Good Calories, Bad Calories Part 1

Good Calories, Bad Calories.

Challenging the Conventional Wisdom on Diet, Weight Control, and Diseas.

by Gary Taubes.

Prologue.

A BRIEF HISTORY OF BANTING.

Farinaceous and vegetable foods are fattening, and saccharine matters are especial y 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 gradual y 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 cal him, weighed in at over two hundred pounds. "Although no very great size or weight," Banting wrote, "stil 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 appet.i.te, 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 eventual y consulted an aural surgeon named Wil iam 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 acc.u.mulates excessively in the bloodstream of diabetics. Harvey then formulated a dietary regimen based on Bernard's revelations. It was wel 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 al ied 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, usual y 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 al owance of alcohol in Banting's regimen -four or five gla.s.ses of wine each day, a cordial every morning, and an evening tumbler of gin, whisky, or brandy-Banting dropped thirty-five pounds by the fol owing 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 wel 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 occasional y 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 a.s.sociation. 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 al which Mr. Banting advises has been written over and over again." Banting responded that this might wel 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 Bril at-Savarin, and Jean-Francois Dancel. (Banting neglected to mention his countrymen Alfred Wil iam Moore and John Harvey, who published treatises on similar meaty, starch-free diets in 1860 and 1861 respectively.) Bril at-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.*1 In it, Bril at-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 wel . 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. "Al food which is not flesh-al 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 whol y upon vegetable matter-rice, mil et, 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 real y 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 actual y 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 "real y 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 tel s 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 sp.a.w.ned a century's worth of variations. By the turn of the twentieth century, when the renowned physician Sir Wil iam 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; overal , 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 Gottingen and author of the 1882 monograph Obesity and Its Treatment, insisted that fatty foods were crucial because they increased satiety and so decreased fat acc.u.mulation. Ebstein's diet al owed no sugar, no sweets, no potatoes, limited bread, and a few green vegetables, but "of meat every kind may be eaten, and fat meat especial y." 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 const.i.tute the bulk of the diet. When seven prominent British clinicians, led by Raymond Greene (brother of the novelist Graham Greene), published a textbook ent.i.tled The Practice of Endocrinology *2 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 Tal er 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 al other white root vegetables 4. Foods containing much sugar 5. Al sweets...

You can eat as much as you like of the following foods: 1. Meat, fish, birds 2. Al 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 col ected epiphanies and anecdotes of those who had successful y 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 careful y 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 preferential y 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 Pa.s.smore wrote in the early 1960s in their cla.s.sic textbook Human Nutrition and Dietetics, "perhaps because foods rich in fat and protein, which satisfy appet.i.te 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 wel . 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 stil 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 mil ion 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 wil get fat. The same, of course, is true of sweets. For over a century, this was the common wisdom. "Al popular 'slimming regimes' involve a restriction in dietary carbohydrate," wrote Davidson and Pa.s.smore in Human Nutrition and Dietetics, offering this advice: "The intake of foods rich in carbohydrate should be drastical y 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, pa.s.s 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-sel ing Good Food Book.

But by that time there had been a sea change. Now even Brody herself was recommending a diet rich in potatoes, rice, and spaghetti for the same purpose. "We need to eat more carbohydrates," Brody declared. "Not only is eating pasta at the height of fas.h.i.+on.... It can help you lose weight." The carbohydrate had become heart-healthy diet food. Now it was the b.u.t.ter rather than the bread, the sour cream on the baked potato that put on the pounds. The bread and the potato themselves were no longer the cause of weight gain but the cure. When a committee of British authorities compiled their "Proposals for Nutritional Guidelines for Health Education in Britain" in 1983, they had to explain that "the previous nutritional advice in the UK to limit the intake of al carbohydrates as a means of weight control now runs counter to current thinking...."

This was one of the more remarkable conceptual s.h.i.+fts in the history of public health. As clinical investigators were demonstrating the singular ability of carbohydrate-restricted diets to generate significant weight loss without hunger,*3 the mainstream medical establishment was insisting, as in a 1973 editorial by the American Medical a.s.sociation, that the diets were dangerous fads-"bizarre concepts of nutrition and dieting [that] should not be promoted to the public as if they were established scientific principles."

Just four months after the AMA publicly censured the use of these diets in The Journal of the American Medical a.s.sociation, obesity researchers from around the world gathered in Bethesda, Maryland, for the first conference on obesity ever hosted by the National Inst.i.tutes of Health. The only talk on the dietary treatment of obesity was presented by Charlotte Young, a wel -known diet.i.tian and nutritionist at Cornel University who had been studying and treating obesity for twenty years.

Young first discussed the work of Margaret Ohlson, chair of nutrition at Michigan State University, who had tested carbohydrate-restricted diets in the early 1950s. "The diets developed by Ohlson," reported Young, "gave excel ent clinical results as measured by freedom from hunger, al aying of excessive fatigue, satisfactory weight loss, suitability for long term weight reduction and subsequent weight control." She then presented the results of her research at Cornel , testing Banting-like diets on overweight young men. As in the other reports over the last century, she noted, her subjects seemed to lose weight by restricting only sugars and starches, without feeling any particular sense of hunger. Moreover, the less carbohydrates in their diets, the greater their weight loss, even though al her subjects were eating equivalent amounts of calories and protein. "No adequate explanation could be given," Young reported, implying that further scientific research might be important to clarify this issue.

None would be forthcoming, and a century of empirical evidence would be rendered irrelevant, as the AMA's spin on Banting's low-carbohydrate diet as fad was quickly adopted as the conventional wisdom, one that has been adhered to faithful y ever since. Dietary fat had been identified as a probable cause of heart disease, and low-fat diets were now being advocated by the American Heart a.s.sociation as the means of prevention. At the same time, the low-fat diet as the ideal treatment for weight loss was adopted as wel , even though a low-fat diet was, by definition, high in the very carbohydrates that were once considered fattening.

This transformation is al the more remarkable because the medical authorities behind it were concerned with heart disease, not obesity. They presented no dramatic scientific data to support their beliefs, only ambiguous evidence, none of which addressed the efficacy of low-fat diets in weight loss. What they did have was the diet-heart hypothesis, which proposed that the excessive consumption of fat in our diets-particularly saturated fats-raises cholesterol levels and so causes atherosclerosis, heart disease, and untimely death. The proponents of this theory believed that Americans-and later the entire developed world-had become gluttons. Americans ate too much of everything-particularly fat-because we could afford to, and because we could not or would not say no. This overnutrition was certainly the cause of obesity. Eating too many calories was the problem, and since fat contains more than twice as many calories per gram as either protein or carbohydrates, "people who cut down on fat usual y lose weight," as the Was.h.i.+ngton Post reported in 1985.

A healthy diet, by definition, had suddenly become a low-fat diet. Beginning in the late 1980s with publication of The Surgeon General's Report on Nutrition and Health, an entire research industry arose to create palatable nonfat fat subst.i.tutes, while the food industry spent bil ions of dol ars marketing the less-fat-is-good-health message. The U.S. Department of Agriculture's (USDA's) booklet on dietary guidelines, and its ubiquitous Food Guide Pyramid, recommended that fats and oils be eaten "sparingly," while we were now to eat six to eleven servings per day of the pasta, potatoes, rice, and bread once considered uniquely fattening.

The reason for this book is straightforward: despite the depth and certainty of our faith that saturated fat is the nutritional bane of our lives and that obesity is caused by overeating and sedentary behavior, there has always been copious evidence to suggest that those a.s.sumptions are incorrect, and that evidence is continuing to mount. "There is always an easy solution to every human problem," H. L. Mencken once said-"neat, plausible, and wrong." It is quite possible, despite al our faith to the contrary, that these concepts are such neat, plausible, and wrong solutions. Moreover, it's also quite possible that the low-fat, high-carbohydrate diets we've been told to eat for the past thirty years are not only making us heavier but contributing to other chronic diseases as wel .

Consider, for instance, that most reliable evidence suggests that Americans have indeed made a conscious effort to eat less fat, and particularly less saturated fat, since the 1960s. According to the USDA, we have been eating less red meat, fewer eggs, and more poultry and fish; our average fat intake has dropped from 45 percent of total calories to less than 35 percent, and National Inst.i.tutes of Health surveys have doc.u.mented a coincident fal in our cholesterol levels. Between 1976 and 1996, there was a 40-percent decline in hypertension in America, and a 28-percent decline in the number of individuals with chronical y high cholesterol levels. But the evidence does not suggest that these decreases have improved our health.

Heart-disease death rates have indeed dropped over those years. The risk of suffering a severe heart attack, what physicians cal an acute myocardial infarction, may have diminished as wel . But there is little evidence that the incidence of heart disease has declined, as would be expected if eating less fat made a difference. This was the conclusion, for instance, of a ten-year study of heart-disease mortality published in The New England Journal of Medicine in 1998, which suggested that the death rates are declining largely because doctors and emergency-medical-service personnel are treating the disease more successful y. American Heart a.s.sociation statistics support this view: between 1979 and 2003, the number of inpatient medical procedures for heart disease increased 470 percent. In 2003 alone, more than a mil ion Americans underwent cardiac catheterizations; more than a quarter-mil ion had coronary-artery bypa.s.s surgery.

The percentage of Americans who smoke cigarettes has also dropped considerably over the years-from 33 percent of Americans over eighteen in 1979 to 25 percent fifteen years later. This should also have significantly reduced the incidence of heart disease. That it hasn't, strongly suggests we're doing something that counteracts the beneficial effect of giving up cigarettes. Indeed, if the last few decades were considered a test of the fat-cholesterol hypothesis of heart disease, the observation that the incidence of heart disease has not noticeably decreased could serve in any functioning scientific environment as compel ing evidence that the hypothesis is wrong.

Throughout the world, on the other hand, the incidence of obesity and diabetes is increasing at an alarm in grate. Obesity levels in the United States remained relatively constant from the early 1960s through 1980, between 12 and 14 percent of the population; over the next twenty-five years, coincident with the official recommendations to eat less fat and so more carbohydrates, it surged to over 30 percent. By 2004, one in three Americans was considered clinical y obese. Diabetes rates have increased apace. Both conditions are a.s.sociated with an increased risk of heart disease, which could explain why the incidence of heart disease is not decreasing. It is also possible that obesity, diabetes, and heart disease al share a single, underlying cause. The surge in obesity and diabetes occurred as the population was being bombarded with the message that dietary fat is dangerous and that carbohydrates are good for the heart and for weight control. This suggests the possibility, however heretical, that this official embrace of carbohydrates might have had unintended consequences.

I first heard this notion in 1998, when I interviewed Wil iam Harlan, then a.s.sociate director of the Office of Disease Prevention at the National Inst.i.tutes of Health. Harlan told me that public-health experts like himself a.s.sumed that if they advised al Americans to eat less fat, with its densely packed calories, weights would go down. "What we see instead," he said, "is actual y weights have gone up, the portion sizes have gone up, the amount we eat has gone up.... Foods lower in fat became higher in carbohydrates and people ate more."

The result has been a polarization on the subject of nutrition. Most people stil believe that saturated fat, if not any and al fat, is the primary dietary evil-that b.u.t.ter, fat, cheese, and eggs wil clog our arteries and put on weight-and have reduced their intakes. Public-health experts and many in the media insist that the obesity epidemic means the population doesn't take their advice and continues to shun physical activity while eating fatty foods to excess. But a large number of people have turned to the message of Banting and one remarkably best-sel ing diet book after another: Eat Fat and Grow Slim (1958), Calories Don't Count (1961), The Doctor's Quick Weight Loss Diet (1968), Dr. Atkins' Diet Revolution (1972), The Complete Scarsdale Medical Diet (1978), The Zone (1995), Protein Power (1996), Sugar Busters! (1998), and The South Beach Diet (2003). Al advocate an alternative hypothesis: that carbohydrates are the problem, not fat, and if we eat less of them, we wil weigh less and live longer. Al have been summarily dismissed by the American Heart a.s.sociation, the American Medical a.s.sociation, and nutritional authorities as part of a misguided fad.

But is it? If 150 years of anecdotal evidence and observation suggest that carbohydrates are uniquely fattening, it would be unjustifiable scientifical y to reject that hypothesis without compel ing evidence to the contrary. Such evidence does not exist. My purpose here is to examine the data that do exist and to demonstrate how we have reached the conclusions we have and whether or not they are justified.

There is a more important issue here as wel , and it extends far beyond the ideal weight-loss diet. Prior to the official acceptance of the low-fat-is-good-health dogma, clinical investigators, predominantly British, had proposed another hypothesis for the cause of heart disease, diabetes, colorectal and breast cancer, tooth decay, and half-dozen or so other chronic diseases, including obesity. The hypothesis was based on decades of eyewitness testimony from missionary and colonial physicians and two consistent observations: that these "diseases of civilization" were rare to nonexistent among isolated populations that lived traditional lifestyles and ate traditional diets, and that these diseases appeared in these populations only after they were exposed to Western foods-in particular, sugar, flour, white rice, and maybe beer. These are known technical y as refined carbohydrates, which are those carbohydrate-containing foods-usual y sugars and starches-that have been machine-processed to make them more easily digestible.

In the early 1970s, the hypothesis that refined carbohydrates cause heart disease and other chronic diseases competed directly with the dietary-fat hypothesis of heart disease. Carbohydrates could not cause heart disease, so the argument went, because fat seemed to cause heart disease. Moreover, any diet that contained a suitably low proportion of calories as fat would, by definition, be high in carbohydrates, and vice versa. The only caveat was that the fat hypothesis was, indeed, only a hypothesis, and the evidence to support it was ambiguous at best. By the mid-1970s, the carbohydrate theory of chronic disease had been transformed into a more political y and commercial y acceptable version: it wasn't the addition of refined and starchy carbohydrates to the diet that caused chronic disease, but the absence of fiber or roughage, removed in the refining process, that was responsible. This conclusion, however, has not been supported by clinical trials, which have shown that fiber has little or no effect on the incidence of any chronic disease.

We have come to accept over the past few decades the hypotheses-and that is what they are-that dietary fat, calories, fiber, and physical activity are the critical variables in obesity and leanness in health and disease. But the fact remains that, over those same decades, medical researchers have elucidated a web of physiological mechanisms and phenomena involving the singular effect of carbohydrates on blood sugar and on insulin, and the effect of blood sugar and insulin, in turn, on cel s, arteries, tissues, and other hormones, that explain the original observations and support this alternative hypothesis of chronic disease.

In this book my aim is to look critical y at a straightforward question to which most of us believe we know the answer: What const.i.tutes a healthy diet? What should we eat if we want to live a long and a healthy life? To address this question, we'l examine the evidence supporting both the prevailing wisdom and this alternative hypothesis, and we'l confront the strong possibility that much of what we've come to believe is wrong.

This scenario would not be uncommon in the history of science, although, if it happened in this case, it would be a particularly dramatic and unfortunate example. If it is true, it would be because medical researchers had a relatively easy, reliable test for blood levels of cholesterol as early as 1934, and therefore fixated on the acc.u.mulation of cholesterol in the arteries as the cause of heart disease, despite considerable evidence to the contrary. By the time they developed reliable methods for measuring what are known as blood lipids, such as triglycerides, and for measuring blood levels of insulin and a condition known as insulin resistance-indicators that may be more reliable and important-a critical ma.s.s of clinicians, politicians, and health reporters had decided that dietary fat and high cholesterol levels were the cause of heart disease, and that low-fat, high-carbohydrate diets were the solution.

In science, researchers often evoke a drunk-in-the-streetlight metaphor to describe such situations: One night a man comes upon a drunk crawling on hands and knees on the pavement under a streetlight. When the man asks the drunk what he's doing, the drunk says that he's looking for his keys. "Is this where you lost them?" asks the man. "I don't know where I lost them," says the drunk, "but this is where the light is." For the past half-century, cholesterol was where the light was.

By critical y examining the research that led to the prevailing wisdom of nutrition and health, this book may appear to be one-sided, but only in that it presents a side that is not often voiced publicly. Since the 1970s, the belief that saturated fat causes heart disease and perhaps other chronic diseases has been justified by a series of expert reports-from the U.S. Department of Agriculture, the Surgeon General's Office, the National Academy of Sciences, and the Department of Health in the U.K., among others. These reports present the evidence in support of the fat-cholesterol hypothesis and mostly omit the evidence in contradiction. This makes for a very compel ing case, but it is not how science is best served. It is a technique used to its greatest advantage by trial lawyers, who a.s.sume correctly that the most persuasive case to a jury is one that presents only one side of a story. The legal system, however, a.s.sures that judge and jury hear both sides by requiring the presence of competing attorneys.

In the case of the fat-cholesterol hypothesis of heart disease, there has always been considerable skepticism of the hypothesis and the data. Why this skepticism is rarely made public is a major theme of this book. In fact, skeptics have often been attacked or ignored, as if disloyal at time of war. Skepticism, however, cannot be removed from the scientific process. Science does not function without it.

An underlying a.s.sumption of this book is that the evolution of medical science has suffered enormously, although unavoidably, by the degree of specialization needed to make progress. "Each science confines itself to a fragment of the evidence and weaves its theories in terms of notions suggested by that fragment," observed the British mathematician and philosopher Alfred North Whitehead. "Such a procedure is necessary by reason of the limitations of human ability. But its dangers should always be kept in mind." Researchers and clinical investigators by necessity focus their attention on a tiny fragment of the whole, and then employ the results of other disciplines to extend the implications of their own research. This means that researchers have to take on faith the critical ac.u.men and scientific ability of those researchers whose results they are borrowing, and, as Whitehead noted, "it wil usual y be the case that these loans real y belong to the state of science thirty or forty years earlier."

This problem is exacerbated in the study of nutrition, obesity, and chronic disease because significant observations emerge from so many diverse disciplines. Indeed, the argument can be made that, to ful y understand obesity alone, researchers should have a working familiarity with the literature in clinical treatment of obesity in humans, body-weight regulation in animals, mammalian reproduction, endocrinology, metabolism, anthropology, exercise physiology, and perhaps human psychology, not to mention having a critical understanding and familiarity with the nuances of clinical trials and observational epidemiology. Most researchers and clinicians barely have time to read the journals in their own subspecialty or sub-sub-specialty, let alone the dozens of significant journals that cover the other disciplines involved. This is a primary reason why the relevant science is plagued with misconceptions propagated about some of the most basic notions. Researchers wil be suitably scientific and critical when addressing the limitations of their own experiments, and then wil cite something as gospel because that's what they were taught in medical school, however many years earlier, or because they read it in The New England Journal of Medicine. Speculations, a.s.sumptions, and erroneous interpretations of the evidence then become truth by virtue of constant repet.i.tion. It is my belief that when all the evidence is taken into account, rather than just a prejudicial subset, the picture that emerges wil be more revealing of the underlying reality.

One consequence of this sub-specialization of modern medicine is the belief, often cited in the lay press, that the causes of obesity and the common chronic diseases are complex and thus no simple answer can be considered seriously.

Individuals involved in treating or studying these ailments wil stay abreast of the latest "breakthroughs" in relevant fields-the discovery of al egedly cancer-fighting phytochemicals in fruits and vegetables, of genes that predispose us to obesity or diabetes, of molecules such as leptin and ghrelin that are involved in the signaling of energy supply and demand around the body. They wil a.s.sume rightful y, perhaps, that the mechanisms of weight regulation and disease are complex, and then make the incorrect a.s.sumption that the fundamental causes must also be complex. They lose sight of the observations that must be explained-the prevalence of obesity and chronic disease in modern societies and the relations.h.i.+p between them -and they forget that Occam's razor applies to this science, just as it does to al sciences: do not invoke a complicated hypothesis to explain the observations, if a simple hypothesis wil suffice. By the same token, molecular biologists have identified a mult.i.tude of genes and proteins involved in the causation and spread of cancer, and so it could be argued, as wel , that cancer is much more complex than we ever imagined. But to say that lung cancer, in over 90 percent of the cases, is caused by anything other than smoking cigarettes is to wil ful y miss the point. In this case, if refined carbohydrates and sugars are indeed the reasons why we fatten-through their effect on insulin and insulin's effect on fat acc.u.mulation-and if our goal is to prevent or remedy the disorder, the salient question is why any deeper explanation, at the moment, is necessary.

This book is divided into three parts. Part I is ent.i.tled "The Fat-Cholesterol Hypothesis" and describes how we came to believe that heart disease is caused by the effect of dietary fat and particularly saturated fat on the cholesterol in our blood. It evaluates the evidence to support that hypothesis. Part I is ent.i.tled "The Carbohydrate Hypothesis." It describes the history of the carbohydrate hypothesis of chronic disease, beginning in the nineteenth century. It then discusses in some detail the science that has evolved since the 1960s to support this hypothesis, and how this evidence was interpreted once public-health authorities established the fat-cholesterol hypothesis as conventional wisdom. Part I ends with the suggestion, which is widely accepted, that those factors of diet and lifestyle that cause us to fatten excessively are also the primary environmental factors in the cause of al of the chronic diseases of civilization. Part I I, ent.i.tled "Obesity and the Regulation of Weight,"

discusses the competing hypotheses of how and why we fatten. It addresses whether or not the conventional wisdom that we get fat because we consume more calories than we expend-i.e., by overeating and sedentary behavior-can explain any of the observations about obesity, whether societal or individual. It then discusses the alternative hypothesis: that obesity is caused by the quality of the calories, rather than the quant.i.ty, and specifical y by the effect of refined and easily digestible carbohydrates on the hormonal regulation of fat storage and metabolism.

My background is as a journalist with scientific training in col ege and graduate school. Since 1984, my journalistic endeavors have focused on controversial science and the excruciating difficulties of getting the right answer in any scientific pursuit. More often than not, I have chronicled the misfortunes of researchers who have come upon the wrong answer and found reason, sooner or later, to regret it. I began writing and reporting on public-health and medical issues in the early 1990s, when I realized that the research in these critical y important disciplines often failed to live up to the strict standards necessary to establish reliable knowledge. In a series of lengthy articles written for the journal Science, I then developed the approach to the conventional wisdom of public-health recommendations that I applied in this book.

It begins with the obvious question: what is the evidence to support the current beliefs? To answer this question, I find the point in time when the conventional wisdom was stil widely considered controversial-the 1970s, for example, in the case of the dietary-fat/cholesterol hypothesis of heart disease, or the 1930s for the overeating hypothesis of obesity. It is during such periods of controversy that researchers wil be most meticulous in doc.u.menting the evidence to support their positions. I then obtain the journal articles, books, or conference reports cited in support of the competing propositions to see if they were interpreted critical y and without bias. And I obtain the references cited by these earlier authors, working ever backward in time, and always asking the same questions: Did the investigators ignore evidence that might have refuted their preferred hypothesis? Did they pay attention to experimental details that might have thrown their preferred interpretation into doubt?

I also search for other evidence in the scientific literature that wasn't included in these discussions but might have shed light on the validity of the competing hypotheses. And, final y, I fol ow the evidence forward in time from the point at which a consensus was reached to the present, to see whether these competing hypotheses were confirmed or refuted by further research. This process also includes interview with clinical investigators and public-health authorities, those stil active in research and those retired, who might point me to research I might have missed or provide further information and details on experimental methods and interpretation of evidence.

Throughout this process, I necessarily made judgments about the quality of the research and about the researchers themselves. I tried to do so using what I consider the fundamental requirement of good science: a relentless honesty in describing precisely what was done in any particular work, and a similar honesty in interpreting the results without distorting them to reflect preconceived opinions or personal preferences. "If science is to progress," as the n.o.bel Prizewinning physicist Richard Feynman wrote forty years ago, "what we need is the ability to experiment, honesty in reporting results-the results must be reported without somebody saying what they would like the results to have been-and final y-an important thing -the intel igence to interpret the results. An important point about this intel igence is that it should not be sure ahead of time what must be." This was the standard to which I held al relevant research and researchers. I hope that I, too, wil be judged by the same standard.

Because this book presents an unorthodox hypothesis as worthy of serious consideration, I want to make the reader aware of several additional details. The research for this book included interviews with over 600 clinicians, investigators, and administrators. When necessary, I cite or quote these individuals to add either credibility or a personal recol ection to the point under discussion. The appearance of their names in the text, however, does not imply that they agree with al or even part of the thesis set forth in this book. It implies solely that the attribution is accurate and reflects their beliefs about the relevant point in that context and no other.

Lastly, I often refer to articles and reports, for the sake of simplicity and narrative flow, as though they were auth.o.r.ed by a single relevant individual, when that is not the case. A more complete list of authors can be found using the notes and bibliography.

Part One

THE FAT-CHOLESTEROL HYPOTHESIS.

Men who have excessive faith in their theories or ideas are not only il prepared for making discoveries; they also make very poor observations. Of necessity, they observe with a preconceived idea, and when they devise an experiment, they can see, in its results, only a confirmation of their theory.

In this way they distort observation and often neglect very important facts because they do not further their aim.... But it happens further quite natural y that men who believe too firmly in their theories, do not believe enough in the theories of others. So the dominant idea of these despisers of their fel ows is to find others' theories faulty and to try to contradict them. The difficulty, for science, is stil the same.

CLAUDE BERNARD, An Introduction to the Study of Experimental Medicine, 1865

Chapter One.

THE EISENHOWER PARADOX.

In medicine, we are often confronted with poorly observed and indefinite facts which form actual obstacles to science, in that men always bring them up, saying: it is a fact, it must be accepted.

CLAUDE BERNARD, An Introduction to the Study of Experimental Medicine, 1865 PRESIDENT DWIGHT D. EISENHOWER SUFFERED his first heart attack at the age of sixty-four. It took place in Denver, Colorado, where he kept a second home.

It may have started on Friday, September 23, 1955. Eisenhower had spent that morning playing golf and lunched on a hamburger with onions, which gave him what appeared to be indigestion. He was asleep by nine-thirty at night but awoke five hours later with "increasingly severe low substernal nonradiating pain," as described by Dr. Howard Snyder, his personal physician, who arrived on the scene and injected Eisenhower with two doses of morphine. When it was clear by Sat.u.r.day afternoon that his condition hadn't improved, he was taken to the hospital. By midday Sunday, Dr. Paul Dudley White, the world-renowned Harvard cardiologist, had been flown in to consult.

For most Americans, Eisenhower's heart attack const.i.tuted a learning experience on coronary heart disease. At a press conference that Monday morning, Dr. White gave a lucid and authoritative description of the disease itself. Over the next six weeks, twice-daily press conferences were held on the president's condition. By the time Eisenhower's health had returned, Americans, particularly middle-aged men, had learned to attend to their cholesterol and the fat in their diets. Eisenhower had learned the same lesson, albeit with counterintuitive results.

Eisenhower was a.s.suredly among the best-chronicled heart-attack survivors in history. We know that he had no family history of heart disease, and no obvious risk factors after he quit smoking in 1949. He exercised regularly; his weight remained close to the 172 pounds considered optimal for his height.

His blood pressure was only occasional y elevated. His cholesterol was below normal: his last measurement before the attack, according to George Mann, who worked with White at Harvard, was 165 mg/dl (mil igrams/deciliter), a level that heart-disease specialists today consider safe.

After his heart attack, Eisenhower dieted religiously and had his cholesterol measured ten times a year. He ate little fat and less cholesterol; his meals were cooked in either soybean oil or a newly developed polyunsaturated margarine, which appeared on the market in 1958 as a nutritional pal iative for high cholesterol.

The more Eisenhower dieted, however, the greater his frustration (meticulously doc.u.mented by Dr. Snyder). In November 1958, when the president's weight had floated upward to 176, he renounced his breakfast of oatmeal and skimmed milk and switched to melba toast and fruit. When his weight remained high, he renounced breakfast altogether. Snyder was mystified how a man could eat so little, exercise regularly, and not lose weight. In March 1959, Eisenhower read about a group of middle-aged New Yorkers attempting to lower their cholesterol by renouncing b.u.t.ter, margarine, lard, and cream and replacing them with corn oil. Eisenhower did the same. His cholesterol continued to rise. Eisenhower managed to stabilize his weight, but not happily.

"He eats nothing for breakfast, nothing for lunch, and therefore is irritable during the noon hour," Snyder wrote in February 1960.

By April 1960, Snyder was lying to Eisenhower about his cholesterol. "He was fussing like the devil about cholesterol," Snyder wrote. "I told him it was 217 on yesterday's [test] (actual y it was 223). He has eaten only one egg in the last four weeks; only one piece of cheese. For breakfast he has skim milk, fruit and Sanka. Lunch is practical y without cholesterol, unless it would be a piece of cold meat occasional y." Eisenhower's last cholesterol test as president came January 19, 1961, his final day in office. "I told him that the cholesterol was 209," Snyder noted, "when it actual y was 259," a level that physicians would come to consider dangerously high.

Eisenhower's cholesterol hit 259 just six days after University of Minnesota physiologist Ancel Keys made the cover of Time magazine, championing precisely the kind of supposedly heart-healthy diet on which Eisenhower had been losing his battle with cholesterol for five years. It was two weeks later that the American Heart a.s.sociation-prompted by Keys's force of wil -published its first official endors.e.m.e.nt of low-fat, low-cholesterol diets as a means to prevent heart disease. Only on such a diet, Keys insisted, could we lower our cholesterol and our weight and forestal a premature death.

"People should know the facts," Keys told Time. "Then if they want to eat themselves to death, let them."

Scientists justifiably dislike anecdotal evidence-the experience of a single individual like Eisenhower. Nonetheless, such cases can raise interesting issues. Eisenhower died of heart disease in 1969, age seventy-eight. By then, he'd had another half-dozen heart attacks or, technical y speaking, myocardial infarctions. Whether his diet extended his life wil never be known. It certainly didn't lower his cholesterol, and so Eisenhower's experience raises important questions.

Establis.h.i.+ng the dangers of cholesterol in our blood and the benefits of low-fat diets has always been portrayed as a struggle between science and corporate interests. And although it's true that corporate interests have been potent forces in the public debates over the definition of a healthy diet, the essence of the diet-heart controversy has always been scientific. It took the AHA ten years to give public support to Keys's hypothesis that heart disease was caused by dietary fat, and closer to thirty years for the rest of the world to fol ow. There was a time lag because the evidence in support of the hypothesis was ambiguous, and the researchers in the field adamantly disagreed about how to interpret it.

From the inception of the diet-heart hypothesis in the early 1950s, those who argued that dietary fat caused heart disease acc.u.mulated the evidential equivalent of a mythology to support their belief. These myths are stil pa.s.sed on faithful y to the present day. Two in particular provided the foundation on which the national policy of low-fat diets was constructed. One was Paul Dudley White's declaration that a "great epidemic" of heart disease had ravaged the country since World War I . The other could be cal ed the story of the changing American diet. Together they told of how a nation turned away from cereals and grains to fat and red meat and paid the price in heart disease. The facts did not support these claims, but the myths served a purpose, and so they remained unquestioned.

The heart-disease epidemic vanishes upon closer inspection. It's based on the proposition that coronary heart disease was uncommon until it emerged in the 1920s and grew to become the nation's number-one kil er. The epidemic was a "drastic development-paral eled only by the arrival of bubonic plague in fourteenth-century Europe, syphilis from the New World at the end of the fifteenth century and pulmonary tuberculosis at the beginning of the nineteenth century," the Harvard nutritionist Jean Mayer noted in 1975. When deaths from coronary heart disease appeared to decline after peaking in the late 1960s, authorities said it was due, at least in part, to the preventive benefits of eating less fat and lowering cholesterol.

The disease itself 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 wil 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 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-typical y where the arteries are already narrowed by atherosclerosis.

The belief that coronary heart disease was rare before the 1920s is based on the accounts of physicians like Wil iam Osler, who wrote in 1910 that he spent a decade at Montreal General Hospital without seeing a single case. In his 1971 memoirs, Paul Dudley White remarked that, of the first hundred papers he published, only two were on coronary heart disease. "If it had been common I would certainly have been aware of it, and would have published more than two papers on the subject." But even White original y considered the disease "part and parcel of the process of growing old," which is what he wrote in his 1929 textbook Heart Disease, while noting that "it also cripples and kil s often in the prime of life and sometimes even in youth." So the salient question is whether the increasing awareness of the disease beginning in the 1920s coincided with the budding of an epidemic or simply better technology for diagnosis.

In 1912, the Chicago physician James Herrick published a seminal paper on the diagnosis of coronary heart disease-fol owing up on the work of two Russian clinicians in Kiev-but only after Herrick used the newly invented electrocardiogram in 1918 to augment the diagnosis was his work taken seriously. This helped launch cardiology as a medical specialty, and it blossomed in the 1920s. White and other pract.i.tioners may have mistaken the new understanding of coronary heart disease for the emergence of the disease itself. "Medical diagnosis depends, in large measure, on fas.h.i.+on," observed the New York heart specialist R. L. Levy in 1932. Between 1920 and 1930, Levy reported, physicians at New York's Presbyterian Hospital increased their diagnosis of coronary disease by 400 percent, whereas the hospital's pathology records indicated that the disease incidence remained constant during that period. "It was after the publication of the papers of Herrick," Levy observed, that "clinicians became more alert in recognizing the disturbances in the coronary circulation and recorded them more frequently."

Over the next thirty years, recorded cases of coronary-heart-disease fatalities increased dramatical y, but this rise-the al eged epidemic-had little to do with increasing incidence of disease. By the 1950s, premature deaths from infectious diseases and nutritional deficiencies had been al but eliminated in the United States, which left more Americans living long enough to die of chronic diseases-in particular, cancer and heart disease.

According to the Bureau of the Census, in 1910, out of every thousand men born in America 250 would die of cardiovascular disease, compared with 110 from degenerative diseases, including diabetes and nephritis; 102 from influenza, pneumonia, and bronchitis; 75 from tuberculosis; and 73 from infections and parasites. Cancer was eighth on the list. By 1950, infectious diseases had been subdued, largely thanks to the discovery of antibiotics: male deaths from pneumonia, influenza, and bronchitis had dropped to 33 per thousand; tuberculosis deaths accounted for only 21; infections and parasites 12. Now cancer was second on the list, accounting for 133 deaths per thousand. Cardiovascular disease accounted for 560 per thousand.

Fortune magazine drew the proper conclusion in a 1950 article: "The conquering of infectious diseases has so spectacularly lengthened the life of Western man-from an average life expectancy of only forty-eight years in 1900 to sixty-seven years today-that more people are living longer to succ.u.mb to the deeper-seated degenerative or malignant diseases, such as heart disease and cancer...." Sir Maurice Ca.s.sidy made a similar point in 1946 about the rising tide of heart-disease deaths in Britain: the number of persons over sixty-five, he explained, the ones most likely to have a heart attack, more than doubled between 1900 and 1937. That heart-attack deaths would more than double with them would be expected.