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DIABESITY: THE CALORIE DECEPTION

DIABESITY IS THE unification of the words diabetes, referring to type 2, and obesity. Just like the evocative “bromance,” it conveys the close relationship between these two ideas. Diabetes and obesity are truly one and the same disease. As strange as it may now sound, physicians did not always recognize this seemingly obvious and basic connection.

Back in 1990, when grunge was taking over the music scene and fanny packs were growing in popularity beyond the middle-aged dad tourist, Dr. Walter Willett, now Professor of Epidemiology and Nutrition at Harvard’s School of Public Health, identified the strong and consistent relationship between weight gain and type 2 diabetes.

The obesity epidemic had only just gotten underway in the late 1970s and was not yet the public health disaster it is today. Type 2 diabetes barely scratched the surface as a public health concern. Instead, AIDS was the hot topic of the day. And type 2 diabetes and obesity were not thought to be related in any way. Indeed, the Report of the Dietary Guidelines Advisory Committee issued by the U.S. Department of Agriculture in 1990 allowed that some weight gain after the age of thirty-five was consistent with good health.

That same year, Dr. Willett challenged the conventional thinking, reporting that weight gain after age eighteen was the major determinant of type 2 diabetes.¹ A weight gain of 20–35 kg (44–77 pounds) increased the risk of type 2 diabetes by 11,300 percent. Gaining more than 35 kg (77 pounds) increased the risk by 17,300 percent! Even smaller amounts of weight gain could raise the risk significantly. But this idea was not an easy sell to a sceptical medical profession.² “We had a hard time getting the first paper published showing that even slight overweight greatly increased the risk of diabetes,” Willett remembers. “They didn’t believe it.”

BODY MASS INDEX: THE RELATIONSHIP BETWEEN OBESITY AND DIABETES

THE BODY MAS index is a standardized measurement of weight, and it is calculated by the following formula:

Body mass index = Weight (kg)/Height² (m²)

A body mass index of 25.0 or higher is considered overweight, while a body mass index of between 18.5 and 24.9 is in the healthy range.

Table 4.1. Body mass index classifications

Body Mass Index	Classification
< 18.5	Underweight
18.5–24.9	Normal weight
25.0–29.9	Overweight
30.0–34.9	Obese
35.0–39.9	Severe Obesity
> 40.0	Morbid Obesity

However, women with a body mass index of 23–23.9 have a 360-percent higher risk of developing type 2 diabetes than women with a body mass index of less than 22, which is even more stunning since a body mass index of 23.9 is considered well within the normal weight range.

By 1995, building on this new realization, researchers had determined that a weight gain of only 5.0–7.9 kg (11–17.5 pounds) increased the risk of type 2 diabetes by 90 percent, and a weight gain of 8.0–10.9 kg (17.5–24 pounds) increased the risk by 270 percent.³ By contrast, weight loss decreased risk by more than 50 percent. This result established an intimate relationship between weight gain and type 2 diabetes. But far more sinister, this excess weight also significantly increased the risk of death.⁴

More supporting evidence would soon surface. Dr. Frank Speizer from the Harvard School of Public Health had established the original Nurses’ Health Study (NHS) in 1976. One of the largest investigations into risk factors for cardiovascular disease and cancer, this long-term epidemiological study included 121,700 female nurses from around the Boston area.

Dr. Willett continued with the Nurses’ Health Study II, which collected data every two years on an additional 116,000 female nurses since 1989. At the start of the study, all the participants were relatively healthy, but over time, many of them developed chronic diseases such as diabetes and heart disease. By looking back at the collected data, some idea of the risk factors for these diseases emerged. In 2001, Dr. Willett⁵ showed that, once again, the single most important risk factor for the development of type 2 diabetes was obesity.

GLYCEMIC INDEX: DIET AND DIABETES

THE NURSES’ HEALTH Study II revealed that other lifestyle variables were also important. Maintaining a normal weight, getting regular physical exercise, not smoking, and eating a healthy diet could prevent a stunning 91 percent of type 2 diabetes. But the million-dollar question is: What is a “healthy” diet? Dr. Willett’s healthy diet was defined as high in cereal fiber, high in polyunsaturated fats, low in trans fat, and low in glycemic load.

When digested, carbohydrates break down into glucose. The glycemic index measures the rise in blood glucose after ingesting 50 grams of carbohydrate-containing foods. However, the amount of carbohydrates contained in a standard serving varies enormously. For example, a standard serving of fruit may contain less than 50 grams of carbohydrates whereas a single pastry may contain far more. The glycemic load refines this measure by multiplying the glycemic index of a food by the grams of carbohydrate in a standard serving of that food.

Generally, foods high in sugar and refined carbohydrates are high in glycemic load. Dietary fats and proteins, since they raise blood glucose very little, have minimal glycemic loads. Contrary to the low-fat diet recommended by all the medical associations around the world, Dr. Willett’s healthy diet was high in dietary fat and protein. His diet was about reducing sugar and refined carbohydrates, not reducing dietary fat.

In 1990, the widespread belief was that dietary fat was evil, that dietary fat was a mass murderer, that dietary fat was vile. The term healthy fats did not exist. It was an oxymoron, like a jumbo shrimp. Fat-laden avocados? A heart attack in a fruit. Fat-laden nuts? A heart attack in a snack. Olive oil? Liquid heart attacks. Most people fervently believed fats were going to clog our arteries, but it was only an illusion.

Dr. Zoë Harcombe, a Cambridge University–trained obesity researcher, reviewed all the data that had been available in the early 1980s, when low-fat guidelines were introduced in the U.S. and U.K. No proof had ever existed that natural dietary fats worsened cardiovascular disease. The evidence for the low-fat guidelines was simply a great work of fiction.⁶ The science was far from settled at the time the government decided to weigh in and make the final decision to vilify dietary fat. Yet this belief had become so entrenched both in the medical establishment and among the general public that it had become heretical to suggest refined grains and sugars were the problem rather than dietary fat.

In the midst of our frenzied low-fat obsession, Dr. Willett’s assertion was considered high treason. But the truth could not be concealed forever. Today, we understand clearly that obesity is the main underlying issue behind type 2 diabetes. But the problem isn’t simply obesity. Rather, it is abdominal obesity.

WAIST CIRCUMFERENCE: FAT DISTRIBUTION AND TYPE 2 DIABETES

IN 2012, Dr. Michael Mosley was a TOFI. A what? Not tofu, the delicious Asian soy delicacy. The acronym TOFI stands for “thin on the outside, fat on the inside.” Dr. Mosley is a medical doctor, British Broadcasting Corporation (BBC) journalist, documentary filmmaker, and international bestselling author. And, in his mid-50s, he was also a ticking time bomb.

He was not particularly overweight, weighing 187 pounds, standing 5 feet 11 inches, with a waist of 36 inches. This equals a body mass index of 26.1, just barely in the overweight range. By standard measurements, he was considered just fine. He felt fine, perhaps carrying a little bit of weight around the mid-section from being middle-aged. Just a little pudge, that’s all.

However, body mass index is not the best indicator of type 2 diabetes risk. The waist circumference, a measure of body fat distribution around the trunk, is a far superior predictor of type 2 diabetes.⁷ Filming a health segment for the BBC, Mosley underwent a magnetic resonance imaging (MRI) body scan. To his shock and consternation, his organs were literally swimming in fat. To look at him, you would not have guessed it because most of the fat was hidden inside his abdomen.

Eighteen months later, during a visit to his own physician, routine screening blood tests revealed type 2 diabetes. Devastated, Dr. Mosley says, “I had assumed I was healthy and suddenly I was discovering I wasn’t, and had to take this visceral fat situation seriously.”⁸ Visceral fat accumulates inside and around the intra-abdominal organs such as the liver, kidneys, and intestines, and can be detected by an increased waist circumference. This pattern of obesity, where most of the fat is carried around the abdomen, is also known as central obesity, or central adiposity. In contrast, subcutaneous fat is the fat deposited directly under the skin.

The different health risks associated with the different fat distributions explain how roughly 30 percent of obese adults are metabolically normal.⁹ These healthy-fat people carry more subcutaneous fat rather than the more dangerous visceral fat. On the other hand, some normal-weight people show the same metabolic abnormalities as in obesity¹⁰ because of excessive visceral fat.

Type 2 diabetes may be diagnosed for patients with a wide range of body mass indexes, following a normal distribution with no distinct subpopulation of “thin” diabetics.¹¹ A full 36 percent of newly diagnosed diabetics have a normal body mass index of less than 25. Look at Figure 4.1. The key clinical indicator is clearly not total body fat as measured by body mass index. Rather, it’s visceral or intra-organic fat.¹²

Figure 4.1. Population BMI distribution for newly diagnosed diabetes¹³

Independent of total weight, central obesity is highly correlated to metabolic abnormalities,¹⁴ increased cardiac risk,¹⁵ and progression to type 2 diabetes.¹⁶ Reducing visceral fat also successfully reduces the risk of progression of type 2 diabetes.¹⁷

Subcutaneous fat, on the other hand, shows little correlation to type 2 diabetes or heart disease. The surgical removal, via liposuction,¹⁸ of almost 10 kilograms of subcutaneous fat brought no significant metabolic benefits whatsoever, which suggests that subcutaneous fat plays little role in the development of type 2 diabetes.

The waist-to-height ratio is a simple measure of central adiposity, calculated by comparing waist circumference to height. This ratio is far more predictive of years of life lost than body mass index.¹⁹ Optimally, your waist circumference should be less than half your height. For example, an average man standing 5 foot 10 inches (70 inches) should strive to maintain a waist size of 35 inches or less. As central obesity increases, risk of metabolic disease skyrockets.

Figure 4.2. Waist-to-height ratio and years of life lost (YLL): A dramatic increase²⁰

There is a distinction even between types of visceral fat. Fat found inside the organs, such as within the liver and pancreas, is called intra-organic fat and is distinctly more dangerous than fat found around the organs, called omental fat. Intra-organic fat increases the risk for the metabolic complications of obesity, including type 2 diabetes, NASH (non-alcoholic steatohepatitis, or fatty liver disease), and cardiovascular disease.²¹ On the other hand, surgical removal of omental fat does not result in any metabolic improvement.²²

Fat within the liver, called intrahepatic fat, plays a crucial role in the development of insulin resistance.²³ Central obesity tracks very closely with intrahepatic fat content.²⁴ Fat within the pancreas also plays a leading role in type 2 diabetes, as we will see in chapter 7.

So, given the principal role of central obesity, what drives this fat deposition into the organs? Isn’t it all about calories?

CALORIE CONFUSION: NO RELATIONSHIP BETWEEN DIABETES AND CALORIES

EAT LES. CUT your calories. Watch your portion size. These mantras have formed the foundation of conventional weight-loss advice over the past fifty years. And the widespread obesity epidemic proves that this advice has been an utter disaster, perhaps only topped by the nuclear meltdown of Chernobyl. This caloric reduction advice is based on a false understanding of what causes weight gain.

What causes obesity? We don’t stop to consider this basic question because we believe that we already know the full answer. It seems so obvious, doesn’t it? Excessive intake of calories causes obesity. Too many calories in compared to too few calories out leads to weight gain. This energy balance model of obesity has been drilled into us since childhood.

Fat Gained = Calories In – Calories Out

For the past fifty years, our best weight-loss advice was primarily to restrict our caloric intake. Specifically, we were told to restrict the amount of dietary fat, which is calorically dense. This means reducing foods high in fat, such as meat, butter, cheese, and nuts, in order to lower our calorie intake and therefore lose weight. We made food guides, food pyramids, and food plates to indoctrinate children into this brand-new, low-calorie religion. “Cut Your Calories,” we declared. “Eat Less, Move More,” we chanted.

Nutrition labels were mandated to include calorie counts. Programs and apps were created to more precisely count calories. We invented small devices such as Fitbits to measure exactly how many calories we were burning. Using all our ingenuity, focused like a laser beam and dogged as a turtle crossing a road, we cut calories.

What was the result? Did the problem of obesity simply fade away like the morning mist on a hot summer day? In a word, no. The underlying, unspoken premise of this model is that energy creation (calories in), energy expenditure (calories out), and fat gain are independent variables fully under our conscious control. It assumes that the number of calories used to keep our bodies running more or less normally remains stable and unchanging. But this is untrue.

The truth is that the body can adjust its basal metabolic rate (BMR)—the energy required to keep the heart pumping, lungs breathing, kidneys and liver detoxifying, brain thinking, body generating heat, and so on—up or down by 40 percent. When you eat fewer calories, your body slows down so it uses fewer calories, which means you don’t lose weight.

This model also completely ignores the multiple overlapping hormonal systems that signal hunger and satiety. That is, we may decide what to eat and when to eat it, but we cannot decide to feel less hungry. We cannot decide when to burn calories as body heat and when to store them as body fat. Hormones make these decisions. The results of the so-called “caloric reduction as primary” advice could hardly have been worse if we had tried. The storm of obesity and type 2 diabetes that began in the late 1970s has today, some forty years later, become a global category 5 hurricane threatening to engulf the entire world in sickness and disability.

Only two possibilities can explain how obesity could spread so rapidly in the face of our shiny new advice to reduce fat and calories: first, perhaps this advice is good but people are simply not following it; second, perhaps the advice is simply wrong.

The idea that the spirit is willing but the flesh is weak—that people have the dream but not the drive—is as absurd as expecting a drowning man to laugh.

Was the entire obesity epidemic simply a sudden, simultaneous, coordinated, worldwide lack of willpower? The world can’t agree which side of the road we should drive on, yet, without discussion, we all decided to eat more and move less so that we could become undesirably fat? This explanation is only the latest iteration of the game called “blame the victim.” It shifts the responsibility from the advice giver (the advice is bad) to the advice taker (the advice is good, but you are not following it).

By declaring that their scientifically unproven caloric reduction advice was flawless, doctors and nutritionists could conveniently shift the blame from themselves to you. It wasn’t their fault. It was yours. Their advice was good. You didn’t follow it. No wonder they love this game so much. To admit that all their precious theories of obesity were simply incorrect was too psychologically difficult. Yet evidence continued to accumulate that this new caloric restriction strategy was about as useful as a comb to a bald man.

The Women’s Health Initiative²⁵ was the most ambitious, important nutrition study ever done. This randomized trial involving almost 50,000 women evaluated the low-fat, low-calorie approach to weight loss. Although it was not specifically a weight-loss trial, one group of women was encouraged through intensive counseling to reduce their daily caloric intake by 342 calories and to increase their level of exercise by 10 percent. These calorie counters expected a weight loss of 32 pounds every single year.

When the final results were tallied in 1997, there was only crushing disappointment. Despite good compliance, more than seven years of calorie counting had led to virtually no weight loss. Not even a single pound. This study was a stunning and severe rebuke to the caloric theory of obesity. Reducing calories did not lead to weight loss.

There were now two choices. First, we could respect the expensive, hard-won, scientific evidence to devise a robust, more correct theory of obesity. Or we could simply keep all our comfortable and convenient preconceived notions and biases and ignore the science. The second choice involved far less work and far less imagination. So this ground-breaking study has largely been ignored and relegated to the dustbins of nutritional history. We have been paying the pied piper every day since, as the twin epidemics of obesity and type 2 diabetes have exploded.

Real-world studies²⁶ have only confirmed this stunning fiasco. The conventional weight-loss advice to eat fewer calories carries an estimated failure rate of 99.4 percent. For morbid obesity, the failure rate is 99.9 percent. These statistics would not surprise anybody in the diet industry or, for that matter, anybody who has ever tried to lose weight.

The Calories-In, Calories-Out theory gained widespread acceptance based on its seemingly intuitive truth. However, like a rotting melon, digging past the outer shell revealed the putrid interior. This simplistic formula is riddled with erroneous assumptions. The most important error is believing that basal metabolic rate, or Calories Out, always remains stable. But a 40-percent reduction in calorie intake is quickly met with a 40-percent decrease in basal metabolic rate. The net result is no weight loss.

The other major false assumption is that weight is consciously regulated. But no system in our body functions like that. The thyroid, parathyroid, sympathetic, parasympathetic, respiratory, circulatory, hepatic, renal, gastrointestinal, and adrenal systems are all closely controlled by hormones. Body weight and body fat are also strictly regulated by hormones. In fact, our bodies contain multiple overlapping systems of body weight control. Body fat, one of the most important determinants of survival in the wild, is simply not left to the vagaries of what we decide to put in our mouths.

HORMONES: FOOD, BODY WEIGHT, AND DIABETES

HORMONES CONTROL HUNGER, telling our body when to eat and when to stop. Ghrelin is a powerful hormone that causes hunger, and cholecystokinin and peptide YY are hormones that tell us when we are full and should stop eating. Imagine you’re at an all-you-can-eat buffet. You’ve already eaten many heaping platefuls of food and you are completely, 110-percent full.

Now, could you eat a few more pork chops? Merely the thought might make you nauseous. Yet these are the same pork chops you ate happily just a few minutes ago. The difference is that satiety hormones are exerting a powerful effect to stop you from eating. Contrary to many popular beliefs, we do not continue eating simply because food is available. Calorie consumption is under tight hormonal regulation.

Fat accumulation is truly not a problem of energy excess. It’s a problem of energy distribution. Too much energy is diverted to producing fat as opposed to, say, increasing body heat or forming new bone tissue. This energy expenditure is controlled hormonally. As long as we believed, wrongly, that excessive caloric intake led to obesity, we were doomed to failure as we uselessly tried to reduce calories.

We cannot “decide” to feel less hungry. We cannot “decide” to increase basal metabolic rate. If we eat fewer calories, our body simply compensates by decreasing its metabolic rate. If calories are not the underlying cause of weight gain, then reducing calories cannot reliably reduce weight. The most important factor in controlling fat accumulation and weight gain is to control the hormonal signals we receive from food, not the total number of calories we eat.

Obesity is a hormonal imbalance, not a caloric one. The hormonal problem in undesired weight gain is mainly excessive insulin. Thus, type 2 diabetes, too, is a disease about insulin imbalance rather than caloric imbalance.