DSI Newsletter: Diabetes Mellitus

DSI Newsletters, Issue 4:
Diabetes Mellitus (DM)

The hallmark of DM is hyperglycemia (high blood sugar). There are two ways this can occur.
In type 1, the pancreatic beta cell breaks and fails to produce insulin. This generally happens to children. Without shots of insulin, type 1 diabetics will die.
In type 2, the defect is at the level of the insulin receptor on the fat cell causing insulin resistance. Type 2s have more insulin than non-diabetics; the problem is the insulin doesn't work properly on the broken malfunctioning insulin receptor.
The goal is to maintain the glucose (blood sugar) normal. What is normal? Well, the quick answer is a HgbA1C (hemoglobin A1C) level of less than 7.0. HgbA1C represents your average glucose over the past three months. If this number is normal, your body won't think you're diabetic. Next is the Fasting Glucose, the blood sugar before you eat breakfast. The goal is to keep it about 100. But, the HgbA1C is a much more important number. If the fasting glucose is high and the HgbA1C is normal, you will be fine. However, if your fasting sugars are normal and your HgbA1C is high, you are bound to get the complications of DM like: heart attack, stroke, blindness, impotence and kidney failure. A Random Glucose is a sugar done anytime that you are not fasting. These become useful in insulin requiring diabetics to guide their treatment.
The history of diabetes is fascinating. In the 1950s, everyone was on insulin, because the pills weren't invented yet. In 1960, the first pill became available. It was in the class Sulfonurea. They work by making more insulin be squeezed out of the pancreas. This was great because it enabled many diabetics to get off of insulin. The common sulfonureas used today have names like: Glucotrol, glyburide, glynase and amaryl. In 1970, we asked the question how much longer a patient would live since we were able to switch them from insulin to the sulfonurea, and we were surprised to learn that there was no difference. That is because the higher than normal insulin level it takes to lower the blood sugar has side effects. It turns out that insulin is a bad hormone. It injures the endothelium (inside lining of the arterial walls) and enables the cholesterol to attach (adhere) itself causing hardening of the arteries (atherosclerosis) and eventually blocks the artery causing a myocardial infarction (heart attack) or a cerebrovascular accident (stroke). So, it didn't matter if you injected yourself with insulin, or if you took a pill (sulfonurea) to increase your own endogenous insulin, both resulted in hyperinsulinemia (high blood insulin level) and hardening of the arteries.
For a long time doctors would tell patients to diet and exercise to lower both the sugar and the insulin to overcome this insulin resistance and prevent a premature vascular event (heart attack or stroke). In 1985 glucophage came out. This was the first drug to lower glucose and lower insulin levels by decreasing the amount of glucose that the liver was making (gluconeogenesis). And, glucophage helps to lose weight.
Then, in the 1990s, the TZDs like rezulin, Actos and avandia became available. They also lower glucose and insulin by helping the sugar into the muscle cells easier. Rezulin was taken off the market for the wrong reason. There were some problems of hepatitis, that is elevated liver blood test. As the doctors learned to use the drug better, we would stop the TZD at the first sign of elevated liver enzymes and they'd return to normal.
The Drug Study Institute is conducting some drug studies on a new treatment for type 2 diabetes. If you are interested in learning about the benefits of participating in an experimental drug research study, please contact us: Joseph Saponaro, MD, DABIM, FACP, CPI, CCI, CCRI, CCRC, CCRP at 866-575-1212.

Return to Table of Contents