articles and books, already indicted such diets, but this had no effect on the developing consensus that fatty diets caused obesity and heart disease. I know it must be annoying to people who read my writings how often I harp on the theme that professional “intellectuals,” especially authorities, rarely have intellectual integrity, but as you can see, the evidence is pretty compelling. To give just one example: [In the 1960s and 1970s, authorities on nutrition] would readily admit that they didn’t know what caused obesity (why [as they saw it] some people ate too much and others didn’t) and that calorie restriction conspicuously failed to cure it. After nearly twenty years in the field, as Jean Mayer wrote in the introduction to his 1968 monograph, Overweight, he was “as aware as any man of the gigantic gaps in our knowledge—and of the likelihood that many of our present concepts may be erroneous.” He also noted, in his discussion of hormonal influences on obesity, that insulin “favors fat synthesis” and that someone who oversecretes insulin could “tend to become hungry as a result.” But when a physician suggested publicly, as Dr. Atkins did, that carbohydrates raised insulin levels, that insulin favors fat 24 synthesis, and that a diet lacking carbohydrates might reverse this process, these nutritionists would denounce it, as Mayer himself did in 1973, as “biochemical mumbojumbo.” The highly respected Harvard nutritionist Fred Stare ridiculed the Atkins diet, which recommended large amounts of meat and eggs, as “nonsense,” and condemned the author as “guilty of malpractice.” Of course, the exact reverse was closer to the truth. The American Medical Association, which has a hideous history (it’s an important reason, for example, why the U.S. doesn’t have national healthcare), even officially censured Atkins’ bestselling book, inadvertently demonstrating in its denunciatory report that a man with no ties to the medical establishment had a better understanding of the science of fat metabolism than the establishment. As I’ve already noted, it isn’t irrelevant that the authorities who were defending sugar and carbs (like Fred Stare’s department at Harvard) received a lot of money from the sugar industry and the soft-drink industry. Taubes gives some sordid examples. The book’s last chapter before the epilogue is an interesting discussion of the causes of the feelings of hunger and satiety, but I won’t go into detail on that. I’ll just say that, based as usual on his prodigious research, Taubes concludes (following the brilliant French scientist Jacques Le Magnen, who died in 2002) that the sensation of satiety is promoted by “anything that induces fatty acids to escape from the fat tissue and then be burned as fuel,” because the body will be getting the energy it needs and won’t have to keep eating. Contrariwise, anything that induces fat synthesis and storage, such as the elevation of insulin caused by carbohydrates, will promote hunger (at least relatively speaking) by removing the available fuel from the bloodstream. And it does seem from experience that a carbohydrate-rich meal is usually less filling than a protein-rich and fat-rich meal. For instance: “why is it that most of us can imagine eating a large bag (twenty ounces) of movie popcorn—more than eleven hundred calories if popped in oil, as it typically is— but not so the equivalent caloric amount of cheese: say, fifteen slices of American cheese, or a cup and a half of melted Brie?” It’s a good question. The simple explanation is that the insulin induced by the carbohydrates serves to deposit both fats and carbohydrates (fatty acids and glucose) as fat in the adipose tissue, and it keeps those calories fixed in the adipose tissue once they get there. As long as we respond 25 to the carbohydrates by secreting more insulin, we continue to remove nutrients from our bloodstream in expectation of the arrival of more, so we remain hungry, or at least absent any feeling of satiation. It’s not so much that fat fills us up as that carbohydrates prevent satiety, and so we remain hungry. The role of insulin in stimulating hunger is also suggested by Le Magnen’s experiments on rats. When he “infused insulin into sleeping rats, they immediately woke and began eating, and they continued eating as long as the insulin infusion continued. When during their waking hours he infused adrenaline—a hormone that promotes the mobilization [i.e., loss] of fatty acids from the fat tissue—they stopped eating.” In short, this book is an epic takedown of high-carb diets. In fact, it’s one of the best works of popular science I’ve ever read, practically a work of genius in its synthesis of an unbelievable amount of research. It isn’t the easiest of reads, and it’s a bit repetitive, but it illuminates a huge range of phenomena that are systematically obscured by most medical, scientific, and political authorities. One reviewer said it’s “easily the most important book on diet and health to be published in the past one hundred years.” Of course it doesn’t clear up everything—I still have a lot of questions about the etiology of heart disease and other conditions—but on what it does cover, it’s darned compelling.