The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally

by Jason Fung

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.

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

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.

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

CALORIE CONFUSION: NO RELATIONSHIP BETWEEN DIABETES AND CALORIES

This caloric reduction advice is

based on a false understanding of what causes weight gain. What causes obesity?

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.

Food energy is stored in two forms: glycogen and body fat. Excess glucose, whether derived from protein or from carbohydrates, is strung together in long chains to form the molecule glycogen, which is stored in the liver. It can be converted to and from glucose easily and released into the bloodstream for

use by any cell in the body.

In essence, the body stores excess food energy in the form of sugar (glycogen) or body fat. Insulin is the signal to stop burning sugar and fat and to start storing it instead.

glucose necessary for normal body functioning. During a prolonged fast, the liver will manufacture new glucose from stored body fat. This process is called gluconeogenesis, meaning literally “the making of new sugar.” In essence, fat is burned to release energy. This is merely the fat-storage process in reverse.

Figure 5.2. Gluconeogenesis: The reverse of the glycogen storage process

This energy storage-and-release process happens every day. Normally this well-designed, balanced system keeps itself in check. We eat, insulin goes up, and we store energy as glycogen and fat. We fast, insulin goes down, and we use our stored glycogen and fat. As long as feeding (insulin high) is balanced with fasting (insulin low), no overall fat is gained.

In this manner, excess carbohydrates and protein can be stored long term offsite as body fat.

Excessive insulin drives fat accumulation and obesity. How? If

our feeding periods predominate over our fasting periods, then the ensuing insulin dominance leads to fat accumulation. Too much insulin signals the liver to keep admitting glucose, resulting in more production of new fat via DNL. Normally, if periods of high insulin (feeding) alternate with periods of low insulin (fasting), weight remains stable. If h...

INSULIN: THE CAUSE OF WEIGHT GAIN...

Although the thiazolidinedione (TZD) drug class, used to treat type 2 diabetes, does not increase insulin

levels, it does increase insulin’s effect. The result? Lower blood glucose, but also weight gain.

Increasing insulin causes weight gain. Decreasing insulin causes weight loss. These are not merely correlations but direct causal factors. Our hormones, mostly insulin, ultimately set our body weight and level of body fat. Remember, obesity is a hormonal imbalance, not a caloric one.

THE CARBOHYDRATE-INSULIN HYPOTHESIS

HYPERINSULINEMIA CAUSES OBESITY. This point is crucial because it immediately makes obvious that successful treatment of obesity depends upon lowering insulin levels. Highly refined, processed carbohydrates—sugars, flour, bread, pasta, muffins, donuts, rice, and potatoes—are well known to raise blood glucose and insulin production. If these highly refined carbohydrates were the main cause of hyperinsulinemia, they would also be the

prime cause of weight gain. This theory of obesity is known as the carbohydrate-insulin hypothesis. It forms the rational basis for many low-carbohydrate diets, such as the Atkins diet. By eliminating many of the “fattening” carbohydrates, we lower insulin levels and prevent weight gain.

For all the success of low-carb diets, the carbohydrate-insulin hypothesis remains incomplete. While refined carbohydrates are certainly an important contributor to hyperinsulinemia, they are not the only contributor. There are many other significant influences. One of the most important is insulin resistance.

As we’ve seen, insulin acts like a key to open a gate for glucose to

enter the cell. But sometimes, in a state of insulin resistance, the usual levels of insulin are not sufficient and glucose piles up in the bloodstream because it cannot get into the cells. To compensate, the body produces more insulin to overcome this resistance and force the blood glucose inside. The effect is to ...

Figure 5.4. Hormonal obesity II: Insulin resistance causes hyperinsulinemia

Fasting insulin, a measure of the amount of insulin in the blood that reflects underlying insulin resistance, increases through the spectrum of obesity, prediabetes, and then type 2 diabetes (see Figure 6.1).1

This suggests that obesity could be the root cause of increased insulin resistance.

After all, if obesity causes insulin resistance, how could type 2 diabetes develop in normal-weight patients? And why do so many obese people not develop type 2 diabetes?

The connection, as we shall see, is too much insulin. The X factor is hyperinsulinemia.

Figure 6.2. Hyperinsulinemia: The X factor causing both obesity and insulin resistance

Insulin causes insulin resistance.

Normally, insulin is released in bursts, preventing insulin resistance from developing. But when the body is constantly

bombarded with insulin, resistance develops.

Dr. Barbara Corkey, the 2011 Banting Medal winner from Boston University’s School of Medicine, called her lecture, “Hyperinsulinemia is the root cause of insulin resistance, obesity and diabetes.”

Figure 6.4. Hyperinsulinemia: The link between obesity and diabetes

Recall that insulin goes up when you eat and acts predominantly in the liver to help store incoming food energy. Insulin instructs the liver to do two things: 1. Stop burning stored food energy (e.g. body fat). 2. Store incoming food energy as glycogen or produce new fat via de novo lipogenesis (DNL).

Despite decades of ongoing research and millions of dollars, all the world’s top researchers were still stumped by this central paradox of insulin resistance until they realized that the old gummed-up, lock-and-key paradigm of insulin resistance with internal starvation was incorrect. The vital clue is that insulin itself

causes insulin resistance, which means that the primary problem is not insulin resistance but the hyperinsulinemia that caused it.

Insulin resistance only refers to the fact that, for a given amount of insulin, it is more difficult to move glucose into the cell. So what if the glucose cannot enter the cell because it is already overflowing? The paradigm of insulin re...

Insulin resistance creates hyperinsulinemia, and vice versa. The vicious cycle goes around and around. The cell is not in a state of internal starvation; instead, it is overflowing with glucose. As it spills out of the cell, blood glucose levels increase.

In other words, too much sugar causes fatty liver, the key problem of insulin resistance, as Figure 6.5 shows.

Ockham’s razor.” This postulate holds that the hypothesis with the fewest assumptions is often true. In other words, the simplest explanation is usually correct. Albert

Only when insulin production fails to keep pace with increasing resistance does the blood glucose rise high enough to make the clinical diagnosis of type 2 diabetes.