The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally

by Jason Fung

“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 Einstein is quoted as saying, “Everything should be made as simple as possible, but not simpler.”

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. Thus, there are two underlying prerequisites of the disease: elevated insulin resistance and beta cell dysfunction.

AS SHOWN IN Figure 7.1, insulin resistance emerges, on average, almost thirteen years prior to type 2 diabetes.

Remember that all fats are not created equal. Excess dietary fat bypasses the liver and can be stored anywhere in the body. Fat carried under the skin (subcutaneous fat) contributes to overall weight and body mass index but has minimal health consequences. It is cosmetically undesirable but seems to be otherwise metabolically innocuous.

Excess dietary carbohydrates and protein are stored first in the liver as glycogen. Once glycogen stores are full, DNL converts glucose to fat, which can then be exported out of the liver to the rest of the body, including to fat stores in and around the abdominal organs.

As shown in Figure 7.2, the cycle proceeds as follows: 1.Hyperinsulinemia causes fatty liver. 2.Fatty liver causes insulin resistance. 3.Insulin resistance leads to compensatory hyperinsulinemia. 4.Repeat cycle.

Fat inside the liver, rather than overall obesity, is the crucial stepping stone toward insulin resistance and diabetes. Fatty

Fatty liver precedes the clinical diagnosis of type 2 diabetes by ten years or more.6 As the liver slowly accumulates fat it becomes increasingly insulin resistant.

Two main types of fatty liver disease exist: alcohol-related liver disease and non-alcoholic fatty liver disease.

But a lot of people who develop fatty liver disease and diabetes are not alcoholics, and it’s only recently that scientists have begun to understand that connection.

Dr. Samuel Zelman, a physician at the Veterans Administration Hospital in Topeka, Kansas, first made the connection in 1952.7 Alcoholism was known to cause fatty liver, but he observed the disease in a hospital aide who drank, not alcohol, but more than twenty bottles of Coca-Cola a day!

Those with NAFLD whose blood tests showed evidence of organ damage were said to have non-alcoholic steatohepatitis (NASH), a term derived from steato, which means “fat,” and hepatitis, which means “inflammation of the liver.” NASH is simply the more serious manifestation of NAFLD.

More importantly, the new recognition of NAFLD confirmed the extraordinarily close association between obesity, hyperinsulinemia/insulin resistance, and fatty liver.

Hepatic steatosis, the deposition of fat in the liver, is consistently one of the most important markers of insulin resistance.

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 only takes three weeks!

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

Fatty liver is a completely reversible process. Emptying the liver of its surplus glucose and dropping insulin levels returns the liver to normal.

Specifically, the sugar fructose, rather than glucose, is the main culprit,21 even though fructose does not produce much insulin response.

Fatty muscle SKELETAL MUSCLES ARE the large muscle groups, such as the biceps, triceps, quadriceps, trunk, and gluteal muscles, that we use to move our limbs voluntarily. This differentiates them from smooth muscles—muscles such as the heart or diaphragm—which are largely not under voluntary control.

With hyperinsulinemia and excess sugar, the liver creates new fat by DNL and distributes these triglycerides throughout the body.

We can see this process of developing fatty muscle more clearly in farm-raised cattle, where the accumulation of fat between muscle fibers is called delicious!

Cattle ranchers know that marbling depends almost entirely on diet. Cows are ruminants, which means they normally eat grass and do not develop marbling. The result is a more flavorful but less tender steak. However, a grain-heavy diet increases the growth rate as well as the marbling. For this reason, many grass-fed cows are “finished” with a period of corn feeding to develop the desired fatty muscle, or marbling.

Fatty liver produces insulin resistance in the liver. In the same manner, fatty muscle produces insulin resistance in skeletal muscles. Hyperinsulinemia forces too much fat and glucose inside the skeletal muscles.

Why can’t the muscle just burn off this fat? The answer lies in the biochemical process known as the Randle cycle.

Randle demonstrated that cells burning glucose could not burn fat and vice versa.

When the body is mostly burning fat, such as during very low–carbohydrate diets or fasting, it cannot burn glucose.

The opposite is also true. When the body is burning glucose, it cannot burn fat, but saves stored fat for later consumption. The Randle cycle ensures the skeletal muscle cells cannot simply burn off the excess fat when they are fully saturated with glucose. They are burning glucose, not fat, so it accumulates. Voilà! Fatty muscle and insulin resistance.

AS WE’VE SEEN previously, the liver lies at the nexus of metabolism and nutrient flow, particularly for carbohydrates and proteins.

The major exception is dietary fat, which is absorbed directly into the lymphatic system as chylomicrons. These chylomicrons empty into the bloodstream without first passing through the liver.

Insulin promotes the storage of food energy for later use, a mechanism that has allowed us to survive the periods of famine inherent in human history.

Think of a refrigerator. We can easily place food (glucose) into the refrigerator (glycogen) and take it out again. Once the glycogen stores are full, the liver must find a different storage form for the excess glucose. It transforms this glucose through de novo lipogenesis (DNL) into newly created molecules of triglycerides, also known as body fat.

THESE NEWLY CREATED triglycerides are made from the substrate glucose, not from dietary fat.

Saturated fats in the blood, not the diet, are highly associated with heart disease.

you stuff more and more fat into the liver, it becomes noticeably engorged and can be diagnosed on ultrasound as fatty liver. But if the liver is not the appropriate place to store this new fat, where should it go?

Your glycogen “fridge” is full, so the only remaining option is to export the newly created fat (excess food) somewhere else. This mechanism is known as the endogenous pathway of lipid transport.

Ultimately, eating too much glucose and too much

High-carbohydrate diets increase VLDL secretion and raise blood triglyceride levels by 30 to 40 percent.16 Called carbohydrate-induced hypertriglyceridemia, this phenomenon can occur with as little as five days of high intake.

AS VLDL PARTICLES circulate through the bloodstream, insulin stimulates the hormone lipoprotein lipase (LPL), which is found in the small blood vessels of muscles, adipocytes, and the heart.

considered the “bad” cholesterol. High blood triglycerides strongly and independently predict cardiovascular disease,18 almost as powerfully as LDL, the marker that typically concerns doctors and patients most. Hypertriglyceridemia increases the risk of heart disease by as much as 61 percent,19 and the average triglyceride level has been rising inexorably in the United States since 1976.

High levels of LDL are pointedly not one of the criteria for developing metabolic syndrome. Instead, the other cholesterol component of the metabolic syndrome is the high-density lipoproteins (HDL, the “good” cholesterol). The landmark Framingham studies established that low levels of HDL are strongly associated with heart disease22 and predicts heart disease much more powerfully than LDL.

transfer protein (CETP), which reduces HDL levels. Given this close association with triglycerides, it should be no surprise that low-carbohydrate diets raise HDL,23 even independent of weight loss. As with triglycerides, low HDL does not cause heart disease, but is a powerful indicator.24

THE ADIPOCYTES GET larger as they take up the triglycerides for storage. This is not particularly dangerous to our health since adipocytes are designed to store fat. But being too fat is dangerous from an evolutionary standpoint, because fat animals get eaten. The adipocytes protect themselves against overexpansion by releasing the hormone leptin. This signals the hypothalamic area of the brain that we need to lose fat. We stop eating, insulin drops, and we lose weight. In this way, obesity serves as the first line of defense against hyperinsulinemia.

If you have too much body fat, leptin is released, which decreases food intake. Insulin should fall, and you should lose weight.

It’s a tug of war between insulin and leptin, and if you are eating too much sugar, ultimately, insulin wins.

allowed to continue, the engorged liver will become distended and injured. The liver cell cannot safely handle any more glucose, yet insulin is still pushing really, really hard to shove more inside. The liver’s only option is to refuse entry. This is known as insulin resistance, and it develops as the body’s second line of defense against hyperinsulinemia.

The predominance of fat around the abdomen becomes noticeable as an increase in waist size, which can be described as a beer belly but more recently is being called a “wheat belly.”

Ectopic fat clogs the pancreas and interferes with normal functioning, so insulin levels fall. When the fatty pancreas fails to produce the compensatory hyperinsulinemia, blood glucose skyrockets and becomes symptomatic when it exceeds the renal threshold. Glucose spills out into the urine, and the classic symptoms of diabetes—excessive urination, thirst, and weight loss—appear.

HIGH BLOOD PREESURE is often called “the silent killer” because there are no symptoms, yet it contributes heavily to the development of heart attacks and strokes. Most cases are called essential hypertension because no specific cause can be found for its development; however, hyperinsulinemia plays a key role.

complete review of all available studies estimates that hyperinsulinemia increases the risk of hypertension by 63 percent.32

Insulin increases blood pressure through multiple mechanisms.33 Insulin increases the cardiac output—the contractile force of the heart34—and the volume of blood in circulation by enhancing the kidney’s ability to reabsorb sodium (salt).