WHY METABOLIC SYNDROME MATTERS
EACH ADDITIONAL COMPONENT of metabolic syndrome, high triglycerides, low HDL, central obesity, high blood glucose, and high blood pressure, significantly increases the risk of all the modern metabolic diseases, such as heart attacks, strokes, peripheral vascular disease, type 2 diabetes, Alzheimer’s disease, and cancer.
These symptoms cluster together, but not every disease manifests in every person: one person may have low triglycerides, another person will have high blood sugars from insulin resistance, and yet another will have high blood pressure.
But having one of these factors increases the likelihood of having the others because they all share the same root cause.
In a typical patient, gaining as little as 2 kilograms (4.4 pounds) of weight is the first detectable abnormality related to hyperinsulinemia/insulin resistance, followed by low HDL cholesterol levels.
High blood pressure, fatty liver, and high triglycerides emerge next, at roughly the same time.
The very last symptom to appear is usually high blood glucose, which clinches the diagnosis of type 2 diabetes.
The West of Scotland study36 confirmed that fatty liver and elevated triglycerides precede the diagnosis of type 2 diabetes.
Fatty liver occurs early in metabolic syndrome.
While virtually all patients with metabolic syndrome have fatty liver, the opposite is not true.
Only a minority of patients with fatty liver have full-blown metabolic syndrome (see Figure 9.4).
Figure 9.4.
Hormonal obesity IX: Full-blown metabolic syndrome
Insulin resistance and type 2 diabetes cannot cause metabolic syndrome because they are part of the syndrome.
Hyperinsulinemia causes it.
The very core of the problem is hyperinsulinemia from excessive fructose and glucose, but especially fructose intake.
Metabolic syndrome, of which obesity and type 2 diabetes are a key part, are ultimately caused by, you guessed it, too much sugar.
Obesity, insulin resistance, and beta cell dysfunction are all protective mechanisms.
Obesity tries to prevent DNL from overwhelming the liver by safely storing the newly created fat in the adipocytes.
We know this because patients with a rare, genetic disorder called lipodystrophy, which is characterized by a lack of fat cells,37 show all the manifestations of metabolic syndrome, fatty liver, elevated triglycerides, and extremely high levels of insulin resistance, without the weight gain.
In rodent models of lipodystrophy, transplanting adipocytes back into these fat-free mice completely cures metabolic syndrome.
Fat cells actually provide protection against metabolic syndrome rather than causing it.
Why?
Because without adipocytes, fat must be stored inside the organs, where it causes metabolic syndrome.
If fat can be stored inside adipocytes instead, no metabolic damage results.
Obesity is the first line of defense against the root problem of hyperinsulinemia/insulin resistance.
Similarly, insulin resistance is the body’s attempt to prevent fat from amassing in the internal organs by preventing it from entering.
The liver refuses to allow more glucose to enter because it is already overfilled,
and the result is visible as insulin resistance, which represents a second protective mechanism.
The final line of defense lies in shutting down pancreatic production of insulin.
Blood glucose rapidly rises above the renal threshold and causes all the classic symptoms of diabetes.
But this toxic load of glucose has been safely discharged out of the body, and is unable to cause further metabolic damage.
The core problems of too much glucose and insulin have been handled, but at the cost of symptomatic diabetes.
The essential problem is too much sugar, and the body is desperately dumping it out in the urine.
All the conditions we thought were problems, obesity, insulin resistance, and beta cell dysfunction, are actually the body’s solutions to a single root cause, too much sugar.
And when we understand the root cause, the answer to all of these problems, and to type 2 diabetes, becomes immediately obvious.
We need to get rid of the sugar and lower insulin.
If we fail to remove the problems of too much sugar, too much insulin, and ectopic fat, then the problem is chronic and progressive.
When we treat the root cause, then type 2 diabetes, and indeed the entire metabolic syndrome, is a completely reversible disease.
BRUNO Bruno, 75, had a thirty-year history of type 2 diabetes, which caused some eye and nerve damage as well as chronic kidney disease.
He also suffered from gout, peripheral vascular disease, and high blood pressure.
When we first met four years ago, he weighed 215 pounds and used 68 units of insulin daily.
Once he began the IDM program, Bruno started on a low- carbohydrate, healthy-fat diet with 36-hour fasts every other day.
Within four weeks, he was able to stop taking insulin completely and has not required any since.
This result still astounds him because he had been using insulin for over twenty years.
In addition, he no longer needs any medication for blood pressure or cholesterol.
His latest A1C is only 6.1%, which classifies him as prediabetic rather than diabetic.
Bruno adjusted quickly to his new diet and fasting regimen and finds it simple to follow, even several years later.
He has maintained a 48-pound weight loss and a 24 cm reduction in waist size over these last four years.
RAVI Ravi, now 40, was diagnosed with type 2 diabetes when he was only 28 years old.
After starting on blood-glucose-lowering medications, he required higher and higher doses until he was finally prescribed insulin, which he was told he would need for life.
In addition, he had developed high cholesterol and hypertension.
He was taking 102 units of insulin daily, in addition to canagliflozin and metformin.
Yet despite these huge doses of medication, his A1C was still 10.8%, which indicates that his blood glucose was completely out of control.
When Ravi entered the IDM program, he switched to a low- carbohydrate, healthy-fat diet and started fasting three times a week for 36 hours each time.
Within two weeks, he was able to stop taking any insulin, and his blood glucose numbers were better than ever.
Within two months, when his cholesterol and blood pressure had returned to normal, he stopped taking metformin and his doctor lowered his cholesterol and blood pressure medications to a quarter of their previous doses.
In addition, he lost 23 pounds and his waist circumference decreased by 18 cm.
Now, ten months into the program, he continues to take a single (non-insulin) medication, but his A1C is 7.4% and continues to improve.
INSULIN: NOT THE ANSWER FOR TYPE 2 DIABETES
THE CONVENTIONAL TREATMENT for both type 1 and type 2 diabetes has long been injection of exogenous (external) insulin.
Human insulin, one of the great triumphs of modern pharmaceutical science, can be produced in a laboratory and packaged for convenient injection.
For most of the early and mid-twentieth century, research focused on type 1 diabetes, which is caused by a severe lack of insulin.
Without exogenous insulin replacement, cells cannot use glucose and they starve, leading to unrelenting weight loss and eventual death.
This formerly fatal disease has become manageable, but injecting insulin comes with its own complications.
It is essential to match the insulin dose with the amount of food being eaten, especially carbohydrates, since complications arise when blood glucose goes too far outside the normal range.
Underdosing causes high blood glucose (hyperglycemia) and overdosing causes low blood glucose (hypoglycemia).
Mild hypoglycemic reactions cause patients to sweat and shake, but more severe reactions can include seizures, loss of consciousness, and death.
In 2014, nearly 100,000 emergency room visits and 30,000 admissions to hospital were directly related to hypoglycemia.1 Extremely high blood glucose can cause diabetic ketoacidosis in type
1 diabetes and non-ketotic hyperosmolar coma in type 2 diabetes, but these complications are relatively uncommon.
On the other hand, until the early 1990s it was unclear whether mildly elevated blood glucose was even all that dangerous.
So for many decades, the standard medical practice was to keep the blood glucose levels slightly high, but below 10 mmol/L, the renal threshold for glucose.
At this level, the kidneys completely reabsorb glucose so that none spills over into the urine, thereby avoiding the typical diabetic symptoms of excessive urination and thirst.
And keeping the levels slightly above normal avoids both hypoglycemia and the symptoms of high blood glucose.
In the past, this was considered an acceptable trade-off, as nobody had yet found definitive proof that this level was harmful.
This point of view changed irrevocably in 1993.
INSULIN AND GLUCOTOXICITY
THE DIABETES CONTROL and Complications Trial (DCCT)2, a large, randomized, controlled trial of patients with type 1 diabetes carried out between 1983 and 1993, proved that intensive insulin therapy, including tight management of blood glucose levels, could have dramatic beneficial results.
Close monitoring and multiple daily insulin injections to keep blood glucose levels as close to normal as possible could prevent the end-organ damage associated with hyperglycemia: diabetic eye disease decreased by 76 percent, kidney disease by 50 percent, and nerve damage by 60 percent.
In 2005, researchers published a follow-up study called the Epidemiology of Diabetes Interventions and Complications (EDIC).3 They followed more than 90 percent of the original DCCT patients for up to seventeen years, and found that the intensive insulin treatment had reduced cardiovascular disease by an astonishing 42 percent.
These two studies clearly established the paradigm of glucotoxicity, that high blood glucose is toxic in type 1 diabetes.