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?