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.
