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HOW OBESITY BECAME AN EPIDEMIC

Of all the parasites that affect humanity, I do not know of, nor can I imagine, any more distressing than that of Obesity.

WILLIAM BANTING

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?

The standard prescription for weight loss is “Eat Less, Move More.” It sounds perfectly reasonable. But why doesn’t it work? Perhaps people wanting to lose weight are not following this advice. The mind is willing, but the flesh is weak. Yet consider the self-discipline and dedication needed to complete an undergraduate degree, medical school, internship, residency and fellowship. It is hardly conceivable that overweight doctors simply lack the willpower to follow their own advice.

This leaves the possibility that the conventional advice is simply wrong. And if it is, then our entire understanding of obesity is fundamentally flawed. Given the current epidemic of obesity, I suspect that such is the most likely scenario. So we need to start at the very beginning, with a thorough understanding of the disease that is human obesity.

We must start with the single most important question regarding obesity or any disease: “What causes it?” We spend no time considering this crucial question because we think we already know the answer. It seems so obvious: it’s a matter of Calories In versus Calories Out.

A calorie is a unit of food energy used by the body for various functions such as breathing, building new muscle and bone, pumping blood and other metabolic tasks. Some food energy is stored as fat. Calories In is the food energy that we eat. Calories Out is the energy expended for all of these various metabolic functions.

When the number of calories we take in exceeds the number of calories we burn, weight gain results, we say. Eating too much and exercising too little causes weight gain, we say. Eating too many calories causes weight gain, we say. These “truths” seem so self-evident that we do not question whether they are actually true. But are they?

PROXIMATE VERSUS ULTIMATE CAUSE

EXCESS CALORIES MAY certainly be the proximate cause of weight gain, but not its ultimate cause.

What’s the difference between proximate and ultimate? The proximate cause is immediately responsible, whereas the ultimate cause is what started the chain of events.

Consider alcoholism. What causes alcoholism? The proximate cause is “drinking too much alcohol”—which is undeniably true, but not particularly useful. The question and the cause here are one and the same, since alcoholism means “drinking too much alcohol.” Treatment advice directed against the proximate cause—“Stop drinking so much alcohol”—is not useful.

The crucial question, the one that we are really interested in, is: What is the ultimate cause of why alcoholism occurs. The ultimate cause includes

•the addictive nature of alcohol,

•any family history of alcoholism,

•excessive stress in the home situation and/or

•an addictive personality.

There we have the real disease, and treatment must be directed against the ultimate, rather than the proximate cause. Understanding the ultimate cause leads to effective treatments such as (in this case) rehabilitation and social support networks.

Let’s take another example. Why does a plane crash? The proximate cause is, “there was not enough lift to overcome gravity”—again, absolutely true, but not in any way useful. The ultimate cause might be

•human error,

•mechanical fault and/or

•inclement weather.

Understanding the ultimate cause leads to effective solutions such as better pilot training or tighter maintenance schedules. Advice to “generate more lift than gravity” (larger wings, more powerful engines) will not reduce plane crashes.

This understanding applies to everything. For instance, why is it so hot in this room?

PROXIMATE CAUSE: Heat energy coming in is greater than heat energy leaving.

SOLUTION: Turn on the fans to increase the amount of heat leaving.

ULTIMATE CAUSE: The thermostat is set too high.

SOLUTION: Turn down the thermostat.

Why is the boat sinking?

PROXIMATE CAUSE: Gravity is stronger than buoyancy.

SOLUTION: Reduce gravity by lightening the boat.

ULTIMATE CAUSE: The boat has a large hole in the hull.

SOLUTION: Patch the hole.

In each case, the solution to the proximate cause of the problem is neither lasting nor meaningful. By contrast, treatment of the ultimate cause is far more successful.

The same applies to obesity: 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: If we already understand what causes obesity, how to treat it, and we’ve spent millions of dollars on education and obesity programs, why are we getting fatter?

ANATOMY OF AN EPIDEMIC

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.”⁴

All foods can be divided into three different macronutrient groups: fat, protein and carbohydrates. The “macro” in “macronutrients” refers to the fact that the bulk of the food we eat is made up of these three groups. Micronutrients, which make up a very small proportion of the food, include vitamins and minerals such as vitamins A, B, C, D, E and K, as well as minerals such as iron and calcium. Starchy foods and sugars are all carbohydrates.

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. Weight gain, he believed, resulted from eating too many “fattening carbohydrates.”

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.

Calorie counting had begun in the early 1900s with the book Eat Your Way to Health, written by Dr. Robert Hugh Rose as a “scientific system of weight control.” That book was followed up in 1918 with the bestseller Diet and Health, with Key to the Calories, written by Dr. Lulu Hunt Peters, an American doctor and newspaper columnist. Herbert Hoover, then the head of the U.S. Food Administration, converted to calorie counting. Dr. Peters advised patients to start with a fast, one to two days abstaining from all foods, and then stick strictly to 1200 calories per day. While the advice to fast was quickly forgotten, modern calorie-counting schedules are not very different.

By the 1950s, a perceived “great epidemic” of heart disease was becoming an increasing public concern. Seemingly healthy Americans were developing heart attacks with growing regularity. In hindsight, it should have been obvious that there was really no such epidemic.

The discovery of vaccines and antibiotics, combined with increased public sanitation, had reshaped the medical landscape. Formerly lethal infections, such as pneumonia, tuberculosis and gastrointestinal infections, became curable. Heart disease and cancer now caused a relatively greater percentage of deaths, giving rise to some of the public misperception of an epidemic. (See Figure 1.1.⁶)

Figure 1.1. Causes of death in the United States 1900 vs. 1960.

The increase in life expectancy from 1900 to 1950 reinforced the perception of a coronary-disease epidemic. For a white male, the life expectancy in 1900 was fifty years.⁷ By 1950, it had reached sixty-six years, and by 1970, almost sixty-eight years. If people were not dying of tuberculosis, then they would live long enough to develop their heart attack. Currently, the average age at first heart attack is sixty-six years.⁸ The risk of a heart attack in a fifty-year-old man is substantially lower than in a sixty-eight-year-old man. So the natural consequence of a longer life expectancy is an increased rate of coronary disease.

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 Best Book Title Ever). Scientific debate raged back and forth about whether the culprit was dietary fat or sugar.

THE DIETARY GUIDELINES

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 Guidelines for Americans, a report released in 1980 for widespread public consumption, followed the recommendations of the McGovern report closely. The nutritional landscape of the world was forever changed.

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 and a 28 percent decline in high cholesterol. When the AHA told us to eat more bread and drink more juice, we ate more bread and drank more juice.

Inevitably, sugar consumption increased. From 1820 to 1920, new sugar plantations in the Caribbean and American South increased the availability of sugar in the U.S. Sugar intake plateaued from 1920 to 1977. Even though “avoid too much sugar” was an explicit goal of the 1977 Dietary Guidelines for Americans, consumption increased anyway until the year 2000. With all our attention focused on fat, we took our eyes off the ball. Everything was “low fat” or “low cholesterol,” and nobody was paying attention to sugar. Food processors, figuring this out, increased the added sugars in processed food for flavor.

Refined grain consumption increased by almost 45 percent. Since carbohydrates in North America tended to be refined, we ate more and more low-fat bread and pasta, not cauliflower and kale.¹¹

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, as illustrated by Figure 1.2.¹²

Figure 1.2. Increase in obese and extremely obese United States adults aged 20–74.

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.