It used to be clear that Juvenile, or Type-I diabetes, occurred only with children, and Type-II ("Adult Onset") diabetes occurred solely among adults. While Type-I diabetes remains a problem of the young, and has a different etiology than Type-II diabetes, both are climbing in incidence. Each has a different cause, and can be treated in different ways.
The classic definition of Type-I diabetes was a reduction in the ability of the pancreas to produce insulin. The insulin-producing parts of the pancreas, the Islets of Langerhans (a good trivia question on your college biology exam), would somehow lose their ability to produce insulin. As a result, children of otherwise normal weight and constitution would need to move relatively quickly to treat their affliction, or die in a diabetic coma.
Recently, we've learned that much of Type-I diabetes occurs because children develop a form of auto-immune reaction to their own pancreatic cells. This hyperreaction to the body's own cells results in a destruction of the Islets of Langerhans, and results in a lifelong need to replace insulin production with injections.
Type-I diabetes is a serious pathology, which can lead to much-increased levels of blindness, heart disease and neuropathies. If not treated properly, Type-I diabetics can contract diabetic ulcers of their feet and legs, leading to amputation.
We've seen a revolution in diabetes treatment with long-term insulin, better diagnosis, and, more recently, insulin pumps. The longer-lasting insulin gives the body a chance to respond in a more normal way to spikes in glucose levels. Diagnosis has been improved through the institution of glycosylated hemoglobin tests, which are more reliable in predicting longer-term glucose levels. Finally, insulin pumps have allowed Type-I diabetics to better match their insulin production with their food intake, thus reducing the deleterious effects of too high glucose in the bloodstream.
Type-II diabetes has been called "adult onset," as it is closely linked to obesity caused by consumption of high-sugar, high-fat diets and a lack of exercise. Once exclusively a preserve of adults, Type-II diabetes has become an increasingly-common fixture amongst teens. It's estimated that 13% of teens today have Type-II diabetes in the US.
This syndrome of early stage obesity and resulting Type-II diabetes was almost unknown 20 years ago. The proliferation of junk foods and a sedentary lifestyle have caused the obesity epidemic, which in turn has resulted in an epidemic of Type-II diabetes throughout the population.
Type-II diabetes affects the body in much the same way as Type-I diabetes over the long term. While some people with Type-II diabetes can become insulin dependent, some drugs (such as glucophages) can diminish the deleterious effects of excess insulin and glucose circulation. People with Type-II diabetes nevertheless encounter higher incidences of heart disease, estimates are three to seven times as high as non-diabetics' and related diseases, such as strokes, neuropathy and kidney disease.
It is clear that more exercise and weight loss can reverse the diabetic effects of insulin resistance. Since few obese patients are willing or able to increase exercise or reduce caloric intake, many are condemned to suffer the lifelong consequences of diabetes.
Type-I diabetes will be treated in the future by drugs and devices which reduce the body's tendency in some people to attack its own cells. Anti-inflammatory drugs, immune suppressants and, in the future, more targeted drugs will improve the outlook for such people. Better and earlier diagnosis, coupled with this better therapy, will reduce the overall rate of Type-I diabetes.
Type-II diabetes, on the other hand, will continue to climb dramatically, along with the rate of obesity in this country. Without a clear strategy to reduce obesity, we must resign ourselves to the fact that more and more people will suffer from Type-II diabetes, and the resulting co-morbidities.