Eat Fat, Get Thin_Why the Fat We Eat Is the Key to Sustained Weight Loss and Vibrant Health

by Mark Hyman

  —Lisa Pelly

  What gives me a unique perspective is one simple fact: I don’t take money from any vested interests, nor have I spent my life proving one particular point of view, be it low-fat or low-carb, or pro– or anti–olive oil, or vegan or meat eater. In fact, I have been both a vegan and an omnivore over the course of my life. I have eaten low-fat, high-carb diets and low-carb, high-fat diets and have used all sorts of different diets with tens of thousands of patients over 30 years of medical practice. At points in my work I advocated for and prescribed low-fat vegetarian diets, but as the research emerged that convinced me that fat was good, I changed my recommendations. I am not married to a particular point of view. I am curious about what lies beneath the money and the egos behind the research. I am interested in one simple thing. What should we eat to stay fit, thin, and healthy? I want the same thing for myself as I do for you. I want to live long, be healthy, and avoid disease, and I would not eat things that I believe would threaten my health or longevity.

  The Fallacy of Focusing on Nutrients Instead of Real Food

  In this book, I will debunk some of the tightly held beliefs and myths that get in the way of our doing the right thing for our bodies and our health. Part of the confusion around nutrition is due to something called nutritionism. Nutritionism is the science of breaking down dietary components into their individual parts, such as one vitamin or one type of fat, and studying those components in isolation. This approach is helpful for studying medication, where there might be a single molecule designed to target one specific pathway and one specific disease. But it is not that helpful for studying individual nutritional components. Why? Because people eat food, not single components. They eat foods that contain often dozens of different ingredients, many different types of fat, proteins, carbohydrates, vitamins, minerals, phytonutrients, and more. For example, olive oil, which people think of as a “monounsaturated fat,” also contains about 20 percent saturated fat and 20 percent polyunsaturated omega-6 fat and even a little bit of omega-3 fat. Beef also contains all different types of fat. The nutrition world is shifting away from focusing on individual nutrients and toward focusing on dietary patterns, whole foods, and complex assortments of foods, that is, the way we actually eat.

  THE CREATION OF THE FAT FALLACY

  In the beginning of our understanding of calories, weight, and metabolism, there were two competing ideas. The first was that all calories were equal. This was based in simple physics: Burn 100 calories from soda or from olive oil in a laboratory and they release exactly the same amount of energy. But think about this rationally when applied to human biology: If you eat the same amount of calories in kale or gummy bears, do they do the same thing to your body? Is your weight affected the same way, regardless of the source of the calories? We are continually told that the regulation of weight is as simple as calories in, calories out. Just eat less and exercise more, and we will lose weight. This is called the energy balance hypothesis. It seems like one of those fundamental self-evident truths, except we now know that it is false.

  The calories in, calories out formula for weight maintenance became embedded in the halls of academia and in government policy, and the calorie counters won. Even the latest food-labeling regulations emphasize calories by making them big and bold on the label. New laws make it mandatory for fast-food restaurants to place calorie counts on menus. It stands to reason that if all calories are equal, and fat contains more than twice as many calories as carbs or protein (9 calories per gram vs. 4 calories per gram), then the best way to cut calories is to cut out fat. You could eat more food if you ate bread and pasta than if you ate butter, because butter is more energy-dense. This is what I was taught and what I believed until new research turned this idea upside down.

  Dr. Frederick Stare, who founded the department of nutrition at the Harvard School of Public Health in 1942 and served as its chairman until he retired in 1976, helped to entrench the idea that obesity was nothing more than a matter of energy imbalance. He stated that all calories had an equal impact on weight gain, “regardless of whether they derive from eggs or eggplant, grapefruit or green beans, skim milk or scotch whisky or soda pop or sirloin steak.” In his books, column, and writings, Stare encouraged the public to accept that “there are no ‘fattening’ foods or ‘slimming’ foods, just too much food.” He wrote, “Calories are all alike, regardless of their source. Patients cannot be misled by a high carbohydrate or high protein or high fat fad if they are aware that surplus calories are surplus calories, whether the source is carbohydrate or protein or fat, or alcohol in various beverages.”

  The idea of energy balance naturally implies that willpower is the key to weight loss, that all one needs to do is limit calories and increase exercise. The logical conclusion of this distorted thinking is this: If you are overweight, it must be because you are a lazy glutton who shuns exercise and loves to eat. The subtle message here is that the overweight person wants to be fat. It is their fault they are fat. Yet, in treating more than 20,000 patients, I have never met a person who wakes up and says, “Hey, today I am going to see how much weight I can gain.” On the contrary, most wake up with every intention of losing weight but can’t, not because of a character defect but because of bad advice based on incorrect scientific assumptions.

  When both the government (the Centers for Disease Control and Prevention) and the American Beverage Association’s websites offer the same dietary advice for weight loss, we should be suspicious. In this model, there is no good or bad food. The answer to obesity and weight regulation is moderation. In fact, in testimony to Congress, under oath, the chair of the American Beverage Association said with a straight face, “In a well balanced diet we need two liters of liquids a day. Soft drinks can be a healthy part of that intake. I would reject any argument that they are in any way harmful.” This is a bald-faced lie contradicted by mountains of research, including the 2015 study in the journal Circulation that found that sugar-sweetened drinks kill 184,000 people a year from obesity, heart disease, and cancer.

  A CALORIE IS NOT A CALORIE

  The conventional wisdom doesn’t stack up against emerging research that shows us that a calorie is not a calorie (when you eat it). In a vacuum or a lab, calories from all foods release the same amount of energy when burned—whether the food is coconut oil or honey. But when you eat, foods have to go through your body, and they can have profoundly different effects on your hormones, brain chemistry, and metabolism. Fat calories burn differently than sugar calories do. Fat calories speed up your metabolism. Fats have to be burned and are not easily stored because they don’t spike insulin—the fat-storage hormone. Fat works on the brain to cut your appetite so you eat less overall during the day. On the other hand, sugar and carb calories do exactly the opposite: They spike insulin, promote fat storage, and are quickly laid down as dangerous belly and organ fat. They slow your metabolism and increase hunger and cravings. Mounds of scientific research support this perspective.

  This hormonal or metabolic hypothesis of weight gain supports the idea that it is the composition and quality of the foods you eat (and the hormones and biochemistry they subsequently trigger) that determine whether you lose or gain weight. In other words, it is not how much you eat but what you eat that controls the metabolic switches. Food’s inherent information—the messages and instructions it contains—is what drives your metabolism. Again, carbs shift your body toward fat storage (anabolism),3 while fats shift your body toward fat burning (catabolism).

  I have lost both in belly fat and hip measurements. It has been many years since I have consumed this many calories while “dieting” and still lost weight!

  —Barbara Chitkara

  This idea was actually quite well described as early as the nineteenth century and was the basis for much of the dietary advice for the last part of the nineteenth and early part of the twentieth century. Leading medical experts in the late nineteenth century believed that the best strategy for treating ob
esity was carbohydrate restriction. It was in the medical textbooks of the day. The fathers of modern medicine, William Harvey, a nineteenth-century English physician, and William Osler, one of the founding physicians of Johns Hopkins, both advised low-carbohydrate diets for weight loss.

  Despite historical evidence to the contrary, however, the idea of energy balance slowly took hold in the 1950s and 1960s. Dr. Frederick Stare at Harvard continued to heavily promote the idea, even while acknowledging obvious holes in the theory: He noted that chronically high blood sugar was looking more and more like a strong driver of weight gain. He called this “obesity of the metabolic type,” caused by eating too much sugar. This is the crack in the theory that all calories are created equal.

  Even if you consume less food and fewer calories, when you eat excess carbs or sugar, you trigger insulin, which turns on a fat-production factory in the liver and your fat-storage system, and you gain weight. Dietary fat, however, doesn’t trigger insulin, and so you don’t store fat. But despite understanding this perspective, which was advocated by other scientists at the time, Stare was unwilling to advocate for almost anything for weight loss but physical activity and calorie restriction.

  At the beginning of the twentieth century, German diabetes specialist Carl von Noorden believed in the metabolic hypothesis, but he later changed his position. In his earlier work, he postulated that obesity was a pre-diabetic state and said, “Obese individuals of this type have already an altered metabolism for sugar, but instead of excreting the sugar in the urine, they transfer it to the fat-producing parts of the body.”4 This concept was pushed under the carpet and ignored despite evidence to the contrary, and the debate smoldered on for years.

  In 1953, in a report in the New England Journal of Medicine titled “A Reorientation on Obesity,” Dr. Alfred Pennington argued that obesity was caused by the hormonal effects of carbs and could be treated by restricting carbs, without worrying about fat and protein.5 That was a radical departure from the idea that weight regulation was just a matter of calories in, calories out.

  In 1977, a study published in the American Journal of Clinical Nutrition showed that the composition of your diet (high-carb, low-fat or high-fat, low-carb) could have profoundly different effects on human biology even though the calories consumed were identical. They kept ten obese men in a metabolic ward in a hospital and strictly controlled their diets. Even though there were only a few people in the study, these metabolic ward studies are relevant because of how carefully their food intake and energy expenditure was measured. For two weeks, these men consumed a high-carb diet of 70 percent carbs, 20 percent protein, and 10 percent fat. Then, after a 7-day rest period, the men were switched to a high-fat diet consisting of 70 percent fat, 20 percent protein, and 10 percent carbs. When the study subjects were on a high-fat diet they lost more weight than when they were on a high-carb diet, and had much greater drops in blood sugar, insulin levels, triglycerides, and cholesterol, even though they ate the same total number of calories.6

  In 2002, Dr. Walter Willett, of the Harvard School of Public Health, summarized all the research on fat and obesity (as well as fat and heart disease) and found no connection. He stated that “diets high in fat do not appear to be the primary cause of the high prevalence of excess body fat in our society, and reductions in fat will not be a solution.”7

  DOES EATING FAT CAUSE HEART DISEASE?

  Besides restricting fat for weight loss, the scientific community embraced and stridently promoted another hypothesis: that fat caused heart disease, our biggest killer. But the history of medicine is full of good ideas that turned out to be wrong and even dangerous. Thalidomide seemed to be a great idea and very effective at preventing morning sickness in pregnancy until it was discovered to cause severe birth defects. Hormone replacement therapy for women was thought to be so effective in preventing heart disease in women that it was considered malpractice not to prescribe it. More than 50 million menopausal women happily took hormones until a large study sponsored by the National Institutes of Health found that hormone replacement actually increased the risk of heart disease, stroke, and breast cancer.

  Before you read any further, you need to know the truth: Eating saturated fat does not cause heart disease.8 I know this might seem startling, given that we’ve spent the better part of a century avoiding everything from butter to egg yolks because we were told they weren’t good for our hearts. But better to know the truth and make new and healthier habits going forward.

  The theory that fat, and specifically saturated fat, is the cause of heart disease all started because of two main findings. First was that rabbits (which are obviously very different from humans) developed atherosclerosis (fatty deposits in the arteries) when they were fed cholesterol, which is completely absent from their vegetable diet. Second, countries that seemed to consume more saturated fat and the most fat generally (for example, Finland and the United States compared to Japan and Greece) had more heart disease. Since saturated fat raised blood levels of cholesterol, it was assumed that saturated fat caused heart disease. Suddenly, a weak hypothesis that was based on shaky observations, not on any real experiments, was taken as fact.

  This idea, spawned in 1953, was the brainchild of a very outspoken, passionate scientist from the University of Minnesota named Ancel Keys. Many questioned Keys’ scientific conclusions, but he was vigorous in criticizing anyone who challenged him. He was a dominant, persuasive, and charismatic man who convinced the world of his hypothesis.

  The history and failure of Keys’ diet-heart hypothesis, that fat is bad, is well documented in Nina Teicholz’s book, The Big Fat Surprise.9 Keys made his conclusions based on observations of heart disease, death rates, and fat consumption in six countries, even though data on twenty-two countries from the Food and Agriculture Organization of the United Nations and data from the World Health Organization (WHO) was available. The diet record keeping was questionable. He selected six countries that he felt had the best data (or perhaps that he knew would best support his ideas) and found a direct correlation between the amount of fat in the diet and heart disease. He ignored data from the other sixteen countries. A more recent 2010 review by the Food and Agriculture Organization found that “there is no probable or convincing evidence” that a high-fat diet causes heart disease.10

  When all twenty-two countries were included in the analysis in 1957 by two who questioned Keys’ conclusions, Drs. Herman Hilleboe, then New York State commissioner of health, and Jacob Yerushalmy, professor of statistics at the University of California, Berkeley, there was zero correlation between fat in the diet and heart disease.11 Yet despite that fact, and the fact that observational or population studies cannot prove cause and effect, Keys’ study took hold.

  Dr. Keys followed up his six countries study with the famous Seven Countries Study, launched in 1956, in which he again carefully selected countries that supported his theory and conveniently omitted countries such as France and Switzerland that had high-fat diets and very little heart disease. He followed 12,770 people but evaluated diet intake for only 499, or 3.9 percent of them. This is poor science, insufficient to make broad conclusions. Yet draw “definitive” conclusions he did, and he further refined his theory to focus on saturated fat as the enemy.

  The theory went something like this: Blood cholesterol was associated with (but not proven to be a factor in) increased risk of heart disease. Saturated fats increased cholesterol. So the enemy was saturated fat. While he did find a correlation between saturated fat and heart disease in the countries he picked, he did not find any reduction in death in countries with lower saturated fat intake. And though he found the correlation of saturated fat and heart disease between countries, when he looked at different regions of the same country—such as different regions of Finland or different islands in Greece, such as Corfu and Crete—he found that they had widely different rates of heart disease. Something didn’t add up.

  There were many problems with Keys’ research, i
ncluding the way in which he collected people’s dietary history and how few people he had dietary information on for a population-type study, which usually requires thousands of participants to be able to draw any conclusions. He studied countries in postwar Europe, when diets were affected by wartime shortages, so they didn’t represent the true diets of these populations. And there were many other severe limitations in his research. Basically, he set up his study to prove his hypothesis.

  CHALLENGES TO THE DIET-HEART HYPOTHESIS

  One of the voices Keys tried to silence was that of John Yudkin, the British physician and founding professor of the Department of Nutrition at Queen Elizabeth College in London. Dr. Yudkin was ahead of his time. As early as 1964, he challenged the unproved assumption that fat in the diet caused fat in the arteries. In the pre-Atkins era, he warned about the dangers of high sugar consumption and the risk of cardiovascular disease and promoted a low-carb, low-sugar diet in his popular 1972 book, Pure, White and Deadly. Dr. Yudkin carried out his own studies looking at the effects of sucrose on coronary risk factors and repeatedly published letters and reviews in leading medical journals arguing that the focus of public health efforts—at least as far as nutrition was concerned—should be on sugar.

  In the American Journal of Clinical Nutrition in 1981, Dr. Yudkin wrote, “As long ago as 1957, it was suggested from epidemiological evidence that the current high sucrose [sugar] consumption in Western countries could be a cause of the high prevalence of coronary heart disease.” He said that a high-sugar diet increases bad cholesterol and decreases good cholesterol, increases insulin and stress hormones (like cortisol), and even makes your blood more likely to clot—all tightly linked to heart attacks and strokes. High-sugar diets, he said, led to diabetes, blindness, and nerve and kidney damage and explained why diabetics have four times the risk of heart attacks as everyone else.