The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally

by Jason Fung

Dr. Jason Fung explains in The Diabetes Code, “you can’t use drugs [or devices] to cure a dietary disease.”

WHAT HAPPENS WHEN excessive glucose piles

up in the body over ten or twenty years?

Every cell in the body starts to rot, which is precisely why type 2 diabetes, unlike virtually any other disease, affects every single organ. Your eyes rot, and you go blind. Your kidneys rot, and you need dialysis. Your heart rots, and you get heart attacks and heart failure. Your brain rots, and you get Alzheimer’s disease. Your liver rots, and you get fatty liver disease and cirrhosis. Your legs rot, and you...

We have overlooked a singular truth: you can’t use drugs to cure a dietary disease.

Adequate protein is required for good health, but excess amino acids cannot be stored in the body and so the liver converts them into glucose. Therefore, eating too much protein adds sugar to the body.

Although insulin and other modern medicines can treat blood glucose efficiently, lowering blood glucose alone does not prevent the complications of diabetes, including heart disease, stroke, and cancer—leading causes of death.

The American Diabetes Association defines an A1C level of 5.7 percent or less to be normal. A level above 6.5 percent is considered diabetic

For the fasting blood glucose test, a patient is asked to have no caloric intake for at least eight hours. A blood sample is then

taken and the amount of glucose in the blood is measured. A level above 7.0 mmol/L (or 126 mg/dL) is considered diabetic.

Occasionally, diabetes is diagnosed using a random blood sugar test. A blood sample is taken at a random time and the level of glucose in the blood is measured. A level above 11.1 mmol/L (or 200 mg/dL) is considered diabetic if accompanied by other symptoms.

Cancer TYPE 2 DIABETES increases the risk of most common cancers, including breast, stomach, colorectal, kidney, and endometrial cancers. This may be related to some of the medications used to treat diabetes and will be further discussed in chapter 10. The survival rate of cancer patients with pre-existing diabetes is far worse than for nondiabetics.

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.

But the story gets worse. Insulin resistance leads to higher fasting insulin levels. Fasting insulin levels are normally low. Now, instead of starting the day with low insulin after the nightly fast, we start with high insulin. The consequences are dire: the fat get fatter. As insulin resistance becomes a larger and larger part of the problem, it can, in fact, become a major driver of high insulin levels. Obesity drives itself.

William of Ockham (1287–1347), is credited with developing the fundamental problem-solving principle known as lex parsimoniae, or “Ockham’s razor.” This postulate holds that the hypothesis with the fewest assumptions is often true.

First, insulin resistance, an overflow phenomenon, is caused by fatty infiltration of the liver and muscle.

Visceral fat deposited in and around the organs4 is the main contributor to high insulin resistance. The very first place this fat starts to accumulate, often before insulin resistance becomes noticeable, is the liver.

Fatty liver is associated at all stages of insulin resistance from obesity to prediabetes to full-blown diabetes. And that relationship holds in all racial groups and ethnicities.

Fatty liver can be diagnosed by ultrasound, but an increased waist circumference or waist-to-height ratio is an important clue to its presence.

Obese individuals have five to fifteen times the rate of fatty liver. Up to 85 percent of type 2 diabetics have fatty liver.

As the liver slowly accumulates fat, insulin resistance escalates in lockstep. In type 2 diabetic patients, a close correlation exists between the amount of liver fat and the insulin dose required,18 reflecting greater insulin resistance. In short, the fattier the liver, the higher the insulin resistance. Therefore, to understand insulin resistance, we must first understand how fatty liver develops.

HERE’S A STARTLING fact: I can give you fatty

liver. Actually, I can give anybody fatty liver.

What’s the scariest part? This crucial first step toward type 2 diabetes ...

This condition can be achieved simply by overeating sugary snacks. Hey presto, fatty liver disease.

When volunteers returned to their usual diets, their weight, liver fat, and markers of liver damage all completely reversed.

Fatty liver is a completely reversible process.

Specifically, the sugar fructose, rather than glucose, is the main culprit,

Deliberate carbohydrate overfeeding provokes the high insulin levels necessary to develop fatty liver. In 1977, the Dietary Guidelines for Americans strongly advised people to eat less fat and more carbohydrates, such as bread and pasta. The result? Dramatically increased insulin levels.

Working with isolated heart and skeletal muscle cell preparations, Randle demonstrated that cells burning glucose could not burn fat and vice versa.

Your body simply cannot use both fuels simultaneously. You either burn sugar or fat, but not both.

When the body is mostly burning fat, such as during very low–carbohydrate diets or fasting, it cannot burn glucose. Therefore, if you start to eat carbohydrates, the cells temporarily cannot handle the

glucose load and your blood glucose levels rise.

The opposite is also true. When the body is burning glucose, it cannot burn fat, but saves stored fat for later consumption.

The more fat found in the pancreas, the less insulin it secretes.

Simply put, fatty pancreas and fatty liver is the difference between a type 2 diabetic and a nondiabetic.

Glucose and fructose are examples of single-sugar carbohydrates.

Eating fructose does not appreciably change the body’s blood glucose level, since they are different sugar molecules. Neither does fructose produce much insulin response directly.

But it had a hidden dark side that was not obvious for many decades. The toxicity of fructose was invisible when looking at the blood glucose; it only became apparent by looking at the slow accumulation of fat in the liver.

fructose is particularly malevolent to human health compared to glucose due to the unique way the body metabolizes it.

Only the liver metabolizes fructose.

Fructose is many times more likely than glucose to cause fatty liver, setting off a vicious cycle.

In fact, the major diseases of the twenty-first century—heart disease, cancer, diabetes—have all been related to metabolic syndrome and its common cause, the X factor. That X factor, as it turns out, is hyperinsulinemia.10

Eating dietary carbohydrates, not dietary saturated fat, increases saturated fat levels in the blood.

The two main activators of DNL are insulin and excessive dietary fructose.

DIABETES, AS WELL as obesity and prediabetes, increases the risk of many different types of cancer, including breast, colon, endometrial, kidney, and bladder cancers.

women with the highest insulin levels carry a 2.4-fold higher risk of breast cancer.

a review of the newly diagnosed diabetics in the Saskatchewan population disclosed that use of insulin raised the risk of cancer by 90 percent.

once cancer has been established, high blood glucose enables it to grow faster.

The main side effect of this class of medications is the increased risk of urinary tract infections and yeast infections due to increased urinary glucose concentration. However, these infections were generally mild and treatable. The most serious side effect was an increased risk of ketoacidosis.