The Diabetes Code. Dr. Jason Fung
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The A1C has largely replaced the fasting blood glucose test and the OGT for diagnosis because of its simplicity and convenience, but all of these tests are considered accurate and acceptable. 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.
Table 2.3 Diagnostic criteria for diabetes
Fasting blood glucose > 7.0 mmol/L (126 mg/dL) |
2 hour blood glucose > 11.1 mmol/L (200 mg/dL) during OGT |
A1C > 6.5% (48 mmol/mol) |
Symptoms of hyperglycemia and random blood glucose > 11.1 mmol/L (200 mg/dL) |
The total amount of glucose circulating in the blood at any time is surprisingly small—roughly a single teaspoonful. Glucose does not float freely around in the blood. Rather, most of the body’s glucose is contained within our cells.
Hormones tightly regulate our blood glucose to avoid excessively low or high levels. Even when we eat large amounts of sugar, the blood glucose level still remains within a remarkably narrow, controlled range due to the coordinated actions of various hormones. As glucose is absorbed through the intestines into the blood, the islet cells within the pancreas secrete the hormone insulin. Insulin allows the glucose to enter the cells as fuel for energy. The body stores any excess glucose in the liver for future use, which keeps our blood glucose from rising out of its normal range.
TYPE 1 DIABETES: THE FACTS
TYPE 1 DIABETES has been previously called juvenile diabetes, since its onset commonly occurs during childhood. However, although three-quarters of all cases are diagnosed in patients under eighteen, it may present at any age. The global incidence of type 1 diabetes has been rising in recent decades for unknown reasons and may be increasing by as much as 5.3 percent annually in the United States.3 In Europe, at present rates, new cases of type 1 diabetes will double between 2005 and 2030.
Type 1 diabetes is an autoimmune disease, meaning that the body’s own immune system damages the cells that secrete insulin. The patient’s blood contains antibodies to normal human islet cells, which provides evidence of an autoimmune attack. Over time, cumulative destruction of the insulin-producing cells causes type 1 diabetes to progress to severe insulin deficiency, whereupon symptoms typically occur.4
There is a strong genetic predisposition to type 1 diabetes, but what eventually triggers the autoimmune destruction is uncertain. Seasonal variation in diagnosis may point to an infectious trigger, but which specific one is unclear. Other environmental agents that may play a role include sensitivity to cow’s milk, wheat protein, and low vitamin D. Type 1 diabetes often occurs together with other autoimmune diseases, such as Graves’ disease (which affects the thyroid) or vitiligo (which affects the skin).
Type 1 diabetics suffer from a severe lack of insulin. Therefore the cornerstone of successful treatment is adequate replacement of the missing hormone insulin. The discovery of insulin injections dramatically improved the prognosis, leading to a widespread feeling that diabetes had been cured. However, the story did not end happily ever after. Over the long term, type 1 diabetics are at much higher risk of complications, which affect almost all organs of the body, than nondiabetics. Type 1 diabetes reduces life expectancy by five to eight years and carries more than ten times the risk of heart disease compared with healthy patients.5
TYPE 2 DIABETES: THE FACTS
TYPE 2 DIABETES has historically afflicted older adults, but the prevalence is rising quickly in children worldwide,6 mirroring the increase in childhood obesity.7 One clinic in New York City reported a tenfold increase in new cases of diabetes from 1990 to 2000, with half of all new cases being type 2.8 In 2001, less than 3 percent of newly diagnosed diabetes in adolescents was type 2. Only a decade later, by 2011, this had increased to 45 percent.9 That is a truly stunning epidemic. In less time than it takes to age a good cheese, type 2 diabetes had risen like a cyclone, leaving only devastation in its wake.
Overall, type 2 diabetes accounts for approximately 90–95 percent of diabetes cases worldwide. It typically develops gradually over many years and progresses in an orderly manner from normal to prediabetes to full-blown type 2 diabetes. The risk increases with age and obesity.
Hyperglycemia occurs due to insulin resistance, rather than the lack of insulin, as in type 1 diabetes. When researchers first developed insulin assays, they expected type 2 diabetes patients to show very low levels, but to their surprise, insulin levels were high, not low.
The failure of insulin to lower blood glucose is called insulin resistance. The body overcomes this resistance by increasing insulin secretion to maintain normal blood glucose levels. The price to be paid is high insulin levels. However, this compensation has a limit. When insulin secretion fails to keep pace with increasing resistance, blood glucose rises, leading to a diagnosis of type 2 diabetes.
DIFFERENT CAUSES REQUIRE DIFFERENT CURES
FUNDAMENTALLY, TYPE 1 and type 2 diabetes are polar opposites, one characterized by very low insulin levels and the other by very high ones. Yet, curiously, standard drug treatment paradigms for the two types are identical. Both primarily target blood glucose, with the goal of lowering it by increasing insulin, even though the high level of blood glucose is only the symptom of the disease and not the disease itself. Insulin helps type 1 diabetes because that disease’s underlying core problem is a lack of naturally occurring insulin in the body. However, the underlying core problem of type 2 diabetes is insulin resistance and it remains virtually untreated because there is no clear consensus upon its cause. Without this understanding, we don’t have a hope of reversing it. That is our challenge. It may appear formidable, but its rewards are equally enticing: a cure for type 2 diabetes.
THE WHOLE BODY EFFECT
DIABETES, UNLIKE VIRTUALLY every other known disease, has the unique and malignant potential to devastate our entire body. Practically no organ system remains unaffected by diabetes. These complications are generally classified as either microvascular (small blood vessels) or macrovascular (large blood vessels).
Certain organs, such as the eyes, kidneys, and nerves, are mostly supplied by small blood vessels. Damage to these small blood vessels results in the visual problems, chronic kidney disease, and nerve damage typically seen in patients with long-standing diabetes. Collectively, these are called microvascular diseases.
Other organs, such as the heart, brain, and legs, are perfused by large blood vessels. Damage to larger blood vessels results in narrowing called atherosclerotic plaque. When this plaque ruptures, it triggers the inflammation and blood clots that cause heart attacks, strokes, and gangrene of the legs. Together, these are known as macrovascular diseases.
How diabetes causes this damage to blood vessels will be discussed throughout this book. It was widely considered to be simply a consequence of high blood glucose, but the truth, as we’ll see, is far different. Beyond the vascular diseases are many other complications, including skin conditions, fatty liver disease, infections, polycystic ovarian syndrome, Alzheimer’s disease, and cancer. However, let’s begin