Diabetes in China is a catastrophic problem.
In 2013, 11.6% of Chinese adults had type 2 diabetes, surpassing the 11.3% in the United States, the long-time champion.
Since 2007, 22 million Chinese people have been diagnosed with diabetes.
This figure is even more shocking when you consider that in 1980, only 1% of Chinese people had type 2 diabetes.
In one generation, the incidence of diabetes increased by a whopping 1160%.
The International Diabetes Federation estimates that by 2040, the global prevalence of diabetes will reach 1 in 10 adults.

This issue is not to be taken lightly.
In the United States, 14.3% of adults have type 2 diabetes, and 38% have prediabetes, making up a total of 52.3%.
This means that for the first time in history, the number of people with a disease exceeds the number of people without a disease.
Prediabetes and diabetes are new phenomena that have never existed before.

--- From "Chapter 1: How did type 2 diabetes become an epidemic?"

Type 2 diabetes accounts for approximately 90-95% of diabetes cases worldwide.
Type 2 usually develops gradually over several years, progressing gradually from normal to prediabetic to full-blown type 2 diabetes.
The older you are and the more obese you are, the greater your risk.

Hyperglycemia is caused by insulin resistance rather than insulin deficiency, as in type 1 diabetes.
When researchers first developed methods to analyze insulin, they expected that people with type 2 diabetes would have very low insulin levels, but surprisingly, their insulin levels were actually high.


A condition in which insulin cannot lower blood sugar levels is called insulin resistance.
The body tries to overcome this resistance by increasing insulin to maintain normal blood sugar levels.
In return, insulin levels increase.
But this compensation has its limitations.
If increasing insulin levels cannot keep up with the increasing resistance, blood sugar levels will rise and you will be diagnosed with type 2 diabetes.

--- From "Chapter 2: Differences between Type 1 and Type 2 Diabetes"

To be honest, your body can regulate your basal metabolic rate (BMR) up and down by up to 40%.
In other words, it can regulate the energy required for the heart to pump, the lungs to breathe, the kidneys and liver to detoxify, the brain to think, and the body to generate heat.
If you eat fewer calories, your body slows down and uses fewer calories, so you don't lose weight.


This model also completely ignores the diverse and multifaceted hormonal systems that signal hunger and satiety.
That is, we can decide what and when to eat, but we cannot avoid being hungry.
You can't decide when to burn calories as body heat and when to store them as body fat.
Hormones make these decisions.
The so-called 'calorie reduction' hypothesis has produced the worst results.
The storm of obesity and type 2 diabetes that began in the late 1970s has now, nearly 40 years later, become a Category 5 hurricane that threatens to engulf the world in disease and disability.

--- From "Chapter 4: Diabetes and Obesity: Calorie Fraud"

Fat accumulation is not really a problem of energy excess.
It's a problem of energy 'distribution'.
Too much energy is diverted to fat production instead of raising body temperature or forming new bone tissue.
This energy expenditure is regulated by hormones.
We were doomed to fail because we mistakenly believed that obesity was caused by excessive calorie intake and tried to cut calories in vain.


We cannot 'decide' to feel less hungry.
We cannot 'decide' to increase our basal metabolic rate.
When you eat fewer calories, your body compensates by lowering your metabolic rate.
Reducing calories won't lead to stable weight loss unless calories are the root cause of your weight gain.
The most important factor in regulating fat storage and weight gain is not the total number of calories consumed, but rather the hormonal signals derived from the foods you eat.


Obesity is not a calorie imbalance, it is a hormonal imbalance.
The hormonal problem that causes unwanted weight gain is mainly insulin excess.
Therefore, type 2 diabetes is a disease caused by insulin imbalance rather than calorie imbalance.

--- From "Chapter 4: Diabetes and Obesity: Calorie Fraud"

The process of making animal foie gras is basically the same as the process of making fatty liver in humans.
To intentionally overfeed carbohydrates and cause fatty liver disease, insulin levels must be high.
In 1977, the U.S. Dietary Guidelines strongly recommended eating less fat and more carbohydrates like bread and pasta.
What was the result? Insulin levels rose dramatically.
Little did we know that we were essentially creating human foie gras.


Fatty liver disease is a precursor to insulin resistance, but it's only the beginning.
Fat within other organs, including skeletal muscle and the pancreas, also plays a leading role in type 2 diabetes.

--- From "Chapter 7: Diabetes, a Double Disease"

Ectopic fat, which accumulates in places other than fat cells, plays a significant role in developing insulin resistance.
These include fatty liver, fatty muscle, and fatty pancreas.
Even severely obese patients do not develop insulin resistance unless ectopic fat accumulates.
This explains why 20% of obese people have a normal metabolic state without insulin resistance.
Conversely, even if your weight is normal, type 2 diabetes can develop if fat accumulates in organs other than fat cells.
Fat inside fat cells is fine, but fat inside organs is not.

Visceral obesity (also known as abdominal obesity), first recognized in the 1950s, is detrimental to metabolism.
Without insulin, ectopic fat cannot accumulate and insulin resistance cannot occur.
In fact, the accumulated fat melts away when insulin levels remain low.
Insulin is needed to convert excess calories into fat and maintain that fat.
Type 2 diabetes not only increases body fat, but also causes fat to accumulate inside your organs.
The problem is not fat, but ectopic fat.

--- From "Chapter 7: Diabetes, a Double Disease"

Obesity, insulin resistance, and beta cell dysfunction are all defense mechanisms.
Obesity is an attempt to prevent the liver from taking over by de novo lipogenesis (DNL) by safely storing newly produced fat in fat cells.
As an example of this, patients with a rare genetic disorder called adiposity syndrome (a disease in which there are no fat cells) show all the symptoms of metabolic syndrome, including fatty liver, triglycerides, and insulin resistance, without gaining weight.
Experiments on mice suffering from this disease showed that transplanting fat cells into fat-free mice completely cured metabolic syndrome.


Fat cells actually do not cause metabolic syndrome, but rather prevent it.
Without fat cells, fat must be stored in organs, leading to metabolic syndrome.
If fat can be stored inside fat cells, no metabolic damage occurs.
Obesity is the first line of defense against the underlying problems of hyperinsulinemia and insulin resistance.
Similarly, insulin resistance is the body's attempt to block incoming fat and prevent it from accumulating in internal organs.
The already over-filled liver refuses to allow more glucose in, and insulin resistance, the second line of defense, appears.

The last line of defense is to stop the pancreas from producing insulin.
Blood sugar levels rise too quickly, beyond what the kidneys can handle, causing all the common symptoms of diabetes.
However, this toxic glucose is safely eliminated from the body and can no longer cause metabolic damage.
The core problem of excessive glucose and insulin has been solved, but at the cost of diabetes symptoms.
Since excess sugar is the main problem, the body desperately tries to get rid of it through urine.
---From "Chapter 9: Association with Metabolic Syndrome"

The traditional diet of the people of Okinawa, a small island in southern Japan, is nearly 85% starch.
Both groups eat mostly sweet potatoes.
They rarely develop type 2 diabetes because they eat very little refined grains like sugar or flour.
The indigenous diet of Kitava, a small island in New Guinea, consists of 69% carbohydrates, mainly from tubers (sweet potatoes, cassava, yams), coconut, and fruit, yet their average insulin levels are lower than those of 90% of the Swedish population.

In other words, higher carbohydrate intake does not necessarily lead to higher insulin levels.
Refining and processing play a major role in enhancing insulin effectiveness.
When you remove the natural fiber, fat, and protein from foods, you're left with pure, concentrated carbohydrates that don't come naturally.
When these carbohydrates are ground into a fine powder (such as flour), they are digested more quickly, causing a spike in blood sugar.
At the same time, refined carbohydrates don't make you feel full like protein, fiber, and fat, so you end up eating more.
Fructose plays a dominant role in the development of fatty liver, insulin resistance, and hyperinsulinemia, and traditional societies consume little or no added sugar.

The fundamental problem of type 2 diabetes is hyperinsulinemia, which may or may not be a result of excessive carbohydrate intake.
Reversing or preventing type 2 diabetes means lowering insulin, which can be achieved with a diet high in carbohydrates.
However, avoiding sugar and refined carbohydrates remains the cornerstone of success.
According to research, a Mediterranean diet that includes olives, is low in carbohydrates, and high in fat reduces the need for medication by a whopping 59%.
Recognizing the potential benefits of consuming natural fats and limiting added sugars and refined carbohydrates can put you on the path to reducing and reversing type 2 diabetes.

---From "Chapter 14: Low-Carb Diet"