After a century of misunderstanding the differences between diet, weight control, and health, The Case for Keto revolutionizes how we think about healthy eating—from the best-selling author of Why We Get Fat and The Case Against Sugar.
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.
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Gary Taubes, an award-winning science and health journalist, is the cofounder and director of the Nutrition Science Initiative (NuSI). He is the author of The Case Against Sugar, Why We Get Fat, and Good Calories, Bad Calories. A former staff writer for Discover and correspondent for Science, he has written three cover articles on nutrition and health for The New York Times Magazine, and his writing has appeared in numerous “Best of” anthologies, including 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 and is the recipient of a Robert Wood Johnson Foundation Investigator Award in Health Policy Research. He lives in Oakland, California, with his wife, the author Sloane Tanen, and their two sons. www.garytaubes.com
1
The Basics
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...
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