It has already been proven that the keto diet can help you lose weight. But how sustainable is it? Bestselling author Gary Taubes, who had a unique bestseller in The Case Against Sugar, brings to focus why our long-held beliefs on weight loss might all be wrong. Could a 21st-century diet be what's needed for today's population?
Based on twenty years of investigative reporting and interviews with 100 practicing physicians who embrace the keto lifestyle as the best prescription for their patients' health, Gary Taubes gives us a manifesto for the twenty-first-century fight against obesity and diabetes.
For years, health organizations have preached the same rules for losing weight: restrict your calories, eat less, exercise more. So why doesn't it work for everyone? Taubes, whose seminal book Good Calories, Bad Calories and cover stories for The New York Times Magazine changed the way we look at nutrition and health, sets the record straight.
The Case for Keto puts the ketogenic diet movement in the necessary historical and scientific perspective. It makes clear the vital misconceptions in how we've come to think about obesity and diet (no, people do not become fat simply because they eat too much; hormones play the critical role) and uses the collected clinical experience of the medical community to provide essential practical advice.
Taubes reveals why the established rules about eating healthy might be the wrong approach to weight loss for millions of people, and how low-carbohydrate, high-fat/ketogenic diets can help so many of us achieve and maintain a healthy weight for life.
Related collections and offers
|Publisher:||Knopf Doubleday Publishing Group|
|Sold by:||Random House|
|File size:||10 MB|
About the Author
Read an Excerpt
A brief lesson in the history of obesity research
On June 22, 1962, a Tufts University Medical School professor named Edwin Astwood tried and failed to correct how we think about the cause of obesity. We have been living with that failure ever since.
Astwood was presenting a counterargument to what had become since the end of the Second World War the dominant thinking among medical authorities and researchers on why we get fat. Astwood called this thinking “the conviction of the primacy of gluttony,” by which he meant the unshakable belief that virtually all cases of obesity, child or adult, mild or extreme, are caused ultimately by the overconsumption of calories; that is, people get fat because they eat too much.
Astwood considered this belief system—for that’s what it is—to be almost willfully naïve and perhaps the primary reason so little progress had been made in understanding obesity, let alone preventing and treating it. It is also the reason those who have the misfortune to suffer from obesity are held responsible for their condition. “Obesity is a disorder,” he said in opening his presentation, “which, like venereal disease, is blamed upon the patient,” the direct consequence of their failing.
Astwood was an endocrinologist; his medical expertise and the subject of his research were hormones and hormone-related disorders. The venue for his talk was the forty-fourth annual meeting of the Endocrine Society. Astwood was its president that year, and his talk, titled “The Heritage of Corpulence,” was his presidential address. Astwood was also a member of the prestigious National Academy of Sciences. According to his NAS biographical essay, his peers considered him “a brilliant scientist” who had contributed more to our understanding of thyroid hormones and how they work than anyone alive. (He won the Lasker Award, considered one step below the Nobel Prize, for the thyroid work.) Of the young men and women who learned to do their medical research in Astwood’s Boston-area laboratory, thirty-five would go on to become full professors by the time Astwood passed away in 1976. He was “not only driven by an insatiable curiosity,” the NAS biography says of Astwood, “but by a curiosity that sought answers with willful determination.”
Although Astwood was known among his friends and colleagues for having little interest in food or eating—he considered meals only “a necessary intervention in the day’s activities solely for the purpose of bodily nutrition”—much of his laboratory work in the latter years of his research career was dedicated to understanding obesity, specifically the influence of hormones on fat accumulation and the use of fat to fuel our metabolism.
In the small world of 1960s-era obesity research, Astwood was something of a throwback to the pre–World War II years. While he had a profound understanding of the research literature on obesity and was a serious if not indeed brilliant scientist, he had been a physician also who treated patients in his clinic. In this he was like the physician researchers in Germany and Austria before the war who had dominated thinking on obesity and had also come to their conclusions on the nature of the obese condition by observing it closely in their human patients, taking their histories and coming to understand what they were going through and living with. Doctors would do that with any other disorder—why not do it with such a seemingly intractable disorder as obesity?
Many of the most influential of those prewar European authorities had become convinced that obesity must be the result of a hormonal or metabolic dysfunction, not caused by overeating, a concept that they recognized as circular logic. (“To attribute obesity to ‘overeating,’” the Harvard nutritionist Jean Mayer had aptly commented eight years before Astwood’s presentation, “is as meaningful as to account for alcoholism by ascribing it to ‘overdrinking.’ ” It’s saying the same thing in two different ways, at best describing the process, not explaining why it’s happening.) Rather, it’s somehow programmed into the very biology of the fat person, a disorder of fat accumulation and fat metabolism, these German and Austrian clinical researchers concluded. They believed, as Astwood came to believe, that obesity is neither a behavioral issue nor an eating disorder, not the result of how much we choose to eat consciously or unconsciously.
That German-Austrian research community had evaporated, beginning in 1933 with the rise of the Nazi Party. By the time the war was over, European thinking on obesity, grounded in decades of clinical experience and observation, had evaporated with it. The very lingua franca of medicine shifted from German prewar to English postwar. German-language medical literature was considered of little interest, even unreadable by the new generation of young American physicians and nutritionists, who repopulated the field and found the conventional, simplistic thinking on obesity all too easy to believe. With just a few exceptions, these newly minted experts weren’t burdened with actually having to help obese patients achieve a relatively healthy weight for life. They were guided instead by a theory—technically, a hypothesis—that they believed in unconditionally. They believed the truth was obvious, which is always an impediment to making progress in any scientific endeavor.
Their truth was the subject of Astwood’s presentation: a “conviction in the primacy of gluttony,” the notion that obesity is almost invariably caused by eating too much, consuming more calories than we expend, and so is ultimately a behavioral or eating disorder. That conviction implied that the only meaningful difference between lean people and people who struggled with obesity is that the lean can control their food intake and hence their appetites—consume only as many calories as they expend—while people with obesity could not, or at least not once they started to get fat. The idea that the fat tissue of those who become obese might have some physiological drive to accumulate fat that the tissues of lean people don’t, some subtle hormonal disruption, was dismissed by the authorities as nothing more than “lame excuses” (quoting the Mayo Clinic’s leading 1960s-era obesity expert) for fat people not to do what came naturally to lean people—eat in moderation.
If anything, the supposedly learned postwar authorities came to consider obesity the result of a psychological defect, not a physiological one. They were not shy in stating that people got fat primarily because of “unresolved emotional conflicts” or because they had “turned toward food to relieve some of the nervous tensions of life.” These authorities counseled those with obesity to embrace a lifetime of walking away from their meals still hungry, of semistarving themselves, ideally after consulting a psychiatrist first.
This is the thinking that Astwood hoped to overturn with his presidential address. He enumerated with elegance and occasional humor the reasons why obesity was surely a genetic disorder, which implied that it almost assuredly had to be a hormonal or endocrinological one. Yes, he acknowledged, this was the implication every time someone afflicted with obesity made a comment along the lines of “everything I eat turns to fat.” It was anything but a lame excuse, according to Astwood; it was a reality. It was true, he said, not just for the kind of extreme obesity that he occasionally saw in patients in his practice, but for “the common or garden varieties . . . the kind that we see every day.”
One thing that seemed to mystify Astwood was that there was nothing subtle about the evidence arguing for a genetic, and so hormonal, influence in obesity and fat accumulation. Obesity ran in families, Astwood said, as the authorities all agreed, but not because fat parents overfed their children. It did so because of a strong genetic component. Identical twins don’t just have the same faces; they have identical body types. If one twin is obese, so almost assuredly will the other one be. Even the distribution of obesity in families suggested genetics were involved. Astwood told his audience about one of his patients who was twenty-four years old, five feet four inches tall, and weighed 457 pounds. This young man had seven siblings, three of whom also suffered from extreme obesity: “His brothers, aged 10, 15, and 21, weighed respectively 275, 380, and 340 pounds.” The four other siblings “were of normal proportions.”
This “looked more like the work of genes,” said Astwood, not the “product of a groaning family board,” an antiquated phrase that refers to a dining table overloaded with food. We know that genes determine stature and hair color, said Astwood, and they determine the size of our feet and a “growing list of metabolic derangements, so why can’t heredity be credited with determining one’s shape?” If we had doubts that this was the case, we only had to look at animals. “Consider the pig,” he said: “His corpulence and gluttony resulted from man’s artificial selection; selective breeding provided us with this hulk with his hoggish ways, and no one will convince me that his gourmandizing is provoked by parental oversolicitude.”
A reasonable picture of how those genes might be expressing themselves, Astwood explained, had been worked out since the 1930s. A series of laboratory researchers had generated an enormous amount of information about how our bodies regulate the fat we store and the fat we use for energy. “To turn what is eaten into fat, to move it and to burn it requires dozens of enzymes and the processes are strongly influenced by a variety of hormones,” he explained. Sex hormones clearly play a role in where fat is stored. Men and women, after all, tend to fatten differently: men above the waist, women below it. Thyroid hormones, adrenaline, and growth hormones all play a role in releasing fat from its depots, as does a hormone known as glucagon, secreted by the pancreas.
“The reverse process,” Astwood said, “reincorporation of fat into the depots and the conversion of other food to fat, tends to be reduced by these hormones, but to be strongly promoted by insulin.” All this demonstrated “what a complex role the endocrine system plays in the regulation of fat.” An important clue to what might be happening, he added, is the fact that the numerous chronic disorders associated with obesity—“particularly those involving the arteries”—resemble those that come with diabetes so closely, it implies “a common defect in the two conditions.”
Now imagine, Astwood suggested to his audience, what would happen if just one of these mechanisms went awry, impeding the release of fat from fat cells or promoting its storage. It was all too easy to imagine a slow, gradual accumulation of fat that could lead to extreme obesity if continued over years and decades. As the fat inexorably accumulated, a likely result would be what Astwood described as “internal starvation,” as the body hoarded calories in fat cells that it would otherwise need for fuel, while simultaneously increasing the weight that had to be carried around, day in and day out, requiring the expenditure of more and more energy to move and fuel that bulk. In other words, the same subtle hormonal disruption that could cause fat to accumulate to excess would also make a fat person hungry while it was happening. This would be exacerbated by the advice given to the fat person from all sides: Eat less, exercise more. Starve yourself, if necessary. If the proposed treatment for a fat accumulation problem that itself caused internal starvation—that is, hunger—was to starve even more, we can imagine all too easily why it would fail, if not in the short run, certainly eventually.
“This theory,” Astwood said, “would explain why dieting is so seldom effective and why most fat people are miserable when they fast. It would also take care of our friends, the psychiatrists, who find all kinds of preoccupation with food, which pervades dreams among patients who are obese. Which of us would not be preoccupied with thoughts of food if we were suffering from internal starvation? Add to the physical discomfort the emotional stresses of being fat, the taunts and teasing from the thin, the constant criticism, the accusations of gluttony and lack of ‘will power,’ and the constant guilt feelings, and we have reasons enough for the emotional disturbances which preoccupy the psychiatrists.”
Maybe the timing was bad, or the audience was wrong—a casualty of the silos in which medical research and medical practice tend to exist. Astwood gave his presentation right on the cusp of a revolution in the science of endocrinology. His comment about the intimate relationship between obesity and type 2 diabetes—the kind we’re increasingly likely to get as we age and fatten—was remarkably prescient. It implied that the treatment and prevention of one would be very similar if not identical to that of the other. But he was talking to an audience of endocrinologists, who didn’t treat the common form of obesity—“the kind we see every day,” as Astwood had said. It wasn’t their responsibility, and perhaps was not their interest, and in the early 1960s, obesity was still relatively uncommon compared with the epidemic confronting us today.
Back then, as Astwood implied, obesity treatment had become the purview primarily of psychiatrists and psychologists. These were the medical professionals charged with teaching fat people to get thin and supposedly elucidating our understanding of the disorder. They saw the obese and overweight, not surprisingly, from their own unique perspective and context, as clearly suffering from mental, emotional, and behavioral disorders. They found it easy to ignore a revolution in endocrinology, because that wasn’t their area of study. (Nutritionists, as I will discuss, did the same.) They read different journals, attended different conferences, and were housed in different university and medical school departments. Even if the endocrinologists solved the problem, the psychiatrists and the psychologists might never know about it or might simply disagree, since they were diligently working to figure out how to get fat people to face up to their unresolved nervous tensions and eat less.
The fact is that by the time Astwood gave his presentation, the conviction in the primacy of gluttony had already won out. The world of obesity research back then was so small that a very few influential and well-placed individuals could and did determine what all the rest of them (and so us) would believe. “Obesity is a matter of balance—faulty balance of dietary intake and energy expenditure,” they said repeatedly and with absolute assurance. It seemed so obvious that virtually all of us came to believe it unconditionally. Even some of the best and most empathic physicians of our era, such as Bernard Lown, a winner of the Nobel Peace Prize, bought in. He wrote in his classic book The Lost Art of Healing, subtitled Practicing Compassion in Medicine, that obesity is the result of “an innate maladaptive behavior,” akin to “alcoholism, cigarette or drug addiction . . . absence of self-esteem, obsessive work habits, or simply a lack of joy in living.” Even those suffering from obesity came to see their condition as their own fault.
By the 1970s, the idea that obesity is a hormonal disorder had effectively vanished from the learned discourse on the subject. The authorities, with only the rarest of exceptions, no longer even considered the possibility that we get fat because the hormones and enzymes that regulate the buildup of our fat stores and the breakdown and use of our fat for fuel are dysregulated in some of us and not in others, so that some of us fatten easily, accumulating excessive fat in our fat tissue or around our organs, and others don’t. It is for this hormonal, physiological reason that some of us spend our lives fighting and losing a battle to remain lean, while others win it effortlessly.
Astwood’s proposition and his theory, and the thinking of the prewar German and Austrian authorities, effectively disappeared. In 1973, after forty years of research had worked out the science of fat metabolism and storage in great detail, Hilde Bruch, the leading U.S. authority on childhood obesity, remarked on its absence. It was “amazing how little of this increasing awareness,” she wrote, “is reflected in the clinical literature on obesity.”
Today, nearly half a century later, this is still the case. While biochemistry and endocrinology textbooks diligently discuss the relevant details of how hormones and enzymes regulate fat storage and metabolism and so imply that a subtle disruption in these systems (particularly the hormone insulin) could easily cause human obesity, just as Astwood had proposed, those very same textbooks will omit this science entirely from the discussions of obesity itself, as will textbooks dedicated entirely to obesity. Those discussions are still dominated by the conviction of the primacy of gluttony: It’s the brain that makes us fat, and it does so by manipulating how much we want to eat and exercise. The absence of a competing theory is remarkable, especially given the stakes and the profound implications.
Imagine learned discussions of cancer—entire books, even textbooks, written on the subject of cause, cure, and prevention—that neglected to mention, let alone discuss in detail, the physiological mechanisms that directly drive a tumor to grow and a cancer cell to divide and multiply and spread its progeny throughout the body. It would never happen. Yet the direct equivalent did happen in obesity research, and it has crippled our thinking on how we should deal with the disorder. The physicians who are left with the job of treating an ever-growing population of patients with obesity and diabetes are expected to give their patients variations on the same advice they would have given in Astwood’s day. And it continues to fail.
Also missing from these discussions has been the direct and virtually unavoidable implications of this hormone-centric view of getting fat: the idea, or at least the possibility, that carbohydrates are uniquely fattening. Dietitians and nutritionists had accepted this as a given through the 1960s, but those researchers who thought of themselves as studying the causes of obesity failed to consider it a relevant piece of information. In 1963, Sir Stanley Davidson and Dr. Reginald Passmore wrote in the textbook Human Nutrition and Dietetics, the definitive source of nutritional wisdom for a generation of British medical practitioners, that “the intake of foods rich in carbohydrate should be drastically reduced since over-indulgence in such foods is the most common cause of obesity.” They didn’t understand yet why physiologically this was the case—it was just then being worked out in laboratories—but the fact seemed undeniable. That same year Passmore coauthored an article in the British Journal of Nutrition that began with the declaration: “Every woman knows that carbohydrate is fattening: this is a piece of common knowledge, which few nutritionists would dispute.”
This observation resonated almost perfectly with what laboratory researchers were learning at the time about the hormonal orchestration of fat storage and fat metabolism. By excluding this thinking and its implications from mainstream medical practice—despite its being textbook medicine—the authorities left it to the doctors themselves to do with it what they could, and they did. They found a way to eat that made it easy to achieve and maintain a healthy weight. Which brings us back to these “fad” diet books.
These books, written by doctors, sold so well not only because those of us who fatten easily have been desperate for answers but also because these carbohydrate-restricted diets—high in fat—provide for relatively quick weight loss and do so typically without hunger. The solutions provided in these books have simply been far more often right than what we’ve been hearing from the nutritional authorities. The advice works, for physiological and metabolic reasons that seem obvious. Yet the authorities, for reasons I’ll discuss, have labored diligently to persuade us either that these diets won’t work, or that we’ll never follow them, or that if we do, they’ll kill us prematurely. It’s as though even trying this way of eating to see if it works were an affront to their expertise, which it is.