12 The Path Well Traveled

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

Someone asked me the other day how I was losing weight. I told them I eat less than 20g of carbs a day. They proceeded to freak the heck out. Told me how dangerous it was. (No.) Asked me if my doc knew. (Yes.) Told me that carbs were essential to human survival….Finally I was like, dude, do you really believe I was healthier 90 pounds heavier than I am now? I really think he wanted to say yes but was worried that I was going to punch his lights out. He probably would’ve been right.

—RACHELLE PLOETZ, on her Instagram account #eatbaconloseweight

The question Rachelle Ploetz asked speaks to the very heart of this endlessly controversial subject: “Dude, do you really believe I was healthier 90 pounds heavier than I am now?” Ultimately the goal is to be healthy. Whether ninety pounds are lost or ten, it’s quite possible that a way of eating that induces fat loss becomes harmful as the years go by.

Rachelle’s experience presents a good case study. Rachelle had wrestled with her weight throughout her life and had tried to eat healthy by the conventional definition. When she began her LCHF/ketogenic program, she weighed 380 pounds. She would eventually lose 150 pounds, documenting it all on her Instagram account and settling in at 230 pounds. Her husband lost seventy-five pounds eating as Rachelle did. Her teenage daughter dropped fifty pounds. They came to believe, as do I, that if they now changed how they were eating, if they went back to eating even “healthy” carbohydrates—say, from whole grains or from beans and legumes (and, of course, cut back on the butter and bacon)—they would eventually gain the weight back. They consider this to be a way of eating for life, out of necessity. Are they healthier for doing so?

When I first wrote about (and still barely understood) the paradox presented by LCHF/ketogenic eating to the medical community in my New York Times Magazine cover story in July 2002, I admitted to trying the Atkins diet as an experiment and effortlessly losing twenty-five pounds by doing so. Those were twenty-five pounds I had essentially been trying to lose every day of my life since I’d hit my thirties, despite an addiction to exercise and the better part of a decade—the 1990s—of low-fat, mostly plant, “healthy” eating. I avoided avocados and peanut butter because they were high in fat, and I thought of red meat, particularly a steak or bacon, as an agent of premature death. I ate only the whites of eggs. Having failed to make noticeable headway, I had come to accept those excess pounds as an inescapable fact of my life. When I changed how I ate—and not, as far as I could tell, how much—those pounds disappeared.

At the time I was simply fascinated by the experience, feeling as though a switch had been flipped (which I now understand to be the case). But I also acknowledged in the article something that remained true for years afterward: my anxiety. Every morning when I sat down to my breakfast of eggs—with the yolks—and sausage or bacon, I wondered whether, how, and when it was going to kill me. I didn’t worry about any lack of green vegetables in my diet because I was eating more of them than ever. I worried about the fat and the red and processed meat. Despite all my reporting and my journalistic skepticism, my thoughts on the nature of a healthy diet were a product of the nutritional belief system that had become firmly ensconced as I was becoming an adult, the theories or, technically, hypotheses of what constituted a healthy diet. Bacon, sausage, eggs (yolks, anyway), red meat, and copious butter were not included.

“After 20 years steeped in a low-fat paradigm,” I wrote in that 2002 article,

I find it hard to see the nutritional world any other way. I have learned that low-fat diets fail in clinical trials and in real life, and they certainly have failed in my life. I have read the papers suggesting that 20 years of low-fat recommendations have not managed to lower the incidence of heart disease in this country, and may have led instead to the steep increase in obesity and Type 2 diabetes. I have interviewed researchers whose computer models have calculated that cutting back on the saturated fats in my diet to the levels recommended by the American Heart Association would not add more than a few months to my life, if that. I have even lost considerable weight with relative ease by giving up carbohydrates on my test diet, and yet I can look down at my eggs and sausage and still imagine the imminent onset of heart disease and obesity, the latter assuredly to be caused by some bizarre rebound phenomena the likes of which science has not yet begun to describe.

Little meaningful evidence existed then, as I also noted, to ease these anxieties. A critical fact in this debate, indeed, the reason it continues to exist at all, is that we still have precious little evidence. What we want to know, after all, is whether LCHF/ketogenic eating—rather than, say, a Mediterranean diet or a very-low-fat diet or a vegetarian diet—will not only lead to more or less weight loss but will kill us prematurely.

To establish this knowledge in any reliable manner, we have to do experiments, the finest of which known to medicine are randomized controlled trials. In concept, they’re simple: Choose two groups of people at random; have one group eat one diet and the other group eat another diet; see what happens. Which group of randomly chosen individuals lives longer, and which has more or less disease? The catch is that it takes decades for these chronic diseases to establish themselves, and to find out how long we live, and the differences between groups in what is technically known as morbidity (sickness) and mortality (age at death) may be subtle. For these reasons the kinds of experiments that shed light on this question of which are the healthiest eating patterns (for all or some subset of the population) require at least a few tens of thousands of subjects, and then they have to proceed for long enough—perhaps decades—to reliably determine if the subjects are getting more or less heart disease, dying sooner or later, in a way that’s clearly the result of what they’re eating.

Medicine is a science, so the concept of hypothesis and test still holds, and these clinical trials are the tests of the relevant hypotheses about diet and health. To do these trials correctly, though, would cost a huge amount of money. Many such trials would have to be done, some just to see if the others got it right, and they are almost unimaginably challenging. The concept is simple, the reality anything but. They can fail in so many different ways that some prominent public health authorities have recently taken to arguing that they shouldn’t be done. They argue that we should trust what they think they know about the nature of a healthy diet, and that this knowledge should apply to all of us, whether we are predisposed to get fat on such a diet or not. I respectfully disagree.

Absent this kind of reliable evidence, we can speculate on whether a diet is likely to kill us prematurely or is healthier than some other way of eating (i.e., we’ll live longer and stay healthy longer) by applying certain rules, but we must always acknowledge that we are guessing. For instance, eating foods that humans have been eating for thousands or hundreds of thousands of years, and in the form in which these foods were originally eaten, is likely to have fewer risks and so to be more benign than eating foods that are relatively new to human diets or processed in a way that is relatively new. This argument was made famously in the context of guidelines for public health by the British epidemiologist Geoffrey Rose in 1981. If the goal is to prevent disease, Rose observed, which is what public health guidelines and recommendations are intended to do, then the only acceptable measures of prevention are those that remove what Rose called “unnatural factors” and restore “ ‘biological normality’—that is…the conditions to which presumably we are genetically adapted.”

Remove and unnatural are the operative words. Removing something unnatural implies that we’re getting rid of something that is likely to be harmful. Take, for example, the advice that we shouldn’t smoke cigarettes. We have very little reason to think that removing cigarettes from our lives will do physical harm, because there’s nothing “natural” about smoking cigarettes. They’re a relatively new addition to the human experience.

If we’re adding something that is new to our diets, hence “unnatural,” thinking it will make us healthier, we’re guessing that the benefits outweigh the harms. There are likely to be both. Now we have to treat that new thing just as we would a drug that we think is good for us and that we’re supposed to take for life (say, a drug that lowers our cholesterol levels or our blood pressure). How do we know it’s safe, even if it seems to be beneficial in the short term?

All this is a judgment call and depends on perspective. One reason all diet authorities now agree more or less that we should cut back on our consumption of highly processed grains (white flour) and sugars (sucrose and high-fructose syrups) is that these refined grains and sweet refined sugars are relatively new to human diets. We assume that no harm can come from not eating them and perhaps quite a bit of good. Eating or drinking sugar, for instance, might have benefits in the short run—the rush of energy might fuel athletic performance or allow us to perform better on a test in school—but that doesn’t tell us whether the long-term consumption is to our detriment. Health authorities have mostly come to believe it is.

The idea that we should all eat tubers, like sweet potatoes, as proponents of the paleo diet suggest, is based on the assumption that our hunter-gatherer ancestors ate them for a couple of million years, implying that they are safe. Some paleo advocates take this assumption a step further and propose that we’d be healthier eating tubers than not. But they’re only guessing. It may be true, or maybe it’s true for some of us but not for others. We have no way to tell, short of doing one of those incredibly expensive, unimaginably challenging clinical trials.

When we’re told that we should consume more omega-3 fatty acids (a kind of polyunsaturated fat in fish oil and flaxseeds, among other sources) and fewer omega-6s (another kind of fat), it is based on the assumption that this shift in the balance of fats we ingest will make us healthier and live longer. In this case, researchers have done a few long-term trials to test the assumption, and the results have been mixed: Maybe they do, maybe they don’t. Nonetheless, we continue to hear that we should eat more omega-3s and fewer omega-6s because we currently consume a lot of omega-6s in our diets (from corn and soybean oil, conspicuously, and from eating animals that have been raised on corn and soybeans), and that’s considered unnatural. By this thinking, we are not genetically adapted to have such a high percentage of fats from omega-6s. It might be the correct assumption, but we don’t know.

One reason I and others promote the idea that eating saturated fat from animal products is most likely benign is that we’ve been consuming these fats as a species for as long as humans have been a species. The evidence isn’t compelling enough to convince us that this assumption is likely to be wrong. We may or may not have been consuming as much of these saturated fats, but we can presume we are genetically adapted to eating them. They are “vintage fats,” to use a term I first saw employed by Jennifer Calihan and Adele Hite, a registered nurse, in their book Dinner Plans: Easy Vintage Meals, and they include some vegetable oils—from olives, peanuts, sesame, avocado, and coconuts—and all animal fats in this category. Calihan and Hite contrast them to “modern fats”—margarine; shortenings of any kind; and industrially processed oils from rapeseeds (canola oil), corn, soy, cottonseed, grapeseed, and safflower. Vintage fats, by this thinking, can be trusted to be benign. Modern fats, not so much.

This is also why we believe that meat from grass-fed, pasture-raised animals is healthier for us than that from grain-fed, factory-farmed animals: The fat content of this meat will be more closely aligned to that of the animals our ancestors ate for the past million or so years. It will be more natural. (Perhaps more important, it is a way of eating that does not support the cruel and inhumane treatment that is common to factory-farming operations.) New foods or old foods in unnatural forms are more likely to be harmful than those foods to which we are presumably genetically adapted.

This belief also, ultimately, underpins the conventional thinking that a healthy diet includes ancient grains—quinoa, for instance, or couscous—or brown rice and whole grains rather than highly refined grains like white rice and white flour. Even without knowing any mechanisms for why this might be true—gluten content or glycemic index (how quickly or slowly the glucose hits our bloodstream)—and absent, once again, any meaningful experimental evidence, the assumption is that our ancestors ate these grains for maybe a few thousand years, in the form in which we’re eating them. Hence they are likely to be benign, at least for people who are predisposed to be lean and can tolerate a higher carbohydrate content in their diet.

The caveat, of course, is that definitions of natural and unnatural can depend on the perspective of the nutrition authority. When we’re parsing the latest diet advice, we have to make judgments about how the proponents of the advice define natural and unnatural. Are ancient grains natural because some populations (but not all) have consumed them for thousands of years, more or less since the invention of agriculture? Or are all grains unnatural because we’ve been consuming them for only a few thousand years, since the invention of agriculture? Are we safe adding something presumably natural to the diet (ancient grains or tubers or omega-3 fatty acids), or is it a better idea to remove only the unnatural elements (refined grains, sugars, some of the omega-6 fatty acids)? I think the latter is the safer bet. But this, too, gets complicated because as we remove sources of energy from the diet, we have to replace them.

What might be the most complicating factor in how we think about how we eat is the influence of the latest news, the latest media report on the latest study that is making a claim sufficiently interesting to constitute news. By definition that is what’s new, which means it either adds significantly to the conventional wisdom or contradicts it or speaks to whatever diets have indeed become particularly faddish these days.*1

The best reason to ignore the latest study results, the latest media reports suggesting we should eat this and not that, is that the interpretation of these latest studies is most likely wrong. A discussion highlighted in the media these days is what science journalists refer to as the “reproducibility crisis”—some large proportion of the studies that are published either get the wrong results or are interpreted incorrectly or maybe both. If we include those studies that are just meaningless, only one in ten or one in twenty studies (that make the press or appear on your home page) may be worth our notice. This percentage may be even smaller in nutrition and lifestyle research, in which the researchers are so poorly trained and the research so challenging to do. This is one reason the committees that decide on Nobel Prizes traditionally wait decades before acknowledging work to be prizeworthy. Far more often than not, if we wait long enough, we’ll see other studies being published making the opposite claims of whatever we’re reading today. We won’t know which is right until long after their publication. Perhaps never.

“Trying to determine what is going on in the world by reading newspapers,” as a famously clever screenwriter/director/journalist named Ben Hecht once wrote, “is like trying to tell the time by watching the second hand of a clock.” The same is true of research and science. Trying to tell what’s true by looking at the latest articles published in a journal—and particularly in nutrition—is another fool’s game. The best idea is to attend little to the latest research and focus instead on the long-term trends, the accumulation of studies (one hopes, interpreted without bias), even if the long-term trends rarely, if ever, appear in the news.

Since the heyday of the Atkins diet in the 1970s, authorities have refused to accept the notion that LCHF/ketogenic eating is safe. (And those that do promptly lose their standing as an authority by doing so.) They believe that the fat content in the foods we think we should eat instead of refined carbohydrates and sugar is too high, so arguably unnatural. Those of us who promote this way of eating can speculate that many hunter-gatherer populations lived on vaguely similar diets and perhaps even in a state of ketosis—the Inuit, pastoralists like the Maasai warriors in Kenya, Native Americans in the winter months—but we’re just speculating. The unusual aspect of these diets leads to legitimate questions about risks outweighing the benefits. This is as it should be.

No matter how much weight people might lose, no matter how easily, the orthodox medical opinion remains that these diets will kill us prematurely. Generations of physicians, medical researchers, dietitians, and nutritionists have been taught to believe (as was I and probably you, too) that we know what a healthy diet is. We know it because this is what healthy people tend to eat. They eat fruits, vegetables, whole grains, pulses (legumes), such as lentils, peas, and beans—mostly plants and plenty of carbohydrates. They avoid red meat and processed meats, and the fats they eat tend to be unsaturated, from plant sources rather than animal. Any radical deviation from this way of eating, regardless of weight loss, according to the consensus of medical opinion, is likely to be unsustainable and ultimately to our detriment.

This is the reason the authorities convened annually by U.S. News & World Report to judge diets and tell us what to eat rank LCHF/ketogenic diets as among the least healthy imaginable, regardless of the copious research and clinical experience that now argues quite the opposite. This is why two of the more media-savvy proponents of conventionally healthy eating—David Katz, a physician formerly associated with Yale University, and the former New York Times columnist Mark Bittman, a best-selling cookbook author—thought it appropriate to suggest recently in New York magazine that losing weight on LCHF/ketogenic eating (let alone maintaining weight for a lifetime) was analogous to getting cholera, an often fatal, infectious diarrheal disease. “Not everything that causes weight loss or apparent metabolic improvement in the short term is a good idea,” they wrote. “Cholera, for instance, causes weight, blood sugar, and blood lipids to come down—that doesn’t mean you want it!”

Despite the hyperbolic rhetoric, Katz and Bittman have our best interests in mind. Their concern is a legitimate one. The world is full of things we can do or take—medications and performance-enhancing substances—that will reverse and maybe even correct some symptoms of ill health in the short run, but will shorten our lives or ruin them if we take them for years or decades. The first rule of medicine is not actually to do well by your patient, but to do no harm. That’s the Hippocratic Oath. As a recent New York Times op-ed said about a drug that seems to do a remarkable job of quickly easing serious suicidal depression, “questions also remain about the safety of long-term use.”

Questions will always remain about the safety of long-term use…of anything. Imagine that you decide to take up running as a hedge against aging. Whether you think about it this way or not, you are implicitly making a judgment about the risks and benefits of the endeavor. Would you suffer more or less damage to your joints, for instance? Will you live longer by stressing your system in these workouts, or will they kill you prematurely? Marathoners die of heart attacks, too, occasionally young. Jim Fixx, author of The Complete Book of Running, a best seller in 1977, tragically died of a heart attack while out for a run. He was fifty-two years old. The conventional wisdom is that there are few things we can do that would be better for us, but we’ll never know for sure. We know that endurance runners seem to be very healthy, but that may not apply to us.

An almost universal misconception about nutrition and modern medicine—one shared by authority figures, physicians, and the journalists who cover the field—involves when clinical trials are necessary to guide our decisions and when they’re not. You do not need a clinical trial (costing tens of millions of dollars with tens of thousands of subjects) to tell you whether LCHF/ketogenic eating, or any regimen from vegan to carnivore, will allow you to achieve significant weight loss easily, without hunger, and make you feel healthier than you did. You can try any of these diets yourself and find out. It doesn’t matter what clinical trials conclude. What matters is what happens to you. Try changing the way you eat, and you will find out, just as you can take a new prescription drug and learn relatively quickly whether it helps whatever ails you and makes you feel better. Clinical trials are necessary to tell us about the long-term risks and benefits of one way of eating versus another—vegan, say, compared to carnivore, the two extremes—not the short-term. Those we can learn about reliably on our own.

“Is it safe?” is always one of two ultimate questions when considering a change of diet or lifestyle, particularly with the goal of preventing chronic disease. “Does it fix what ails us?” is the other. The two questions are so intimately related that we cannot discuss one without the other.

This is one of the many conspicuous problems with the argument that LCHF/ketogenic eating is simply too risky, if not for the short term, then for the long. The authorities who make this argument assume, as we’ve discussed, that we have viable alternatives, that we can achieve and maintain a healthy weight via any number of dietary approaches (so long as we eat less), like the Mediterranean diet, which they assume to be safe. For them, the observation that lean, healthy people eat this way—not all of them, though—seals the deal. To believe that it applies to all of us, you have to believe that those of us who fatten easily, as I’ve discussed and disagreed with strongly, are no different from those lean folks physiologically and hormonally.

By this orthodox thinking, LCHF/ketogenic eating is just another of many routes to doing what’s necessary: restricting calories and eating less. It’s seen as a particularly radical way to accomplish that, and radical ways to do anything are unnatural and entail, by definition, considerable risk, hence a relatively high likelihood of doing harm. According to orthodox thinking, eating a conventionally healthy diet as lean and healthy people appear to do, but less of it, is clearly an alternative for heavy people, one they can assume to be safe. These authorities simply will not confront the possibility that eating less or not too much of a conventionally healthy diet will not fix what ails many of us. If eating a conventionally healthy diet but less of it, and achieving and maintaining a healthy weight by doing so, is not a viable reality for us, then this argument falls apart.

It’s also critically important to understand the basis of the faith upholding these arguments. The authorities who make them—whether they are the experts convened for U.S. News & World Report or the U.S. Department of Agriculture’s dietary guidelines or the Katzes and Bittmans of the world or the well-meaning friends (“dude!”) who advise us to ease off the bacon—derive their opinions not from experience but from theoretical concepts about a healthy diet. They have merely embraced, as virtually all of us once did, the conventional hypotheses about the nature of a healthy diet. This way of thinking seems intuitively obvious and seems to work for them. In this sense, it’s helpful to think of the half-century-old controversy about the nature of a healthy diet as a conflict between hypothesis and experience.^*2

On the one hand, we have ideas about how best to eat to be healthy, ideas we think are true or that seem to be true. On the other, we have what physicians observe in their clinics and what happens to us, what we experience, when we try different diets. The conventional wisdom on nutrition is dominated by the hypothesis that saturated fats cause heart attacks by raising cholesterol levels, specifically the “bad cholesterol” in low-density lipoproteins (LDLs). This hypothesis has dominated orthodox thinking on diet and health, much as the one ring in J. R. R. Tolkien’s The Lord of the Rings “rules them all.” Hence, eating polyunsaturated fats from corn, soy, or canola oil, instead of saturated fats, by implication, will make us live longer. The ideas that we should avoid animal products (red meat, eggs, and dairy in particular), that they do us harm, and that we will live longer and healthier lives if we eat a mostly or all-plant diet are also based largely on the fear of saturated fats.

Physicians and dietitians are expected to base their diet and lifestyle advice on these hypotheses, but they have no way to know whether their advice makes a difference. When a patient dies, as all eventually will, regardless of age or cause of death, regardless of whether her cholesterol levels changed or not, the physician is privy to no information about what role the low-fat diet might have played. By the same token, should I die tomorrow or in my hundredth year, my next of kin will not know if my unconventional high-fat eating shortened my life or lengthened it. (Critics of my nutrition work will insist that the fat killed me prematurely, regardless, but they’ll be guessing.) Maybe Jim Fixx would have had his tragic fatal heart attack a decade younger had he not taken up running. Maybe he would have died in his early fifties regardless. We’ll never know.

Even if we had strong clinical trial evidence to support these hypotheses, which we don’t, we wouldn’t know the answer to these questions. The hypotheses and the evidence on which the authorities come to these conclusions—i.e., to embrace these assumptions—suggest only that we’re more likely to live longer if we eat conventionally healthy diets and exercise, not that we will. So we will have to make a risk-benefit analysis as to whether the likelihood that we’ll live longer makes it worth engaging in the relevant behavior for the rest of our lives. This raises another obvious question: If the authorities are right, for instance, that eating saturated fat will shorten our lives, can we quantify it? How much longer can we expect to live if we restrict our fat consumption?

This is yet another question the authorities seem to avoid, perhaps because the answer is not to their liking. If the conventional wisdom is right and eating saturated fat raises your LDL cholesterol (as for many of us it will) and so gives you a heart attack and kills you prematurely, how many years of life would you have gained if you avoided fat-rich foods and particularly those with saturated fat, or replaced at least some of that saturated fat (from animals) with polyunsaturated fats from seed oils, as the authorities concerned with our heart health advise? In other words, assuming the experts are right, what kind of culinary sacrifice is our fear of saturated fat worth?

As I noted in my 2002 New York Times Magazine article, the answer to that question was worked out long ago by three groups of researchers, all in agreement: at Harvard (published in 1987), at McGill University in Montreal, and at the University of California San Francisco (both 1994). These researchers estimated the benefit to longevity if we cut our fat consumption by a quarter and our saturated fat consumption by a third from what we might have typically eaten back then, lowering our cholesterol significantly, and they all concluded that absent other serious risk factors for heart disease, we’d live on average from a few days to a few months longer.

As one of these researchers pointed out to me when I interviewed him, the added time is not in the prime of our lives but rather at the very end of our lives. This seems obvious, but it’s a point worth pondering. Instead of dying, say, in March of our seventy-fifth year, we die in April or May. A ninety-year-old is likely to get a few more months being ninety or maybe will make it to ninety-one. That could be a good thing when you’re ninety, or maybe not, depending on the quality of your life at the time. A sixty-year-old is likely to gain only a couple of extra weeks. It’s not even clear that this dietary intervention prevents any heart attacks. Even in the best of all worlds, it may delay them merely by those few weeks or months.

After the 1987 Harvard analysis was published in the Annals of Internal Medicine, Marshall Becker, a professor of public health at the University of Michigan, suggested that avoiding fat or saturated fat to prevent heart disease is “analogous to stewards rearranging the deck chairs on the Titanic.” Even that analogy, though, assumes that all the fat-restricted diet does is prevent heart disease and doesn’t do us harm—for instance, make us fatter and more diabetic because of its carbohydrate content.

There is another way to parse these statistics of population averages, and this is the one the authorities seem to prefer. It is indeed possible that a few of us will die prematurely, perhaps at fifty instead of eighty, as a direct result of elevated cholesterol. If those people eat a cholesterol-lowering diet, they will live significantly longer. But they don’t know who they are in advance—nobody does—so we all have to eat the cholesterol-lowering diet for those lucky people to benefit. The rest of us would get no benefit at all. We may even be harmed by such a diet, as many doctors now believe. In 1999 one of the legendary experts in cholesterol research, Scott Grundy of the University of Texas, described this to me as the I-have-to-eat-a-low-fat-diet-for-life-so-my-neighbor-down-the-street-doesn’t-get-a-heart-attack scenario. Ninety-nine out of one hundred of us who avoid butter and bacon for a lifetime may well do it for no health benefit whatsoever, even if the conventional wisdom on saturated fat is right.

Physicians who embrace and prescribe LCHF/ketogenic eating believe that these conventional healthy-diet hypotheses are refuted daily in their lives and in their practices. After all, many of them and their patients had lived and eaten by these conventional guidelines while they got progressively fatter and sicker (as had I). Some had been vegetarians, even vegans, but LCHF/ketogenic eating was what eventually allowed them to easily lose their excess fat and reverse any progression toward hypertension or diabetes. That’s what they directly observed, and that, in turn, is what their patients experience. No faith is necessary to observe or experience these benefits.

Recall what the hundred-plus Canadian physicians wrote in HuffPost about their observations, their experiences, when their patients embraced LCHF/ketogenic eating: “What we see in our clinics: blood sugar values go down, blood pressure drops, chronic pain decreases or disappears, lipid profiles improve, inflammatory markers improve, energy increases, weight decreases, sleep is improved, IBS [irritable bowel syndrome] symptoms are lessened, etc. Medication is adjusted downward, or even eliminated, which reduces the side-effects for patients and the costs to society. The results we achieve with our patients are impressive and durable.” Physicians who now prescribe these diets commonly say that they rarely if ever prescribe drugs to their patients for blood sugar control or hypertension; rather, they de-prescribe, they get patients off medications. That’s compelling testimony.

One physician I interviewed put this trade-off in perhaps its starkest perspective. Caroline Richardson is a family medicine doctor at the University of Michigan and a health services researcher who also works for the university’s Institute for Healthcare Policy and Innovation. She started her career doing physical activity research and then gradually transitioned into diabetes prevention. For years, she told me, she counseled her patients to follow the Diabetes Prevention Program regimen of low-fat, calorie-restricted diets plus exercise. Most of her patients, though, were extremely obese and half were diabetic. Slowly she shifted into studying and prescribing LCHF/ketogenic eating—typically, after finding out how well a relatively low-carb diet worked for her.

Now Richardson tells her patients to read Always Hungry?: Conquer Cravings, Retrain Your Fat Cells, and Lose Weight Permanently by David Ludwig, a physician and professor of nutrition at Harvard, and to study its low-carb recipes. “One thing I love about the low-carb, high-fat diet, which I say again and again to my patients, is it makes you feel better.” The situation is similar to that of exercising, she told me. She advises her patients to exercise not because they’ll be healthier five years from now. She suggests they do it because they’ll feel better now. “When my patients cut out the carbohydrates, every single one comes back saying, ‘Wow, I feel like a new person.’ And one thing my patients tell me all the time is, ‘I don’t care if I die in ten years, I feel like crap today, I want to stop feeling like crap today.’ ”

Dan Murtagh’s take on this trade-off is also worth hearing. Murtagh is a general practitioner working in Northern Ireland with a patient population of mostly middle- and working-class families. He told me that when he was in medical school—he graduated in 2002—he heard little discussion about an obesity or diabetes epidemic. By the time we spoke fifteen years later, he was diagnosing a new case of type 2 diabetes in his clinical practice weekly. He became interested in diet and nutrition in 2009 when a patient asked him about the safety and efficacy of a paleo diet.

Murtagh did his homework and went “down the rabbit hole.” First he read The Paleo Diet by Loren Cordain, the Colorado State University exercise physiologist who did the formative thinking on this way of eating. That led Murtagh to books on LCHF/ketogenic eating. He says the arguments in these books (including mine) made sense to him, so he experimented on himself and then tried it on his patients. “It’s all very well waxing on about what you think is going to happen on these diets,” he said to me, “but eventually you have to roll up your sleeves and get to work and see what happens.”

When I interviewed Murtagh, he told me about several patients whom he had counseled to avoid carbohydrates and to replace those calories with natural (vintage) fats. About one diabetic patient, “not particularly heavy-set,” he said, “I don’t think remission is a strong enough word for what happened to his diabetes.” He described another patient, in his early fifties, as “textbook obese”: six foot one, 320 pounds, on his way to becoming diabetic, but already with fatty liver disease, gout, and hypertension. Prior to changing how he ate, this patient was taking two medications daily for his blood pressure, another medication for his gout, and another for chronic indigestion and heartburn. After a year of LCHF/ketogenic eating, he had lost upward of 110 pounds and was medication-free.

Surely he was healthier, but Murtagh’s medical colleagues who were still bound to the conventional thinking were not sanguine. “I discuss the same patients with them I’ve discussed with you,” he said, and he gets pushback. “I’m thinking, ‘Look, you’re telling me I should go back to this patient who’s lost 110 pounds and got off all his medications, and tell him to go back to eating his bread and cut the fat off his bacon.’ ”

The fact that LCHF/ketogenic eating produces such remarkable results in the clinic has always represented a tremendous challenge to the conventional thinking on nutrition. It creates an essential conflict, a cognitive dissonance, between two seemingly mutually exclusive definitions of what it means to “eat healthy.” Over the last fifty years, healthy eating has conventionally been defined and institutionalized to mean eating fruits, vegetables, whole grains, and pulses in abundance, with plenty of carbohydrates—mostly plants—and minimal animal fats and little or no red or processed meats. The other definition is what many people appear to need to maintain a “healthy” weight: ideally little or no fruit, no whole grains, no legumes or pulses, very few carbohydrates, and plenty of fat, which often translates to plenty of red and even processed meat. How do we resolve the discrepancy? If achieving and maintaining a “healthy” weight requires us to eat an “unhealthy” diet, are we healthier or not?

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?^*3 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 (without 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.^*4 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 prematurely 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 eating 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.

Nutritional authorities (or at least those quoted in the media) still argue with the same dogmatic assurance as ever that they’ve always been right and so their credibility should not be doubted, but the conventional thinking on nutrition and the nature of a healthy diet has clearly changed considerably in the past twenty years. The slow, relentless accumulation of clinical trial and clinical evidence supporting what I’m arguing for in this book, and what thousands of physicians have now come to believe, has had an effect, which is how science is supposed to work.

Twenty years ago, when I first began reporting on this subject, the conventional wisdom was that the only way to lose weight was to consciously restrict calories (or exercise more); that diets that prevented heart disease had to be low in fat; and that LCHF/ketogenic eating was deadly. Now, with the notable exception of Katz and Bittman in their hyperbolic moods and U.S. News & World Report (where Katz has played a significant role in the authoritative committee), proponents of the orthodoxy in the media are typically arguing or defending a much different position: that calorie-restricted and/or low-fat diets are as good or as healthy as LCHF/ketogenic eating, about which there is nothing special. These conventional eating experts want people to know we still have a choice when it comes to weight loss (therefore these experts weren’t completely wrong, only partly). The informed argument is no longer that LCHF/ketogenic eating will shorten our lives but that other ways of eating may work just as well. The implication is that these other eating patterns aren’t as radical, making them easier to sustain and surely less of a risk.

A handful of prominent physicians and nutritional authorities will still actively argue—as they do, for instance, in the Netflix film What the Health—that the healthiest way to eat for all of us is to minimize animal fats and animal products. Not just to consume mostly plants but perhaps to eat only food that is plant-based, vegetarian, or even vegan. But these physicians or researchers have not compared these two approaches—whether in their own clinics or in clinical trials—to conclude that mostly plant diets work better for their patients or that LCHF/ketogenic eating does harm. (A reminder: The relevant trials that can do this reliably don’t exist.) These physicians, nutritionists, and even epidemiologists surveying populations have strong beliefs that mostly or all-plant diets are beneficial, which may be valid. But that tells us (and them) nothing about the relative benefits or harms of LCHF/ketogenic eating. These physicians don’t know, in effect, whether their patients would do better or worse abstaining from carbohydrate-rich foods specifically, rather than from animal products. They’re only guessing. Those who insist so vehemently that these diets are dangerous do so not because they have clinical experience to that effect, and not because they’re familiar with the clinical research literature, but because they don’t.

So is it safe? Can you follow an LCHF/ketogenic eating plan indefinitely without fearing that you’re slowly killing yourself? The existing evidence says that if you have metabolic syndrome, if you’re getting fatter or are already obese, if you’re prediabetic or already diabetic, avoiding carbohydrate-rich foods and replacing them with fat may be the single healthiest thing you can do for yourself. That’s why so many physicians have now become evangelists.

No one can guarantee what happens in the long run. The evidence to do so, as I’ve said repeatedly, doesn’t exist and may never exist. Anyone who makes an ironclad guarantee for any way of eating—that one diet will assuredly make you live longer than others—as Gladwell suggested and I tend to agree, is probably selling something (although perhaps with the best of intentions).

Over the years, both the media and the research community have fallen into the habit of discussing the constituents of healthy diets in terms of the benefits they may confer. Eating abundant fruits and vegetables, as a recent New York Times article said, “can promote health,” as though these foods contain indispensable ingredients that work to make us healthy and keep us healthy. By this logic, the more fruits and vegetables in a diet, the better. This may be true, but the only way we can get some reliable information is by adding them to our diets or taking them away and seeing what happens. Do we get leaner? Do we get healthier? Do we feel better or worse?

A more useful way to discuss the pros and cons of dietary changes, as implied earlier in this chapter and by Geoffrey Rose’s observation about natural and unnatural factors, is in terms of how well they do at removing whatever it is that makes us ill, while keeping the essential fats, minerals, and vitamins that we know reliably are necessary for health. (If we eat in a way deficient in these fats, minerals, and vitamins, we get deficiency diseases.) By this standard, we know that when carbohydrates are removed (including fruits and starchy vegetables) and replaced with fat, people get leaner and healthier. What was wrong with these folks has seemingly been corrected by the simple removal of nonessential constituents of the diet.

As such, LCHF/ketogenic eating can be thought of as working to correct our health rather than improve it. I’m proposing that’s how we should think about it.^*5 A diet that restricts carbohydrates and replaces those calories with fat corrects your weight by lowering it. It corrects your blood pressure by lowering it. It corrects your inability to control your blood sugar. It’s not the equivalent of taking a pill that will make you healthy; rather, it removes what makes you unhealthy, replaces those calories with a benign macronutrient (fat), and in so doing, fixes what ails you. These corrections are noticeable in real time, by patient, by physician, and by any individuals who try this approach on their own.

The gamble is that improving health in the short run will lead to improvements in the long run. We’re gambling that if something happens in the future, if a symptom of ill health develops, we can experiment with how we’re eating to see if that’s the cause, then fix it appropriately. We’re taking our health into our own hands. There are no ironclad guarantees, though. There never are.

In considering the question of what’s safe and what isn’t, one more vitally important aspect has to be taken into account. It’s no longer just our health that we’re worried about or our children’s—it’s the planet’s. So we must ask if LCHF/ketogenic eating is justifiable if it means increasing your “climate footprint” compared to alternatives. Given what may be a trade-off between humanity’s future and your own health (and that of your children), how do you decide?

In the last few years, the conventional wisdom has emerged that eating animal products results in a greater contribution to greenhouse warming of the planet than does eating plants. Because we worry with good reason that global warming is a major threat to planetary health and humanity’s future, we believe we should do whatever we can personally to mitigate it. This has led newspapers to publish analyses of “how to shop, cook and eat in a warming world,” as The New York Times did in April 2019, and to suggest that the fewer animal products we consume (and certainly the less beef, lamb, and dairy, as these seemingly have the greatest climate footprints), the healthier the planet will be.

This may indeed be true. While acknowledging that livestock can be raised in ways that are relatively climate friendly and much of it is (in the United States, for instance, more, say, than in Brazil), the implication is that the most climate-friendly eating pattern is one that omits these foods—a vegan diet—and that that’s how we should eat. For those who don’t think they can become a vegan, the Times suggests, then “another approach would be to simply eat less meat and dairy, and more protein-rich plants like beans, legumes, nuts and grains.”

The problem, of course, is that this thinking once again assumes that the conventional healthy diet—or even an unconventional and arguably unnatural diet, per Geoffrey Rose’s thinking, like the vegan diet—is indeed healthy for all of us. It builds on a foundation of the bad science in nutrition research of the past fifty years, and it shows little concern for the absence of clinical trials that might actually test it. It’s also the lean person’s perspective. If those of us who are predisposed to be insulin resistant, obese, and/or diabetic in the modern food environment get fat or stay fat eating beans, legumes, and grains, we have a conflict that must be resolved.

It’s certainly possible to eat a vegan or vegetarian LCHF/ketogenic diet, and many people now do. Whether it is a healthier option for some of us (rather than for the environment) in the long run than LCHF/ketogenic eating with some or even mostly animal products is an open question. I’m skeptical (as is my nature). Without the clinical trials, the only evidence we have on which to base our conclusions is how our weight and health status responds to these eating patterns. As we try to do what we can for the environment, the planet, and our future, we’ll have to take into consideration what we have to eat to remain healthy and how important that is to us. Until we know the trade-offs, both personally and as a society, it may be a costly mistake, regrettably, to assume that a way of eating that is healthiest for the planet is healthiest for us.