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Fats, Carbs, and the Controversial Science of Diet and Health

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On Sale: September 25, 2007
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For decades we have been taught that fat is bad for us, carbohydrates better, and that the key to a healthy weight is eating less and exercising more. Yet despite this advice, we have seen unprecedented epidemics of obesity and diabetes. Taubes argues that the problem lies in refined carbohydrates, like white flour, easily digested starches, and sugars, and that the key to good health is the kind of calories we take in, not the number. In this groundbreaking book, award-winning science writer Gary Taubes shows us that almost everything we believe about the nature of a healthy diet is wrong.


Prologue: A Brief History of Banting

Farinaceous and vegetable foods are fattening, and saccharine matters are especially so….In sugar-growing countries the negroes and cattle employed on the plantations grow remarkably stout while the cane is being gathered and the sugar extracted. During this harvest the saccharine juices are freely consumed; but when the season is over, the superabundant adipose tissue is gradually lost.
–Thomas Hawkes Tanner, The Practice of Medicine, 1869

William Banting was a fat man. In 1862, at age sixty-six, the five-foot-five Banting, or “Mr. Banting of corpulence notoriety,” as the British Medical Journal would later call him, weighed in at over two hundred pounds. “Although no very great size or weight,” Banting wrote, “still I could not stoop to tie my shoe, so to speak, nor attend to the little offices humanity requires without considerable pain and difficulty, which only the corpulent can understand.” Banting was recently retired from his job as an upscale London undertaker; he had no family history of obesity, nor did he consider himself either lazy, inactive, or given to excessive indulgence at the table. Nonetheless, corpulence had crept up on him in his thirties, as with many of us today, despite his best efforts. He took up daily rowing and gained muscular vigor, a prodigious appetite, and yet more weight. He cut back on calories, which failed to induce weight loss but did leave him exhausted and beset by boils. He tried walking, riding horseback, and manual labor. His weight increased. He consulted the best doctors of his day. He tried purgatives and diuretics. His weight increased.

Luckily for Banting, he eventually consulted an aural surgeon named William Harvey, who had recently been to Paris, where he had heard the great physiologist Claude Bernard lecture on diabetes. The liver secretes glucose, the substance of both sugar and starch, Bernard had reported, and it was this glucose that accumulates excessively in the bloodstream of diabetics. Harvey then formulated a dietary regimen based on Bernard’s revelations. It was well known, Harvey later explained, that a diet of only meat and dairy would check the secretion of sugar in the urine of a diabetic. This in turn suggested that complete abstinence from sugars and starches might do the same. “Knowing too that a saccharine and farinaceous diet is used to fatten certain animals,” Harvey wrote, “and that in diabetes the whole of the fat of the body rapidly disappears, it occurred to me that excessive obesity might be allied to diabetes as to its cause, although widely diverse in its development; and that if a purely animal diet were useful in the latter disease, a combination of animal food with such vegetable diet as contained neither sugar nor starch, might serve to arrest the undue formation of fat.”

Harvey prescribed the regimen to Banting, who began dieting in August 1862. He ate three meals a day of meat, fish, or game, usually five or six ounces at a meal, with an ounce or two of stale toast or cooked fruit on the side. He had his evening tea with a few more ounces of fruit or toast. He scrupulously avoided any other food that might contain either sugar or starch, in particular bread, milk, beer, sweets, and potatoes. Despite a considerable allowance of alcohol in Banting’s regimen–four or five glasses of wine each day, a cordial every morning, and an evening tumbler of gin, whisky, or brandy–Banting dropped thirty-five pounds by the following May and fifty pounds by early 1864. “I have not felt better in health than now for the last twenty-six years,” he wrote. “My other bodily ailments have become mere matters of history.”

We know this because Banting published a sixteen-page pamphlet describing his dietary experience in 1863–Letter on Corpulence, Addressed to the Public–promptly launching the first popular diet craze, known farther and wider than Banting could have imagined as Bantingism. His Letter on Corpulence was widely translated and sold particularly well in the United States, Germany, Austria, and France, where according to the British Medical Journal, “the emperor of the French is trying the Banting system and is said to have already profited greatly thereby.” Within a year, “Banting” had entered the English language as a verb meaning “to diet.” “If he is gouty, obese, and nervous, we strongly recommend him to ‘bant,’ ” suggested the Pall Mall Gazette in June 1865.

The medical community of Banting’s day didn’t quite know what to make of him or his diet. Correspondents to the British Medical Journal seemed occasionally open-minded, albeit suitably skeptical; a formal paper was presented on the efficacy and safety of Banting’s diet at the 1864 meeting of the British Medical Association. Others did what members of established societies often do when confronted with a radical new concept: they attacked both the message and the messenger. The editors of The Lancet, which is to the BMJ what Newsweek is to Time, were particularly ruthless. First, they insisted that Banting’s diet was old news, which it was, although Banting never claimed otherwise. The medical literature, wrote The Lancet, “is tolerably complete, and supplies abundant evidence that all which Mr. Banting advises has been written over and over again.” Banting responded that this might well have been so, but it was news to him and other corpulent individuals.

In fact, Banting properly acknowledged his medical adviser Harvey, and in later editions of his pamphlet he apologized for not being familiar with the three Frenchmen who probably should have gotten credit: Claude Bernard, Jean Anthelme Brillat-Savarin, and Jean-François Dancel. (Banting neglected to mention his countrymen Alfred William Moore and John Harvey, who published treatises on similar meaty, starch-free diets in 1860 and 1861 respectively.)

Brillat-Savarin had been a lawyer and gourmand who wrote what may be the single most famous book ever written about food, The Physiology of Taste, first published in 1825.* In it, Brillat-Savarin claimed that he could easily identify the cause of obesity after thirty years of talking with one “fat” or “particularly fat” individual after another who proclaimed the joys of bread, rice, and potatoes. He added that the effects of this intake were exacerbated when sugar was consumed as well. His recommended reducing diet, not surprisingly, was “more or less rigid abstinence from everything that is starchy or floury.”

Dancel was a physician and former military surgeon who publicly presented his ideas on obesity in 1844 to the French Academy of Sciences and then published a popular treatise, Obesity, or Excessive Corpulence, The Various Causes and the Rational Means of Cure. Dancel’s thinking was based in part on the research of the German chemist Justus von Liebig, who, at the time, was defending his belief that fat is formed in animals primarily from the ingestion of fats, starches, and sugars, and that protein is used exclusively for the restoration or creation of muscular tissue. “All food which is not flesh–all food rich in carbon and hydrogen–must have a tendency to produce fat,” wrote Dancel. “Upon these principles only can any rational treatment for the cure of obesity satisfactorily rest.” Dancel also noted that carnivores are never fat, whereas herbivores, living exclusively on plants, often are: “The hippopotamus, for example,” wrote Dancel, “so uncouth in form from its immense amount of fat, feeds wholly upon vegetable matter–rice, millet, sugar-cane, &c.”

The second primary grievance that The Lancet’s editors had with Banting, which has been echoed by critics of such diets ever since, was that his diet could be dangerous, and particularly so for the credibility of those physicians who did not embrace his ideas. “We advise Mr. Banting, and everyone of his kind, not to meddle with medical literature again, but be content to mind his own business,” The Lancet said.

When Bantingism showed little sign of fading from the scene, however, The Lancet’s editors adopted a more scientific approach. They suggested that a “fair trial” be given to Banting’s diet and to the supposition that “the sugary and starchy elements of food be really the chief cause of undue corpulence.”

Banting’s diet plays a pivotal role in the science of obesity–and, in fact, chronic disease–for two reasons. First, if the diet worked, if it actually helped people lose weight safely and keep it off, then that is worth knowing. More important, knowing whether “the sugary and starchy elements of food” are “really the chief cause of undue corpulence” is as vital to the public health as knowing, for example, that cigarettes cause lung cancer, or that HIV causes AIDS. If we choose to quit smoking to avoid the former, or to use condoms or abstinence to avoid the latter, that is our choice. The scientific obligation is first to establish the cause of the disease beyond reasonable doubt. It is easy to insist, as public-health authorities inevitably have, that calories count and obesity must be caused by overeating or sedentary behavior, but it tells us remarkably little about the underlying process of weight regulation and obesity. “To attribute obesity to ‘overeating,’ ” as the Harvard nutritionist Jean Mayer suggested back in 1968, “is as meaningful as to account for alcoholism by ascribing it to ‘overdrinking.’ ”

After the publication of Banting’s “Letter on Corpulence,” his diet spawned a century’s worth of variations. By the turn of the twentieth century, when the renowned physician Sir William Osler discussed the treatment of obesity in his textbook The Principles and Practice of Medicine, he listed Banting’s method and versions by the German clinicians Max Joseph Oertel and Wilhelm Ebstein. Oertel, director of a Munich sanitorium, prescribed a diet that featured lean beef, veal, or mutton, and eggs; overall, his regimen was more restrictive of fats than Banting’s and a little more lenient with vegetables and bread. When the 244-pound Prince Otto von Bismarck lost sixty pounds in under a year, it was with Oertel’s regimen. Ebstein, a professor of medicine at the University of Göttingen and author of the 1882 monograph Obesity and Its Treatment, insisted that fatty foods were crucial because they increased satiety and so decreased fat accumulation. Ebstein’s diet allowed no sugar, no sweets, no potatoes, limited bread, and a few green vegetables, but “of meat every kind may be eaten, and fat meat especially.” As for Osler himself, he advised obese women to “avoid taking too much food, and particularly to reduce the starches and sugars.”

The two constants over the years were the ideas that starches and sugars–i.e., carbohydrates–must be minimized to reduce weight, and that meat, fish, or fowl would constitute the bulk of the diet. When seven prominent British clinicians, led by Raymond Greene (brother of the novelist Graham Greene), published a textbook entitled The Practice of Endocrinology** in 1951, their prescribed diet for obesity was almost identical to that recommended by Banting, and that which would be prescribed by such iconoclasts as Herman Taller and Robert Atkins in the United States ten and twenty years later.

Foods to be avoided:

1. Bread, and everything else made with flour . . .
2. Cereals, including breakfast cereals and milk puddings
3. Potatoes and all other white root vegetables
4. Foods containing much sugar
5. All sweets . . .

You can eat as much as you like of the following foods:

1. Meat, fish, birds
2. All green vegetables
3. Eggs, dried or fresh
4. Cheese
5. Fruit, if unsweetened or sweetened with saccharin, except bananas and grapes

“The great progress in dietary control of obesity,” wrote Hilde Bruch, considered the foremost authority on childhood obesity, in 1957, “was the recognition that meat . . . was not fat producing; but that it was the innocent foodstuffs, such as bread and sweets, which lead to obesity.”

The scientific rationale behind this supposed cause and effect was based on observation, experimental evidence, and maybe the collected epiphanies and anecdotes of those who had successfully managed to bant. “The overappropriation of nourishment seen in obesity is derived in part from the fat ingested with the food, but more particularly from the carbohydrates,” noted James French in 1907 in his Textbook of the Practice of Medicine. Copious opinions were offered, but no specific hypotheses. In his 1940 monograph Obesity and Leanness, Hugo Rony, director of the Endocrinology Clinic at the Northwestern University Medical School in Chicago, reported that he had carefully questioned fifty of his obese patients, and forty-one professed a “more or less marked preference for starchy and sweet foods; only 1 patient claimed preference for fatty foods.” Rony had one unusual patient, “an extremely obese laundress,” who had no taste for sweets, but “a craving for laundry starch which she used to eat by the handful, as much as a pound a day. . . .” So maybe carbohydrates are fattening because that’s what those with a tendency to gain weight eat to excess.

To others, carbohydrates carry some inherent quality that makes them uniquely fattening. Maybe they induce a continued sensation of hunger, or even a specific hunger for more carbohydrates. Maybe they induce less satiation per calorie consumed. Maybe they somehow cause the human body to preferentially store away calories as fat. “In Great Britain obesity is probably more common among poor women than among the rich,” Sir Stanley Davidson and Reginald Passmore wrote in the early 1960s in their classic textbook Human Nutrition and Dietetics, “perhaps because foods rich in fat and protein, which satisfy appetite more readily than carbohydrates, are more expensive than the starchy foods which provide the bulk of cheap meals.”

This belief in the fattening powers of carbohydrates can be found in literature as well. In Tolstoy’s Anna Karenina, for instance, written in the mid-1870s, Anna’s lover, Count Vronsky, abstains from starches and sweets in preparation for what turns out to be the climactic horse race. “On the day of the races at Krasnoe Selo,” writes Tolstoy, “Vronsky had come earlier than usual to eat beefsteak in the officers’ mess of the regiment. He had no need to be in strict training, as he had very quickly been brought down to the required weight of one hundred and sixty pounds, but still he had to avoid gaining weight, and he avoided starchy foods and desserts.” In Giuseppe di Lampedusa’s The Leopard, published in 1958, the protagonist, Prince Fabrizio, expresses his distaste for the plump young ladies of Palermo, while blaming their condition on, among other factors, “the dearth of proteins and the overabundance of starch in the food.”

This was what Dr. Spock taught our parents and our grandparents in the first five decades, six editions, and almost 50 million copies of Baby and Child Care, the bible of child-rearing in the latter half of the twentieth century. “Rich desserts,” Spock wrote, and “the amount of plain, starchy foods (cereals, breads, potatoes) taken is what determines, in the case of most people, how much [weight] they gain or lose.” It’s what my Brooklyn-born mother taught me forty-odd years ago. If we eat too much bread or too much spaghetti, we will get fat. The same, of course, is true of sweets. For over a century, this was the common wisdom. “All popular ‘slimming regimes’ involve a restriction in dietary carbohydrate,” wrote Davidson and Passmore in Human Nutrition and Dietetics, offering this advice: “The intake of foods rich in carbohydrate should be drastically reduced since over-indulgence in such foods is the most common cause of obesity.” “The first thing most Americans do when they decide to shed unwanted pounds is to cut out bread, pass up the potatoes and rice, and cross spaghetti dinners off the menu entirely,” wrote the New York Times personal-health reporter, Jane Brody, in her 1985 best-selling Good Food Book.

* When the first American edition of The Physiology of Taste was published in 1865, it was entitled The Handbook of Dining, or Corpulence and Leanness Scientifically Considered, perhaps to capitalize on the Banting craze.
** Endocrinology is the study of the glands that secrete hormones and the hormones themselves.

From the Hardcover edition.
Gary Taubes|Author Q&A

About Gary Taubes

Gary Taubes - Good Calories, Bad Calories

Photo © Kristen Lara Getchell

Gary Taubes is a contributing correspondent for Science magazine. His writing has appeared in The Atlantic, The New York Times Magazine, Esquire, and The Best of the Best American Science Writing (2010). He has received three Science in Society Journalism Awards from the National Association of Science Writers, the only print journalist so recognized. He is currently a Robert Wood Johnson Foundation Investigator in Health Policy Research at the University of California, Berkeley School of Public Health. He lives in Oakland.

Gary Taubes is represented by Random House Speakers Bureau (www.rhspeakers.com)

Author Q&A

A conversation with


author of


Q: You make claims in this book that counter everything we’ve been told. You argue that exercise has little or no effect on how much we weigh, that fattening is not about how many calories we eat but what kind of calories we eat. Really?

A: I spend the second half of my book making a very simple point: obesity is not a disorder of over-eating or sedentary behavior, but rather a disorder of excess fat accumulation. If you consider obesity as a disorder of fat accumulation, then the natural question is: what regulates fat accumulation? Simple answer: insulin. And what regulates insulin levels? Again a simple answer: carbohydrates. This explains why carbohydrates were considered uniquely fattening from the 1830s until the 1960s. And it explains why carbohydrate-restricted diets, unrestricted in calories (like the Atkins and South Beach diets), seem to be so effective at causing weight loss. One of the most bizarre aspects of the story in Good Calories, Bad Calories is why obesity researchers and clinicians in this country decided that the hormonal regulation of fat tissue is somehow irrelevant to the question of why we grow fat. I still have trouble believing that this actually happened, but it’s all too easy to find obesity authorities who have spent their entire professional careers studying obesity and giving advice, and yet don’t have any idea what hormones actually regulate fat accumulation.

Q: Everywhere we look, from Cheerios boxes to New York City’s recent ban on trans fats, we see the message that minimizing dietary fat will help prevent obesity and heart disease. How did we come to believe this “conventional wisdom” and when/how did you begin to doubt it?

A: We first came to believe this fifty years ago primarily because a handful of medical researchers of very dubious quality came to believe it unconditionally. They managed to get the American Heart Association to go along, which in turn convinced the health reporters and the politicians and it spread from there. The evidence never came around to support it, but after a while nobody cared. Or at least they didn’t consider the copious evidence refuting the hypothesis to be an impediment to believing that it was true.I came to doubt it initially because I had interviewed some of these people when I was doing an investigative article for the journal Science on the equally unsubstantiated belief that eating salt causes hypertension. My previous two books were about how hard it is to conduct good science, how rigorous and skeptical the scientists have to be, and here I was interviewing these prestigious and respected medical authorities, and they didn’t seem to have a clue what real science was all about. I decided to look into the fat story, knowing nothing about it, simply because these people were involved and claimed to have played significant roles. What I found was the scientific equivalent of a house of cards. These people would do a study to test their beliefs and it would come out either negative or just ambiguous. Then they’d interpret it as supporting their preferred hypothesis—that all fat or just saturated fat was harmful—in light of the fact that there were other studies that also supported their beliefs. And when I looked at the other studies, those were equally ambiguous but were in turn interpreted as supportive because still other studies appeared to support the fat-is-bad hypothesis. And that’s how it went, all the way down and back to the beginning. To mix my metaphors, there was a lot of smoke, but never any fire.

Q: Insulin plays a vital role in food digestion. Its function (and dysfunction) is central to Type II diabetes, the most common form of the disease. When we eat certain types of foods (sweets versus fats, refined versus unrefined), what effects do these foods have on insulin levels in the body?

A: Insulin is the hormone that our body uses to partition the fuels we consume. It tells us to store fats and protein and burn carbohydrates. So we secrete it when we eat carbohydrates and, to a lesser extent, protein, and the easier it is for us to digest the carbs, the more insulin we secrete. So we secrete more insulin in response to white rice, for instance, than brown rice, or white bread than pumpernickel. Because insulin plays such a fundamental role in how our bodies work, this over-secretion of insulin has profound effects all over. It causes a condition called insulin resistance, which means we have to secrete even more insulin to handle the carbohydrates we eat. The result is this vicious cycle that then seems to lead to virtually every common chronic disease. What it certainly does is make us fat, because insulin works directly on the cells of our fat tissue to tell them to accumulate ever more fat. In general, the higher your insulin levels, the fatter you’ll be.

Q: You not only relate the consumption of refined carbohydrates and sugars to weight gain and the escalation of Type II diabetes, you also relate our eating habits to cancer and dementia. Can’t these phenomena be caused by other factors, such as toxic chemicals in our environment?

A: It’s possible, but what I’m talking about is a common pattern with all of these diseases. Certainly with cancer, when researchers have looked at the cancer patterns of populations and how their incidence changes over time, they’ve concluded that most cancers are indeed preventable, in that inevitably you can find some population that doesn’t get a particular cancer or gets it at a very low level. But whereas a tiny percent of these cancers might be explicable by pollutants or toxic chemicals in the workplace, the great majority of them seem to be caused by cigarettes and, even more so, by some aspect of our diet or lifestyle.

Type II diabetics have a higher risk of Alzheimer’s and cancer, just as they have a higher risk of heart disease and obesity. And when you consider that Type II diabetes is characterized by this condition of insulin resistance, it suggests that having relatively high blood sugar and insulin levels makes you more susceptible to these diseases or even somehow causes them. I looked in the scientific literature for mechanisms that could explain how insulin and blood sugar could actually play a causal role in these diseases, and these mechanisms are very easy to find. So while toxic chemicals in our environment play a role, the evidence suggests that it’s a much, much smaller role than we might think. Diet and lifestyle are more likely culprits, which makes one wonder about foods that raise insulin and blood sugar levels—i.e., refined and easily digestible carbohydrates and sugars.

Q: Tell us about the dangers of the high-fructose corn syrup Americans have been consuming in large quantities over the last few decades, just as the rate of obesity has been increasing.

A: The dangers of high-fructose corn syrup or HFCS, as it’s called, are real, but we actually pay it too much attention because HFCS in the form that it’s usually found—in sodas and fruit juices and yogurts, etc.—is effectively equivalent to sugar. Both are effectively half glucose and half fructose. It’s the fructose that makes them so sweet. In our bodies, the glucose works to raise our insulin and blood sugar levels. The fructose is dumped directly on the liver, and so increases the amount of fat we store and also, probably, leads to insulin resistance in the long run. When you talk to biochemists who specialize in fructose metabolism, as opposed to say, diabetes specialists who only worry about blood sugar, they’ll tell you that HFCS or table sugar are the worst of all carbohydrates because they have this dual effect.

Q: If we want to lose weight (and thus avoid related health problems), can’t we simply eat fewer calories and exercise more? Why focus on carbohydrates versus fats?

A: First of all, the actual evidence suggests that eating less and exercising more doesn’t make a bit of difference. Secondly, obese people spend their whole life eating less or at least trying to and it doesn’t help. If it did, they wouldn’t be obese. The fact that a doctor or a health agency or a newspaper reporter tells them they should eat less, doesn’t make it work any better. The thing everyone ignores in this business is that our fat tissue seems to be very well regulated—just as it is in every animal. That’s why we get fat in some places and not in others. We’ve all seen men with big pot bellies and skinny legs. That’s the result of the hormonal regulation of fat tissue. It’s also why men and women fatten differently. Why when men go through puberty they lose fat and women tend to gain it. It’s why women put on fat when they get pregnant.

So the obvious question is: what regulates fat accumulation? And it turns out that sex hormones are involved and, more than anything, insulin. Insulin is the only hormone that tells our fat cells to accumulate fat. When insulin levels are elevated, we store fat. And we can’t get rid of that fat without first lowering insulin levels. So what determines how much insulin we secrete? Carbohydrates. It’s actually that simple. As one former Harvard professor of medicine said to me, “carbohydrates is driving insulin is driving fat.” We do not secrete insulin in response to the fat we eat. What else do you need to know? One reason my book is relatively lengthy is because I spend a lot of time explaining why something so simple could be ignored for so long.

Q: When you discuss blood cholesterol levels in your book, the evidence you present challenges the emphasis doctors put on lowering cholesterol levels. Should we stop worrying about cholesterol, and if so, why?

A: The point is that it’s not the cholesterol itself in the blood that determines your risk of heart disease. It’s not even the LDL cholesterol. It appears to be the LDL particle itself. LDL stands for low density lipoprotein and that’s one of the particles that carries cholesterol and fats around in your blood stream. The idea that cholesterol itself is bad is an idea that dates to the 1970s. Since then, research has shown pretty conclusively that it’s the size and density of the LDL particle that is the risk factor for heart disease. Small, dense LDL is dangerous. Large fluffy LDL is not. And what makes for small, dense LDL: eating a lot of carbohydrates. Fat seems to have no effect. This has been a problem for policy makers, because they’d like to include small, dense LDL as an “official” risk factor for heart disease, but when they try to do so, they’re stuck with this evidence that it’s not fat or even saturated fat that increases the risk of heart disease, but carbs.

Q: What do you, as a science journalist rather than a doctor, bring to the subject that will change our minds?

A: Perspective. I had no vested interest. I wasn’t taught in graduate or medical school that something was true and so never thought to question it. As a journalist, I question everything. And because my initial training was in physics and I had spent the last 20 years writing about controversial science, I know what’s required to do good science, the need to be skeptical of everything and, perhaps most importantly, to be skeptical of your own pet theories. Once I started my research, I just followed the evidence, not just a study here and there that supports a given point of view but all of the science. All the disciplines, not just a given one. I had no investment in any particular point of view, though I had my hunches based on preliminary research. Some of these hunches turned out to be right; some were wrong. One advantage I had working in the 21st century was that I could do an immense amount of research in a relatively short period of time. The internet allowed me to identify and locate virtually every source, every paper, every book of relevance. Then whatever I couldn’t download or buy or have mailed to me, I had researchers get from various libraries. At one point I had five young researchers working for me, going to different libraries in different cities, getting me the books and articles I needed to make sense of this stuff.

Q: What makes us feel hungry? What keeps us feeling full?

A: The current theories on hunger all aim to explain what’s happening in the brain that prompts us to eat. Is it leptin levels rising or falling? Glucose? Is it fatty acids? Things like that. The idea I lay out in the book is that hunger and satiety are the body’s response to the ebbing and flowing of fuels at the cellular level. After all, it’s the cells of our tissues and organs that use the fuel. In fact, our brain is pretty much protected against fuel shortages until we’re in the end stages of starvation. So the question becomes: what is it that regulates the availability of fuel at a cellular level? That job once again is handled fundamentally by insulin. One of the things that insulin does is empty the blood stream of available fuel—of glucose and fatty acids. This would explain why true hunger often begins only after we start eating. This is why the first course of a meal is known as an appetizer. It increases our appetite and it does so by prompting us to secrete insulin. The insulin empties our blood stream of fuels, and we get hungry and eat. Because carbohydrates make us over-secrete insulin, they not only make us hungrier than fats and proteins do, but they tend to keep us hungry longer. This is why it’s considerably easier to over-eat carbohydrate-rich foods—pasta, for instance, or popcorn. On the other hand, when we eat foods that are mostly fat and protein, we tend to feel sated.

Q: How should the research into nutrition actually be conducted? Why has so little research been conducted effectively?

A: The only way to establish with any certainty which foods or diets are healthy in the long run is to do what are known as randomized controlled trials, and to run them for a long time. Take a few thousand or tens of thousands of willing subjects, assign half of them at random to eat one diet and half to another, and keep them at it for a decade or more. This kind of study was planned in the 1960s to test the idea that low-fat diets are good for us, but it never got done because these studies are very hard to do correctly and ludicrously expensive. They can cost hundreds of millions or even a few billion dollars each. The problem is that you can’t know the truth without doing them. So the medical and public health authorities have tried to get around this problem by doing what are called observational studies: look at a huge population people—say, once again, tens of thousands —and try to get an accurate record of what they eat, then follow them to assess their relative health and well-being. But these observational studies can never reliably establish cause and effect. This is a subject I discuss at length in my September 16th New York Times Magazine cover story. These studies can never be trusted to get the right answer, no matter how large they are or how consistently they see the same associations. A lot of the things we’re told these days about what constitutes a healthy diet and lifestyle comes from these observational studies, and there’s simply no way to know if they’re right. As I argue in the epilogue of Good Calories, Bad Calories, we have to bite the bullet and pay for long-term randomized trials—and perhaps figure out more effective ways to do them—or we’ll never know the truth.

Q: When you’re not pouring over medical studies, what do you observe about the health and habits of people around you? If you could offer them a few pieces of advice, what would you say?

A: It’s hard to spend a significant portion of your life studying diet and health and not want to interject yourself into someone’s life when you see them eating in a way you’ve come to consider unhealthy. Nonetheless, I treasure my friends and family and try to keep my thoughts buried far beneath the surface. If anyone asks for advice, I tell them, of course, to avoid the easily digestible carbohydrates, stay away from sugar in any form, and eat the foods we evolved to eat: meat, fish, fowl, eggs and the non-starchy vegetables.

Q: What’s for dinner at your house tonight?

A: Well, living in Manhattan and having a kitchen smaller than most peoples’ closets, we tend to have dinner delivered and that decision is always a last minute thing. If it helps any, I had eggs and sausage for breakfast and a hamburger (without the bun) for lunch. I’m a creature of habit.

From the Hardcover edition.



“A vitally important book, destined to change the way we think about food.” —Michael Pollan, author of In Defense of Food“Gary Taubes is a brave and bold science journalist who does not accept conventional wisdom.” —The New York Times“A very important book.” —Dr. Andrew Weil “Brilliant and enlightening. . . . Taubes is a relentless researcher.” —The Washington Post“Easily the most important book on diet and health to be published in the past one hundred years. It is clear, fast-paced and exciting to read, rigorous, authoritative, and a beacon of hope for all those who struggle with problems of weight regulation and general health.” —Richard Rhodes“A watershed. . . . Lucid and lively. . . . It could literally change the way you eat, the way you look and how long you live.” —Minneapolis Star Tribune“Taubes tackles the subject with the seriousness and scientific insight it deserves, building a devastating case against the low-fat, high-carb way of life endorsed by so many nutrition experts in recent years.” —Barbara Ehrenreich
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