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The Case for Keto — Exclusive Preview #3

ByGary TaubesDecember 28, 2020

The article below is a portion of Chapter 12 from Gary Taubes’ book The Case For Keto, presented here with permission from the author and publisher. The book is set for publication on Dec. 29, 2020, and is available for pre-order here.


Chapter 12: The Path Well Traveled, Part 3

Given a choice between a hypothesis and an experience, go with the experience.

As clinical experience with these trials has been accumulating, so, finally, has the clinical trial evidence. When I first reported on this subject for that 2002 New York Times Magazine article, we were seeing only the very first clinical trials assessing the relative benefits and risks of these eating patterns. These trials informed my decision to take the unorthodox position that I did in the article. Once researchers and authorities in the 1960s chose to believe that all obesity was caused by eating too much and then embraced the notion that saturated fat was a primary cause of heart disease, they did their best to put the entire nation and then the entire world on diets that would hypothetically prevent heart disease. No meaningful research was done on even the short-term effects of LCHF/ketogenic eating. That remained the case through the end of the century. (In the course of my research, I interviewed researchers in Germany who had done clinical trials on LCHF/ketogenic diets through the mid-1980s, then stopped doing them when they decided that the consensus opinion on the dangers of fat must be right, even though that was the opposite of what their own research implied.)

Only at the turn of this century, with the awareness of an obesity epidemic and typically motivated by a personal conversion experience, did physicians begin once again to conduct clinical trials on LCHF/ketogenic eating. In my article, I noted that five clinical trials had recently been completed (albeit not yet published) comparing the LCHF/ketogenic Atkins diet to the kind of low-fat, calorie-restricted (semistarvation) diet recommended then and still by the American Heart Association. The trial participants ranged from overweight adolescents in Long Island, who followed the diets for twelve weeks, to Philadelphia adults whose weight averaged 295 pounds and who followed these diets for six months.

The results of those five studies were consistent. The participants eating the LCHF/ketogenic high-fat diet lost more weight, despite the advice to eat to satiety, than those who ate the AHA-recommended low-fat, low-saturated-fat diet. Moreover, their heart disease risk factors showed greater improvement. In other words, the results of these trials were the opposite of what physicians and medical researchers would have predicted. And this is what I reported.

Since then, as of the spring of 2019, close to one hundred, if not more, clinical trials have published results, and they confirm these observations with remarkable consistency. The trials are still incapable of telling us whether embracing LCHF/ketogenic eating will extend our lives (compared to other patterns of eating the authorities might recommend), but they continue to challenge, relentlessly, the conventional thinking on the dangers of high-fat diets, and they tell us that in the short term, this way of eating is safe and beneficial.

Following LCHF/ketogenic eating for the duration of these clinical trials (at most two years), or at least being assigned to eat that way, results in equal or greater weight loss than any eating pattern to which it has been compared, and that happens without requiring the study participants to count and consciously restrict calories. And the benefits to health are clear. As with the first five studies and the clinical experience, virtually all measures of metabolic health, all risk factors for heart disease and diabetes, improve with LCHF/ketogenic eating. Along with achieving a healthier weight, the study participants became healthier overall, and they become healthier than the participants who are counseled to eat conventionally “healthy,” even calorie-restricted, diets. One particularly compelling trial was recently completed at Indiana University, led by Dr. Sarah Hallberg, working with a San Francisco–based start-up called Virta Health that was founded by Steve Phinney and Jeff Volek. Hallberg and her colleagues counseled patients with type 2 diabetes to follow LCHF/ketogenic eating. They provided 24/7 guidance from health coaches and physicians to address any issues that arose and to help them stick with it. Even in participants with type 2 diabetes, LCHF/ketogenic eating consistently produced the kind of results that we should now expect: These people were not counseled to eat less, yet they experienced significant weight loss. Their cardiovascular risk factors improved significantly. And perhaps most important, many of the 262 participants assigned to the LCHF/ketogenic eating arm of the IU/Virta Health trial had their diabetes effectively go into remission. Blood sugar control improved even while they discontinued their blood sugar medications, including insulin. (“Insulin therapy was reduced or eliminated in 94% of users,” the Virta Health team reported.) Blood pressure also improved, and so blood pressure medications were stopped as well.

In June 2019 Hallberg and Virta Health published a paper on how two years of LCHF/ketogenic eating had influenced heart disease risk factors in its subjects. The bottom line was that twenty-two of twenty-six established risk factors improved (compared to what these physician researchers call “usual care”), three remained unchanged, and only one—LDL cholesterol—on average got worse. When the Virta Health researchers worked out the numbers for what’s called the “aggregate atherosclerotic cardiovascular disease risk score,” a measure of ten-year risk of having a heart attack developed by the American College of Cardiology and the American Heart Association, the Virta Health patients decreased their risk of having a heart attack by over 20 percent, compared to the usual treatment program for diabetes and all the drug therapies typically prescribed. Even with the rise in their LDL cholesterol, these patients got significantly healthier, as did their hearts.

So here’s yet another way to ask the critical question: Can a pattern of eating that has so many beneficial effects be unhealthy because it contains considerable saturated fat or allows for the conspicuous consumption of a processed meat like bacon? (Not that bacon or meat of any kind is required in LCHF/ketogenic diets, but as foods that contain (essentially) only protein and fat, they can be eaten freely. With the exception of avocados, olives, and vegetable oils, plant-based foods come with carbohydrates as a significant source of available energy. Lower-carb, higher-fat versions of plant-based diets can be consumed, but they take significantly more thought and work and may or may not be as effective. These are discussed in Chapter 16.) In one of my favorite Rachelle Ploetz Instagram postings, she noted that her friends never criticized her diet when she weighed 380 pounds, but having switched to LCHF/ketogenic eating and lost by then 120, they would often express concern about how much bacon she was eating, as though the dangers of eating bacon regularly outweighed the benefits of losing 120 excess pounds with relative ease.

The definitive evidence to answer this question does not exist. It may never exist. But it’s hard to imagine that a way of eating that makes people so much healthier in the short run, that can even reverse diabetes, which is considered a progressive chronic disease—one that only gets worse as time goes by—will harm us in the long run. The authorities are willing to think in terms of hypotheticals and hold on dearly to their cherished beliefs. Those beliefs have already failed us. We have to take the gamble and leave them behind.

Our institutional condemnation of dietary fat and the wisdom behind prescribing diets by hypothesis would be more understandable if the evidence to support these hypotheses were indeed compelling. I don’t believe it is. Just as the evidence has inexorably accumulated over the years supporting the observation that LCHF/ketogenic diets make us healthier, the evidence supporting the idea that saturated fat is deadly and that we should all eat low-fat diets has been fading, despite the best efforts of the orthodoxy to prop it up. The more research that’s been done, the less compelling it becomes. This is always a bad sign in science and a persuasive reason to believe that a theory or a belief is simply wrong. Outside mathematics, it’s impossible to prove anything definitively one way or the other. Evidence always exists to support reasonable hypotheses (and even some unreasonable ones), because studies will always be done that get the wrong answer or that are interpreted incorrectly. That’s why I suggest we follow the trends.

The better scientists and philosophers of science have been advising this approach at least since Francis Bacon (his name, of course, is only coincidental) pioneered the scientific method four hundred years ago: The way to judge the viability of a hypothesis is to judge whether the evidence has grown significantly stronger with time. As Bacon suggested, you can tell what is not correct in science—what he called “wishful science,” which is based on fancies, opinions, and the exclusion of contrary evidence—because these are the propositions that “have stuck fast in their tracks and remained in virtually the same position, without any noticeable development; rather the reverse, flourishing most under their first authors, but going downhill ever since.”

The dietary fat–heart disease hypothesis, the one on which we base our anxieties about eating saturated fat, should be a case study in this kind of downhill progression. In 1952, while acknowledging he had no meaningful evidence to support his proposition, Ancel Keys suggested Americans should eat one-third less fat than they were at the time if they wanted to avoid heart disease. In 1970, still without hard clinical trial evidence, the American Heart Association recommended low-fat diets for everyone in America literally old enough to walk. In 1988, after the publication of two hundred-million-dollar-plus clinical trials, the results of which happened to be contradictory, followed by what one NIH administrator later described to me as a “leap of faith,” the U.S. surgeon general was blaming two-thirds of the two million yearly deaths in the United States on the overconsumption of fat-rich foods, and maintaining that the “depth of the science base” was “even more impressive than that for tobacco and health.” That report was part of a concerted public relations campaign by the federal government to do all it could (apparently with the best of intentions) to get us to fear eating any fat that didn’t come from vegetable sources. It worked. That’s why we bought into the idea that we should avoid eating saturated fat if at all possible. Animal fat consumption in America went down; plant oil consumption went up.

Now, thirty years later, the most recent unbiased review of this evidence—from the Cochrane Collaboration, an international organization founded to do such impartial reviews—concluded that clinical trials have failed to demonstrate any meaningful benefit from eating low-fat diets and so, implicitly, any harm from eating fat-rich foods. The Cochrane review described the evidence as only “suggestive” that avoiding saturated fat specifically might avert a single heart attack, and said it’s even “less clear” whether this would lengthen anyone’s life.

Despite its prominent role in pushing the anti-fat frenzy, the American Heart Association recently acknowledged (in an otherwise biased assessment) that its conception of healthy low-fat eating gets support primarily, still, from the ambiguous results of a handful of poorly done trials that all date to the 1960s and ’70s, and that if this murky evidence is to take precedence, the results of later studies, including the enormous (49,000 participants) and exorbitantly expensive (half a billion dollars at least) Women’s Health Initiative, have to be ignored or rejected as inadequate. Of course, the hundred-some trials consistently finding that LCHF/ ketogenic eating makes us healthier, despite being saturated-fat- rich, also refute the idea that we should be listening to the authorities. For the past half century, evidence supporting the idea that the saturated fat in our diet is a cause of heart disease and premature death has simply been eroding away.

The notion (i.e., hypothesis) that fat-rich foods cause cancer has had similar setbacks. In 1982 this proposition was considered so likely to be true that the National Academy of Sciences published a report—Diet, Nutrition, and Cancer—recommending that to prevent cancer, Americans cut fat consumption from 40 percent of our calories, as we were then eating, to 30 percent. It asserted that the evidence was so compelling, it “could be used to justify an even greater reduction.” This is also what health-conscious people grew up believing and were taught. By the mid- 1990s, though, the experts who assembled a seven-hundred-page report on this question for the World Cancer Research Fund and American Institute for Cancer Research—Food, Nutrition and the Prevention of Cancer—could find neither “convincing” nor even “probable” reason to believe that fat-rich diets were carcinogenic. When I interviewed Arthur Schatzkin, chief of the nutritional epidemiology branch of the National Cancer Institute, in 2003, he described the evidence from clinical trials designed to test this dietary fat–cancer hypothesis as “largely null.” In short, the proposition that fat caused cancer had also gone steeply downhill with further study, but our fear of fat did not go with it.

As for the idea that a healthy diet must be mostly plants, that it must include fruits, vegetables, whole grains, pulses, and legumes, we don’t have even the ambiguous 1960s-era studies to support it. We have no meaningful clinical trial evidence to support this idea, as Michael Pollan infers in In Defense of Food, the book that brought us the mantra “Eat food. Not too much. Mostly plants.” What we have instead, he notes, is the idea that people who eat a lot of plant foods tend to be healthier than people who eat the standard American diet (given the appropriate acronym SAD), that is, who eat at fast-food restaurants and buy the packaged, highly processed, sugary foods in the supermarket that Pollan aptly calls “foodlike substances,” food that health-conscious people naturally avoid. More than anything, says Pollan, we have the simple fact that virtually all nutritionists believe eating mostly plants is a good idea. In the very contentious world of nutritional beliefs, he says, this is something on which they can all agree.

Yet they believe this, and Pollan argues for it, not because they have compelling experimental evidence (i.e., clinical trial results) that it is true, and not because they’ve seen obese and diabetic patients switch from omnivorous or meat-rich diets (without sugar and foodlike substances) to mostly or all-plant diets (with- out sugar and foodlike substances) and get healthier for doing so, but because they, well, all seem to believe it. This is what cognitive psychologists would call a “cascade” or “groupthink,” and it’s exceedingly common in this kind of soft science. It’s even common in the harder sciences—physics, for instance, where the Nobel laureate Louis Alvarez called it “intellectual phase lock.” People believe something because people they respect believe it, and if they’re doing research, they report what they’re supposed to find, and they see what they expect to see, whether it’s really there or not.

Eating mostly plants, in other words, just seems right to those who recommend it to us. It seems right, in part, because we’ve been hearing it our whole lives. It’s what my health-conscious mother was teaching me in the 1960s every time she told me to eat my vegetables (if it wasn’t green or cauliflower, in her worldview, it was not a vegetable) and suggested that too much red meat would cause colon cancer. I’m now badgering my children to eat their green vegetables, even if I primarily believe they should because that’s what my mother taught me. Eating mostly plants may be better for the environment than the alternatives, and better for the animals that won’t be killed prematurely and eaten for our pleasure. (Sophocles counsels at the end of Oedipus Rex that we should look upon that last day always and count no mortal lucky or happy until he (or she) lives his last day without pain. If the same is true of animals, then this assumption, too, is questionable.) When epidemiological surveys look at what healthy, health-conscious people eat, not surprisingly this mostly plants wisdom wins out. Health-conscious people have not been sitting down to breakfasts of eggs and bacon every morning, because they’ve been told eggs and bacon will kill them. They’re drinking kale-almond smoothies with their low-sugar granola because that’s what they’ve been counseled, no matter the weakness in the underlying evidence. Shouldn’t we all?

The answer, once again, is probably not. The last thirty years of medical research have resulted in a sea change in our understanding of heart disease risk factors and their relationship with obesity, diabetes, and the condition we discussed earlier called insulin resistance. A critical factor in the pushback against LCHF/ketogenic eating has always been the belief that the animal fat content will cause premature heart disease—the “artery-clogging” saturated fat argument. Most people believe butter and bacon and full-fat dairy products are deadly because we’ve been taught that these foods high in saturated fats will raise our cholesterol, specifically the cholesterol in LDL particles known as the “bad” cholesterol, and that this will lead to premature death from a heart attack.

One of many problems with this way of thinking is that it focuses all dietary attention on one disease state, heart disease, and one biological entity, LDL cholesterol. This is at best misguided 1970s-era medical science. While physicians have been taught to believe it with dogmatic certainty, and a large proportion still do, the scientific understanding has evolved over the years, as scientific understanding has a way of doing.

While LDL does seem to play a role in the atherosclerotic process, it’s not the cholesterol in the particle that’s the active player but rather the LDL particle itself and specifically the number and maybe the size of particles in circulation. Public health and medical authorities have slowly come to accept what research and physician iconoclasts had argued as early as the 1960s, that heart disease is a complex process and the end result of a metabolic disruption that manifests itself throughout the human body. We cannot ascertain whether we will live a long and healthy life from a single number and a single biological entity. (The measures that are best at doing that, in any case, are far better indicators than LDL cholesterol.) For most of us, the primary sign that we’re at high risk of heart disease or premature death from any chronic disease, including cancer, is not whether our LDL cholesterol is elevated, but whether we have the cluster of metabolic disorders now known as metabolic syndrome, which itself seems to be a consequence or manifestation of insulin resistance.

Physicians are instructed to diagnose metabolic syndrome if their patients have at least three of five characteristic signs. The most important, the one physicians are told to look for first, is whether the patient is getting fatter, specifically above the waist. In this sense, the metabolic syndrome concept is, perversely, a direct descendant of Ancel Keys’s thinking and observations in 1960 that the people most likely to get heart attacks and die pre- maturely are fat middle-aged men, those fat men that Keys was so ardently imploring to “think.” Some heart specialists were referring to these men as “fat cardiacs” even a century ago. Keys and the medical community became obsessed with dietary fat and cholesterol as the key to solving the fat-man-heart-attack connection and so focused all attention on LDL cholesterol and dietary fat. But other researchers—at Stanford, Yale, and Rockefeller universities in the United States and at Queens Elizabeth College and Queen’s University in Belfast, among others—focused on carbohydrates and their effect not just on insulin and elevated blood sugar but also on blood pressure and “blood lipids,” in particular HDL cholesterol (the “good cholesterol”) and triglycerides (one form in which fat is found in the circulation). This is what Edwin Astwood was referring to in his 1962 lecture when he observed that the disorders associated with obesity—“particularly those involving the arteries”—closely resemble those of type 2 diabetes, implying “a common defect in the two conditions.”

By the late 1980s, as the National Institutes of Health, the Surgeon General’s Office, and even the National Academy of Sciences in the United States—not to mention the National Health Service in the United Kingdom—were convincing us all to avoid fat and eat carbohydrates, researchers led by the late Stanford University endocrinologist Gerald Reaven began to convince first diabetes specialists and then eventually cardiologists that their patients should be worried less about LDL cholesterol than about metabolic syndrome. It was metabolic syndrome, these physician researchers argued, that was the manifestation of the fundamental physiological disruption that would eventually kill their patients (and us). This is what journalists are referring to when they write, as Trymaine Lee, an NBC correspondent, recently did, that “obesity and high blood pressure [are] key contributors to heart disease.” Lee was writing about his own near-fatal heart attack at age thirty-eight. Obesity and high blood pressure are manifestations of metabolic syndrome; they go hand in hand.

The revelations about metabolic syndrome can be understood if we think of obesity, diabetes, heart disease, hypertension, and even stroke all as consequences of the same disruptive force: disordered insulin signaling, poor blood sugar control, and all the metabolic and physiological disruptions, including systemic inflammation, that then occur. All these conditions are intimately associated. Those who have obesity are at high risk of type 2 diabetes, and most people with diabetes are overweight or obese. They’re all likely to get heart disease (as Astwood noted), but those with diabetes are at the highest risk, and they all tend to have high blood pressure. Medical textbooks refer to obesity, diabetes, heart disease, gout, and stroke (cerebrovascular disease) as “hypertensive” disorders, meaning high blood pressure is common in all of them. Additionally, all these disorders associate with these abnormalities in blood lipids, specifically low HDL cholesterol and high triglycerides (and high LDL particle number, but not high LDL cholesterol).

These risk factors are the diagnostic criteria of metabolic syndrome. Individually, each of these factors is associated with an increased likelihood that you’ll have heart disease: As your waist circumference expands, your risk of heart disease goes up. As your blood pressure elevates, so does your risk for heart disease, and stroke as well. The worse your blood sugar control (glucose intolerance), the more likely you are to be diabetic, and the more plaque deposition you’re likely to have in your arteries. In 1930 Elliott Joslin, the leading U.S. authority on diabetes, observed that “every other diabetic now dies of arteriosclerosis,” and the situation hasn’t changed much since then. The arteries of a sixty-year-old with untreated diabetes will look like the arteries of a ninety-year-old who doesn’t have the disease. Finally, the medical community has known since 1977 (if not twenty years earlier) that low HDL cholesterol is a far better predictor of heart disease than high LDL cholesterol, many times more likely to be regrettably right, and that high triglycerides are at least as predictive as high LDL. The likelihood is that when you have a heart attack, metabolic syndrome will be the reason, not your elevated LDL cholesterol.

If you have metabolic syndrome, it means you’re sliding down the slope from health to chronic disease, and the first obvious sign is that you’re getting fatter or you’ve got high blood pressure. According to Centers for Disease Control (CDC) statistics, one in three Americans has metabolic syndrome. But that proportion includes children, in whom it is relatively rare. The older we get and the fatter we get, the more likely we are to have metabolic syndrome, to be insulin resistant. Among adults over fifty, one in two have it. If you’re reading this book to help bring your weight under control (and particularly if you’re male), it’s a good sign that you either have metabolic syndrome or are going to get it.

All these physiological disturbances that characterize metabolic syndrome, all the risk factors that physicians are told to look for to diagnose metabolic syndrome, are linked directly to the carbohydrates we eat, not to the fat. If you have metabolic syndrome, it’s the quantity and quality of carbohydrates you’re eating that are slowly shortening your life. Saturated fat is not responsible. Both clinical trial data and clinical experience tell us that this body-wide disruption of metabolic syndrome—the disruption that appears to begin with insulin resistance and so elevated levels of insulin and poor blood sugar control—is normalized or corrected by removing the carbohydrates from the diet and replacing them with fat. That’s the twenty-two of twenty-six risk factors that improved in the Virta Health trial.

All this—what happens to the human body when blood sugar and insulin move in and out of healthy ranges—can be explained by textbook medicine. By this I mean that the beneficial effects observed when patients or clinical trial participants restrict carbohydrates and replace them with fat are what medical textbooks tell us should happen. Eating fewer carbohydrates, for instance, will, by definition, result in lower blood sugar, at least in the short term after a meal. This almost has to be beneficial, considering it’s high blood sugar that causes many of the deleterious side effects of diabetes. Researchers have known, at least since the 1970s, that carbohydrate consumption lowers the apparently beneficial HDL cholesterol compared to eating fats, and that it raises triglycerides as well. Their understanding of how the liver processes these “lipids” and lipoproteins explains why.

As for blood pressure, insulin induces your kidneys to hold on to sodium. (Salt is sodium chloride, and the sodium is the player here.) This is one of the many things insulin does. When your insulin levels are high, your kidneys retain sodium rather than excreting it in urine. Now blood pressure will increase as your body retains water to keep the sodium concentration in your circulation constant. When the medical authorities blame hypertension and high blood pressure on eating too much salt, they’re thinking of the same mechanism—increasing the sodium concentration in the circulation leads to more water being retained and higher blood pressure—but typically simplistically. They’re putting the blame on consuming too much salt—a behavioral problem or maybe the food industry’s fault for oversalting processed food—rather than on excreting too little, which results from chronically elevated insulin levels and insulin resistance. Lowering insulin by avoiding carbohydrates and replacing them with fat reverses this sodium-retention phenomenon, and so blood pressure should drop with LCHF/ketogenic eating, as it typically does.

Once again, knowing the history of nutrition science makes the fact that orthodox medicine has ignored this connection all that much more disturbing. As early as the 1860s, the German biochemists who pioneered the science of nutrition were commenting that carbohydrate-rich diets elevated blood pressure and fat-rich diets did not. In the 1970s Harvard researchers came to understand the role of insulin in this process. By then, though, we were all being told that high blood pressure was caused by eat- ing too much salt, another speculative hypothesis that continues to suffer from a dearth of experimental, clinical trial evidence. It was embraced nonetheless. It sounded right, and so the authorities believed it. We believed it because they did, and we never let it go.

Meanwhile business in blood pressure medications boomed—tens of billions of dollars a year worldwide—and the carbohydrate-insulin–blood pressure connection was relegated to the textbooks. Like most things insulin-related, it is assumed to have no relevance to anyone other than maybe those with diabetes. By the mid-1990s diabetes textbooks, such as Joslin’s Diabetes Mellitus, described chronically elevated levels of insulin as likely to be “the major pathogenic defect initiating the hypertensive process” in patients with type 2 diabetes. Patients with type 2 diabetes are just further down the metabolic syndrome spectrum than the rest of us, but this idea that chronically elevated levels of insulin might be the pathogenic defect initiating the hypertensive process in the rest of us was not thought to be relevant. But it is, though, certainly to those of us who want to be lean and healthy.

Purchase or preview the book here.

Published December 29, 2020 by Alfred A. Knopf, an imprint of The Knopf Doubleday Publishing Group, a division of Penguin Random House LLC. Copyright © 2020 by Gary Taubes.


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