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 with the problems associated with small blood vessels.
MICROVASCULAR COMPLICATIONS
Retinopathy
DIABETES IS THE leading cause of blindness in the United States.1 Eye disease—characteristically retinal damage (retinopathy)—is one of the most frequent complications of diabetes. The retina is the light-sensitive nerve layer at the back of the eye that sends its “picture” to the brain. Diabetes weakens the small, retinal blood vessels, which causes blood and other fluids to leak out. During routine physical eye examinations, this leakage can be visualized with a standard ophthalmoscope.
In response to this damage, new retinal blood vessels form, but they are fragile and easily broken. The result is more bleeding and the eventual formation of scar tissue. In severe cases, this scar tissue can lift the retina and pull it away from its normal position, ultimately leading to blindness. Laser treatment can prevent retinopathy by sealing or destroying the leaky new blood vessels.
Approximately 10,000 new cases of blindness in the United States are caused by diabetic retinopathy each year.2 Whether retinopathy develops depends on how long a person has had diabetes as well as how severe the disease is.3 In type 1 diabetes, most patients develop some degree of retinopathy within twenty years. In type 2 diabetes, retinopathy may actually develop up to seven years before the diabetes itself is diagnosed.
Nephropathy
THE MAIN JOB of the kidneys is to clean the blood. When they fail, toxins build up in the body, which leads to loss of appetite, weight loss, and persistent nausea and vomiting. If the disease goes untreated, it eventually leads to coma and death. In the United States, more than 100,000 patients are diagnosed with chronic kidney disease annually, costing $32 billion in 2005. The burden is not only financially enormous, but emotionally devastating.
Diabetic kidney disease (nephropathy) is the leading cause of end stage renal disease (ESRD) in the United States, accounting for 44 percent of all new cases in 2005.4 Patients whose kidneys have lost over 90 percent of their intrinsic function require dialysis to artificially remove the accumulated toxins in the blood. This procedure involves removing the patient’s “dirty” blood, running it through the dialysis machine to clean out its impurities, and then returning the clean blood to the body. To stay alive, patients require four hours of dialysis, three times per week, indefinitely, unless they receive a transplant.
Figure 3.1. Adjusted prevalence rates of end stage renal disease5
Diabetic kidney disease often takes fifteen to twenty-five years to develop, but, like retinopathy, it may occasionally be diagnosed before type 2 diabetes, itself. Approximately 2 percent of type 2 diabetic patients develop kidney disease each year. Ten years after diagnosis, 25 percent of patients will have evidence of kidney disease.6 Once established, diabetic nephropathy tends to progress, leading to more and more kidney impairment until eventually the patient requires dialysis or transplantation.
Neuropathy
DIABETIC NERVE DAMAGE (neuropathy) affects approximately 60–70 percent of patients with diabetes.7 Once again, the longer the duration and severity of diabetes, the greater the risk of neuropathy.8
There are many different types of diabetic nerve damage. Commonly, diabetic neuropathy affects the peripheral nerves, first in the feet, and then progressively in the hands and arms as well, in a characteristic stocking-and-glove distribution. Damage to different types of nerves will result in different symptoms, including
•tingling,
•numbness,
•burning, and
•pain.