Living Well: A diabetes tale

From two types to more

Steven Brooks, MD
BY STEVEN BROOKS, MD
Ministry Medical Group
Once upon a time, classifying diabetes was easy; we had type 1 and type 2. Type 1 was known as juvenile onset; type 2 was adult onset. They were also called insulin-dependent and non-insulin-dependent diabetes.
The tale was never that simple, of course, and it seems to be getting more complicated.
Today, we are seeing more and more children and adolescents being diagnosed with “adult-onset” diabetes; and adults in later life being diagnosed with type 1 diabetes.
The dichotomy between type 1 and type 2 diabetes has been useful. It identifies two major causes of diabetes which are an autoimmune reaction, often occurring in childhood that destroys the cells of the pancreas that are necessary to produce insulin; and insulin resistance or other changes in the body that make it impossible for cells to get the energy they need.
Carbohydrates you eat are broken down into glucose or blood sugar that is needed to fuel the cells of the body. In order to take in the glucose, though, the cells need insulin, a hormone that allows glucose to enter. Without insulin, glucose builds up in the blood, causing damage, while the cells go without the fuel they need.
TYPE 1 DIABETES: The autoimmune reaction that causes type 1 diabetes strikes suddenly and definitively, often in childhood or the teen years. Because the pancreas becomes unable to produce insulin, the patient must have daily insulin injections, hence, the term “insulin dependent” diabetes.
In addition to making changes in diet and exercise patterns, patients must monitor their glucose and adjust their insulin accordingly.
TYPE 2 DIABETES: is by far the most common type, affecting 95 percent of patients. In most cases, the pancreas still produces insulin but not enough to meet the body’s needs. Most type 2 patients have what is known as insulin resistance; their cells do not respond normally to insulin. As a result, the pancreas is asked to produce increasingly larger amounts of insulin until it becomes unable to meet the demand. Insulin resistance is strongly associated with obesity. And that is one reason that this type of diabetes is now being found more frequently among children and adolescents.
EARLY ONSET TYPE 2 DIABETES: has been increasing dramatically in many countries of the world. And more than 80 percent of those diagnosed at an early age are obese (compared to only 56 percent of those diagnosed after age 45). These young diabetics have a substantially higher risk of cardiovascular and other serious complications, even compared to type 1 diabetics. A patient diagnosed before age 45, for example, has a 14-fold increased risk of a heart attack, compared to a 4-fold increased risk for a patient diagnosed after that age. Kidney failure starts to become a danger as early as 10 years after diagnosis.
LADA DIABETES, or latent autoimmune diabetes in adults, has sometimes been called type 1.5 diabetes. It accounts for about 10 percent of diabetes diagnoses, so it may be even more prevalent than type 1.
Like type 1 diabetes, LADA occurs because of an autoimmune destruction of cells in the pancreas, but one that progresses slowly and as a result, is often mistaken for type 2 diabetes. Researchers in the 1970s found a way of identifying autoantibodies in the blood that indicate an attack on the pancreas by one’s own immune system. This test confirmed for the first time that type 1 diabetes is an autoimmune disorder. These autoantibodies are virtually absent in the general population but present in about 10 percent of persons diagnosed with type 2 diabetes.
The concept of LADA is now fairly well accepted. Persons with a higher number and greater variety of autoantibodies undergo quicker and more complete destruction of beta cells in the pancreas. They are type 1 diabetics. Patients with LADA undergo a much slower decline, but are still more likely to require insulin injections than type 2 diabetics who have few or no autoantibodies. Unlike patients with insulin resistance, those with LADA are more likely to be lean, physically active and otherwise healthy.
What’s important in distinguishing this type is the difference in treatment that may be helpful. Some evidence suggests that giving LADA patient’s insulin treatment at an early stage might be beneficial in protecting beta cells.
The simplified type 1 and type 2 system has been useful for many years. Doctors hope that a few changes to the system will make it even more useful.
Steven R. Brooks, MD, is a board certified internal medicine physician with Ministry Medical Group
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