The Obesity Code: Unlocking the Secrets of Weight Loss (Why Intermittent Fasting Is the Key to Controlling Your Weight)

by Jason Fung

In treating patients with end-stage kidney disease, Dr. Fung learned two key lessons. First, that type 2 diabetes is the single commonest cause of kidney failure.

Gradually, it dawned on Dr. Fung that he was practicing medicine exactly as he had been taught: by reactively treating the symptoms of complex diseases without first trying to understand or correct their root causes.

Dr. Jason Fung’s existence. Then one day I chanced upon his two lectures—“The Two Big Lies of Type 2 Diabetes” and “How to Reverse Type 2 Diabetes Naturally”—on YouTube.

According to Dr. Fung, the first big lie in the management of type 2 diabetes is the claim that it is a chronically progressive disease that simply gets worse with time, even in those who comply with the best treatments modern medicine offers. But, Dr. Fung argues, this is simply not true.

So why are we unable to acknowledge the truth? Dr. Fung’s answer is simple: we doctors lie to ourselves. If type 2 diabetes is a curable disease but all our patients are getting worse on the treatments we prescribe, then we must be bad doctors. And since we did not study for so long at such great cost to become bad doctors, this failure cannot be our fault. Instead, we must believe we are doing the best for our patients, who must unfortunately be suffering from a chronically progressive and incurable disease. It is not a deliberate lie, Dr. Fung concludes, but one of cognitive dissonance—the inability to accept a blatant truth because accepting it would be too emotionally devastating.

The second lie, according to Dr. Fung, is our belief that type 2 diabetes is a disease of abnormal blood glucose levels for which the only correct treatment is progressively increasing insulin dosages. He argues, instead, that type 2 diabetes is a disease of insulin resistance with excessive insulin secretion—in contrast to type 1 diabetes, a condition of true insulin lack. To treat both conditions the same way—by injecting insulin—makes no sense. Why treat a condition of insulin excess with yet more insulin, he asks? That is the equivalent of prescribing alcohol for the treatment of alcoholism.

Dr. Fung’s novel contribution is his insight that treatment in type 2 diabetes focuses on the symptom of the disease—an elevated blood glucose concentration—rather than its root cause, insulin resistance. And the initial treatment for insulin resistance is to limit carbohydrate intake. Understanding this simple biology explains why this disease may be reversible in some cases—and, conversely, why...

Unfortunately, the treatment of obesity is also one such example. Obesity is defined in terms of a person’s body mass index, calculated as a person’s weight in kilograms divided by the square of their height in meters. A body mass index greater than 30 is defined as obese. For more than thirty years, doctors have recommended a low-fat, calorie-reduced diet as the treatment of choice for obesity. Yet the obesity epidemic accelerates. From 1985 to 2011, the prevalence of obesity in Canada tripled, from 6 percent to 18 percent.1 This phenomenon is not unique to North America, but involves most of the nations of the world. Virtually every person who has used caloric reduction for weight loss has failed. And, really, who hasn’t tried it? By every objective measure, this treatment is completely and utterly ineffective. Yet it remains the treatment of choice, defended vigorously by nutritional authorities.

As a nephrologist, I specialize in kidney disease, the most common cause of which is type 2 diabetes with its associated obesity. I’ve often watched patients start insulin treatment for their diabetes, knowing that most will gain weight. Patients are rightly concerned. “Doctor,” they say, “you’ve always told me to lose weight. But the insulin you gave me makes me gain so much weight. How is this helpful?” For a long time, I didn’t have a good answer for them.

That nagging unease grew. Like many doctors, I believed that weight gain was a caloric imbalance—eating too much and moving too little. But if that were so, why did the medication I prescribed—insulin—cause such relentless weight gain? Everybody, health professionals and patients alike, understood that the root cause of type 2 diabetes lay in weight gain. There were rare cases of highly motivated patients who had lost significant amounts of weight. Their type 2 diabetes would also reverse course. Logically, since weight was the underlying problem, it deserved significant attention. Still, it seemed that the health profession was not even the least bit intereste...

Treatment of this terrible disease—obesity—was left to large corporations like Weight Watchers, as well as various hucksters and charlatans mostly interested in peddling the latest weight-loss “miracle.” Doctors were not even remotely interested in nutrition. Instead, the medical profession seemed obsessed with finding and prescribing the next new drug: •You have type 2 diabetes? Here, let me give you a pill. •You have high blood pressure? Here, let me give you ...

The conventional view of obesity as a caloric imbalance did not make sense. Caloric reduction had been prescribed for the last fifty years with startling ineffectiveness.

Reading books on nutrition was no help. That was mostly a game of “he said, she said,” with many quoting “authoritative” doctors. For example, Dr. Dean Ornish says that dietary fat is bad and carbohydrates are good. He is a respected doctor, so we should listen to him. But Dr. Robert Atkins said dietary fat is good and carbohydrates are bad. He was also a respected doctor, so we should listen to him. Who is right? Who is wrong? In the science of nutrition, there is rarely any consensus about anything: •Dietary fat is bad. No, dietary fat is good. There are good fats and bad fats. •Carbohydrates are bad. No, carbohydrates are good. There are good carbs and bad carbs. •You should eat more meals a day. No, you should eat fewer meals a day. •Count your calories. No, calories don’t count. •Milk is good for you. No, milk is bad for you. •Meat is good for you. No, meat is bad for you. To discover the answers, we need to turn to evidence-based medicine rather than vague opinion.

The major problem is the complete lack of a theoretical framework for understanding obesity. Current theories are ridiculously simplistic, often taking only one factor into account: •Excess calories cause obesity. •Excess carbohydrates cause obesity. •Excess meat consumption causes obesity. •Excess dietary fat causes obesity. •Too little exercise causes obesity. But all chronic diseases are multifactorial, and these factors are not mutually exclusive. They may all contribute to varying degrees.

For example, heart disease has numerous contributing factors—family history, gender, smoking, diabetes, high cholesterol, high blood pressure and a lack of physical activity, to name only a few—and that fact is well accepted. But such is not the case in obesity research. The other major barrier to understanding is the focus on short-term studies. Obesity usually takes decades to fully develop. Yet we often rely on information about it from studies that are only of several weeks’ duration. If we study how rust develops, we would need to observe metal over a period of weeks to months, not hours. Obesity, similarly, is a long-term disease. Short-term studies may not be informative.

Evidence-based medicine does not mean taking every piece of low-quality evidence at face value. I often read statements such as “low-fat diets proven to completely reverse heart disease.” The reference will be a study of five rats. That hardly qualifies as evidence. I will reference only studies done on humans, and mostly only those that have been published in high-quality, peer-reviewed journals. No animal studies will be discussed in this book.

“The Parable of the Cow”: Two cows were discussing the latest nutritional research, which had been done on lions. One cow says to the other, “Did you hear that we’ve been wrong these last 200 years? The latest research shows that eating grass is bad for you and eating meat is good.” So the two cows began eating meat. Shortly afterward, they got sick and they died. One year later, two lions were discussing the latest nutritional research, which was done on cows. One lion said to the other that the latest research showed that eating meat kills you and eating grass is good. So, the two lions started eating grass, and they died.

HERE’S THE QUESTION that has always bothered me: Why are there doctors who are fat? Accepted as authorities in human physiology, doctors should be true experts on the causes and treatments of obesity. Most doctors are also very hardworking and self-disciplined. Since nobody wants to be fat, doctors in particular should have both the knowledge and the dedication to stay thin and healthy. So why are there fat doctors?

What causes weight gain? Proximate cause: Consuming more calories than you expend. If more calories in than out is the proximate cause, the unspoken answer to that last question is that the ultimate cause is “personal choice.” We choose to eat chips instead of broccoli. We choose to watch TV instead of exercise. Through this reasoning, obesity is transformed from a disease that needs to be investigated and understood into a personal failing, a character defect. Instead of searching for the ultimate cause of obesity, we transform the problem into •eating too much (gluttony) and/or •exercising too little (sloth). Gluttony and sloth are two of the seven deadly sins. So we say of the obese that they “brought it on themselves.” They “let themselves go.” It gives us the comforting illusion that we understand ultimate cause of the problem. In a 2012 online poll,1 61 percent of U.S. adults believed that “personal choices about eating and exercise” were responsible for the obesity epidemic. So we discriminate against people who are obese. We both pity and loathe them. However, on simple reflection, this idea simply cannot be true. Prior to puberty, boys and girls average the same body-fat percentage. After puberty, women on average carry close to 50 percent more body fat than men. This change occurs despite the fact that men consume more calories on average than women. But why is this true?

What is the ultimate cause? It has nothing to do with personal choices. It is not a character defect. Women are not more gluttonous or lazier than men. The hormonal cocktail that differentiates men and women must make it more likely that women will accumulate excess calories as fat as opposed to burning them off. Pregnancy also induces significant weight gain. What is the ultimate cause? Again, it is obviously the hormonal changes resulting from the pregnancy—not personal choice—that encourages weight gain. Having erred in understanding the proximate and ultimate causes, we believe the solution to obesity is to eat fewer calories.

The “authorities” all agree. The U.S. Department of Agriculture’s Dietary Guidelines for Americans, updated in 2010, forcefully proclaims its key recommendation: “Control total calorie intake to manage body weight.” The Centers for Disease Control2 exhort patients to balance their calories. The advice from the National Institutes of Health’s pamphlet “Aim for a Healthy Weight” is “to cut down on the number of calories . . . they get from food and beverages and increase their physical activity.”3 All this advice forms the famous “Eat Less, Move More” strategy so beloved by obesity “experts.” But here’s a peculiar thought:...

WE WEREN’T ALWAYS so obsessed with calories. Throughout most of human history, obesity has been rare. Individuals in traditional societies eating traditional diets seldom became obese, even in times of abundant food. As civilizations developed, obesity followed. Speculating on the cause, many identified the refined carbohydrates of sugar and starches. Sometimes considered the father of the low-carbohydrate diet, Jean Anthelme Brillat-Savarin (1755–1826) wrote the influential textbook The Physiology of Taste in 1825. There he wrote: “The second of the chief causes of obesity is the floury and starchy substances which man makes the prime ingredients of his daily nourishment. As we have said already, all animals that live on farinaceous food grow fat willy-nilly; and man is no exception to the universal law.”

Several decades later, William Banting (1796–1878), an English undertaker, rediscovered the fattening properties of the refined carbohydrate. In 1863, he published the pamphlet Letter on Corpulence, Addressed to the Public, which is often considered the world’s first diet book. His story is rather unremarkable. He was not an obese child, nor did he have a family history of obesity. In his mid-thirties, however, he started to gain weight. Not much; perhaps a pound or two per year. By age sixty-two, he stood five foot five and weighed 202 pounds (92 kilograms). Perhaps unremarkable by modern standards, he was considered quite portly at the time. Distressed, he sought advice on weight loss from his physicians. First, he tried to eat less, but that only left him hungry. Worse, he failed to lose weight. Next, he increased his exercise by rowing along the River Thames, near his home in London. While his physical fitness improved, he developed a “prodigious appetite, which I was compelled to indulge.”5 Still, he failed to lose weight. Finally, on the advice of his surgeon, Banting tried a new approach. With the idea that sugary and starchy foods were fattening, he strenuously avoided all breads, milk, beer, sweets and potatoes that had previously made up a large portion of his diet. (Today we would call this diet low in refined carbohydrates.) William Banting not only lost the weight and kept it off, but he also felt so well that he was compelled to write his famous pamphlet. Wei...

For most of the next century, diets low in refined carbohydrates were accepted as the standard treatment for obesity. By the 1950s, it was fairly standard advice. If you were to ask your grandparents what caused obesity, they would not talk about calories. Instead, they would tell you to stop eating sugary and starchy foods. Common sense and empiric observation served to confirm the truth. Nutritional “experts” and government opinion were not needed.

But all great stories need a villain, and dietary fat was cast into that role. Dietary fat was thought to increase the amount of cholesterol, a fatty substance that is thought to contribute to heart disease, in the blood. Soon, physicians began to advocate lower-fat diets. With great enthusiasm and shaky science, the demonization of dietary fat began in earnest. There was a problem, though we didn’t see it at the time. The three macronutrients are fat, protein and carbohydrates: lowering dietary fat meant replacing it with either protein or carbohydrates. Since many high-protein foods like meat and dairy are also high in fat, it is difficult to lower fat in the diet without lowering protein as well. So, if one were to restrict dietary fats, then one must increase dietary carbohydrates and vice versa. In the developed world, these carbohydrates all tend to be highly refined. Low Fat = High Carbohydrate

This dilemma created significant cognitive dissonance. Refined carbohydrates could not simultaneously be both good (because they are low in fat) and bad (because they are fattening). The solution adopted by most nutrition experts was to suggest that carbohydrates were no longer fattening. Instead, calories were fattening. Without evidence or historical precedent, it was arbitrarily decided that excess calories caused weight gain, not specific foods. Fat, as the dietary villain, was now deemed fattening—a previously unknown concept. The Calories-In/Calories-Out model began to displace the prevailing “fattening carbohydrates” model.

But not everybody bought in. One of the most famous dissidents was the prominent British nutritionist John Yudkin (1910–1995). Studying diet and heart disease, he found no relationship between dietary fat and heart disease. He believed that the main culprit of both obesity and heart disease was sugar.9, 10 His 1972 book, Pure, White and Deadly: How Sugar Is Killing Us, is eerily prescient (and should certainly win the award for B...

THE ISSUE WAS finally settled in 1977, not by scientific debate and discovery, but by governmental decree. George McGovern, then chairman of the United States Senate Select Committee on Nutrition and Human Needs, convened a tribunal, and after several days of deliberation, it was decided that henceforth, dietary fat was guilty as charged. Not only was dietary fat guilty of causing heart disease, but it also caused obesity, since fat is calorically dense.

The resulting declaration became the Dietary Goals for the United States. An entire nation, and soon the entire world, would now follow nutritional advice from a politician. This was a remarkable break from tradition. For the first time, a government institution intruded into the kitchens of America. Mom used to tell us what we should and should not eat. But from now on, Big Brother would be telling us. And he said, “Eat less fat and more carbohydrates.”

Several specific dietary goals were set forth. These included •raise consumption of carbohydrates until they constituted 55 percent to 60 percent of calories, and •decrease fat consumption from approximately 40 percent of calories to 30 percent, of which no more than one-third should come from saturated fat. With no scientific evidence, the formerly “fattening” carbohydrate made a stunning transformation. While the guidelines still recognized the evils of sugar, refined grain was as innocent as a nun in a convent. Its nutritional sins were exonerated, and it was henceforth reborn and baptized as the healthy whole grain. Was there any evidence? It hardly mattered. The goals were now the nutritional orthodoxy. Everything else was heathen. If you didn’t toe the line, you were ridiculed. The Dietary G...

The Dietary Guidelines for Americans, now updated every five years, spawned the infamous food pyramid in all its counterfactual glory. The foods that formed the base of the pyramid—the foods we should eat every single day—were breads, pastas and potatoes. These were the precise foods that we had previously avoided to stay thin. For example, the American Heart Association’s 1995 pamphlet, The American Heart Association Diet: An Eating Plan for Healthy Americans, declared we should eat six or more servings of “breads, cereals, pasta and starchy vegetables (that) are low in fat and cholesterol.” To drink, “Choose . . . fruit punches, carbonated soft drinks.” Ahhh. White bread and carbonated soft drinks—the dinner of champions. Thank you, American Heart Association (AHA). Entering this brave new world, Americans tried to comply with the nutritional authorities of the day and made a conscious effort to eat less fat, less red meat, fewer eggs and more carbohydrates. When doctors advised people to stop smoking, rates dropped from 33 percent in 1979 to 25 percent by 1994. When doctors said to control blood pressure and cholesterol, there was a 40 percent decline in high blood pressure a...

Success! From 1976 to 1996, the average fat intake decreased from 45 percent of calories to 35 percent. Butter consumption decreased 38 percent. Animal protein decreased 13 percent. Egg consumption decreased 18 percent. Grains and sugars increased. Until that point, the widespread adoption of the low-fat diet was completely untested. We had no idea what effect it would have on human health. But we had the fatal conceit that we were somehow smarter than 200,000 years of Mother Nature. So, turning away from the natural fats, we embraced refined low-fat carbohydrates such as bread and pasta. Ironically, the American Heart Association, even as late as the year 2000, felt that low-carbohydrate diets were dangerous fads, despite the fact that these diets had been in use almost continuously since 1863. What was the result? The incidence of heart disease certainly did not decrease as expected. But there was definitely a consequence to this dietary manipulation—an unintentional one. Rates of obesity, defined as having a body mass index greater than 30, dramatically increased, starting almost exactly in 1977,

The abrupt increase in obesity began exactly with the officially sanctioned move toward a low-fat, high-carbohydrate diet. Was it mere coincidence? Perhaps the fault lay in our genetic makeup instead.

No relationship whatsoever was discovered between the weight of the adoptive parents and the adoptees. Whether adoptive parents were thin or fat made no difference to the eventual weight of the adopted child. The environment provided by the adoptive parents was largely irrelevant.

Comparing adoptees to their biological parents yielded a considerably different result. Here there was a strong, consistent correlation between their weights. The biological parents had very little or nothing to do with raising these children, or teaching them nutritional values or attitudes toward exercise. Yet the tendency toward obesity followed them like ducklings. When you took a child away from obese parents and placed them into a “thin” household, the child still became obese.

Studying identical twins raised apart is another classic strategy to distinguish environmental and genetic factors. Identical twins share identical genetic material, and fraternal twins share 25 percent of their genes. In 1991, Dr. Stunkard examined sets of fraternal and identical twins in both conditions of being reared apart and reared together.4 Comparison of their weights would determine the effect of the different environments. The results sent a shockwave through the obesity-research community. Approximately 70 percent of the variance in obesity is familial. Seventy percent.

Seventy percent of your tendency to gain weight is determined by your parentage. Obesity is overwhelmingly inherited.

THE FIRST ATTEMPT to explain the genetic basis of obesity was the thrifty-gene hypothesis, which became popular in the 1970s. This hypothesis assumes that all humans are evolutionarily predisposed to gain weight as a survival mechanism. The argument goes something like this: In Paleolithic times, food was scarce and difficult to obtain. Hunger is one of the most powerful and basic of human instincts. The thrifty gene compels us to eat as much as possible, and this genetic predisposition to gain weight had a survival advantage. Increasing the body’s food stores (fat) permitted longer survival during times of scarce or no food. Those who tended to burn the calories instead of storing them were selectively wiped out. However, the thrifty gene is ill adapted to the modern all-you-can-eat world, as it causes weight gain and obesity. But we are simply following our genetic urge to gain fat. Like a decomposing watermelon, this hypothesis seems quite reasonable on the surface. Cut a little deeper, and you find the rotten core. This theory has long ceased to be taken seriously. However, it is still mentioned in the media, and so its flaws bear some examination. The most obvious problem is that survival in the wild depends on not being either underweight or overweight. A fat animal is slower and less agile than its leaner brethren. Predators would preferentially eat the fatter prey over the harder-to-catch, lean prey. By the same token, fat predators would find it much more difficul...

As we will see in Part 3, “A New Model of Obesity,” the root cause of obesity is a complex hormonal imbalance with high blood insulin as its central feature. The hormonal profile of a baby is influenced by the environment in the mother’s body before birth, setting up a tendency for high insulin levels and associated obesity later in life. The explanation of obesity as a caloric imbalance simply cannot account for this predominantly genetic effect, since eating and exercise are voluntary behaviors. Obesity as a hormonal imbalance more effectively explains this genetic effect. But inherited factors account for only 70 percent of the tendency to obesity that we observe. The other 30 percent of factors are under our control, but what should we do to make the most of this? Are diet and exercise the answer?

TRADITIONALLY, OBESITY HAS been seen as a result of how people process calories, that is, that a person’s weight could be predicted by a simple equation: Calories In – Calories Out = Body Fat This key equation perpetrates what I call the calorie deception. It is dangerous precisely because it appears so simple and intuitive. But what you need to understand is that many false assumptions are built in.

Assumption 1: Calories In and Calories Out are independent of each other This assumption is a crucial mistake. As we’ll see later on in this chapter, experiments and experience have proven this assumption false. Caloric intake and expenditure are intimately dependent variables. Decreasing Calories In triggers a decrease in Calories Out. A 30 percent reduction in caloric intake results in a 30 percent decrease in caloric expenditure. The end result is minimal weight loss.

Assumption 2: Basal metabolic rate is stable We obsess about caloric intake with barely a thought for caloric expenditure, except for exercise. Measuring caloric intake is simple, but measuring the body’s total energy expenditure is complicated. Therefore, the simple but completely erroneous assumption is made that energy expenditure remains constant except for exercise. Total energy expenditure is the sum of basal metabolic rate, thermogenic effect of food, nonexercise activity thermogenesis, excess post-exercise oxygen consumption and e...

Assumption 3: We exert conscious control over Calories In Eating is a deliberate act, so we assume that eating is a conscious decision and that hunger plays only a minor role in it. But numerous overlapping hormonal systems influence the decision of when to eat and when to stop. We consciously decide to eat in response to hunger signals that are largely hormonally mediated. We consciously stop eating when the body sends signals of satiety (fullness) that are largely hormonally mediated. For example, the smell of frying food makes you hungry at lunchtime. However, if you have jus...

Our bodies possess an intricate system guiding us to eat or not. Body-fat regulation is under automatic control, like breathing. We do not consciously remind ourselves to breathe, nor do we remind our hearts to beat. The only way to achieve such control is to have homeostatic mechanisms. Since hormones control ...

Assumption 4: Fat stores are essentially unregulated Every single system in the body is regulated. Growth in height is regulated by growth hormone. Blood sugars are regulated by the hormones insulin and glucagon, among others. Sexual maturation is regulated by testosterone and estrogen. Body temperature is regulated by a thyroid-stimulating hormone and free thyroxine. The list is endless. We are asked to believe, however, that growth of fat cells is essentially unregulated. The simple act of eating, without any interference from any hormones, will result in fat growth. Extra calories are dumped into fat cells like doorknobs into a sack. This assumption has already been proven false. New hormonal pathways in the regulation of fat growth are being discovere...

If hormones regulate fat growth, then obesity is a hormonal, not...

Assumption 5: A calorie is a calorie This assumption is the most dangerous of all. It’s obviously true. Just like a dog is a dog or a desk is a desk. There are many different kinds of dogs and desks, but the simple statement that a dog is a dog is true. However, the real issue is this: Are all calories equally likely to cause fat gain? “A calorie is a calorie” implies that the only important variable in weight gain is the total caloric intake, and thus, all foods can be reduced to their caloric energy. But does a calorie of olive oil cause the same metabolic response as a calorie of sugar? The answer is, obviously, no. These two foods have many easily measurable differences. Sugar will increase the blood glucose level and provoke an insulin response from the pancreas. Olive oil will not. When olive oil...

Reducing Calories In works only if Calories Out remains stable. What we find instead is that a sudden reduction of Calories In causes a similar reduction in Calories Out, and no weight is lost as the body balances its energy budget. Some historic experiments in calorie reduction have shown exactly this.

A detailed study of total energy expenditure under conditions of reduced caloric intake was done in 1919 at the Carnegie Institute of Washington.5 Volunteers consumed “semi-starvation” diets of 1400 to 2100 calories per day, an amount calculated to be approximately 30 percent lower than their usual intake. (Many current weight-loss diets target very similar levels of caloric intake.) The question was whether total energy expenditure (Calories Out) decreases in response to caloric reduction (Calories In). What happened? The participants experienced a whopping 30 percent decrease in total energy expenditure, from an initial caloric expenditure of roughly 3000 calories to approximately 1950 calories. Even nearly 100 years ago, it was clear that Calories Out is highly dependent on Calories In. A 30 percent reduction in caloric intake resulted in a nearly identical 30 percent reduction in caloric expenditure. The energy budget is balanced. The First Law of Thermodynamics is not broken.

Several decades later, in 1944 and 1945, Dr. Ancel Keys performed the most complete experiment of starvation ever done—the Minnesota Starvation Experiment, the details of which were published in 1950 in a two-volume publication entitled The Biology of Human Starvation.6 In the aftermath of World War II, millions of people were on the verge of starvation. Yet the physiologic effects of starvation were virtually unknown, having never been scientifically studied. The Minnesota study was an attempt to understand both the caloric-reduction and recovery phases of starvation. Improved knowledge would help guide Europe’s recovery from the brink. Indeed, as a result of this study, a relief-worker’s field manual was written detailing psychological aspects of starvation.7 Thirty-six young, healthy, normal men were selected with an average height of five foot ten inches (1.78 meters) and an average weight of 153 pounds (69.3 kilograms). For the first three months, subjects received a standard diet of 3200 calories per day. Over the next six months of semi-starvation, only 1570 calories were given to them. However, caloric intake was continually adjusted to reach a target total weight loss of 24 percent (compared to baseline), averaging 2.5 pounds (1.1 kilograms) per week. Some men eventually received less than 1000 calories per day. The foods given were high in carbohydrates, similar to those available in war-torn Europe at the time—potatoes, turnips, bread and macaroni. Meat and dair...