A form of diabetes sometimes called “double diabetes,” in which an adult has aspects of both Type 1 and Type 2 diabetes.
Over the past three decades, diabetes researchers have gradually fine-tuned the classification of different underlying diseases that comprise diabetes. In the early 1970’s, they spoke of “juvenile-onset” and “adult-onset” diabetes to distinguish between two seemingly different forms of the disease based on when they tended to appear; however, sometimes the “juvenile” form showed up in adults. They later coined the terms “insulin-dependent” and “non-insulin-dependent” diabetes to distinguish between the two basic forms of the disease based on how they were treated rather than the age of onset. But this, too, was confusing because some people with non-insulin-dependent diabetes also used insulin. So scientists had to come up with yet another classification system.
In the late 1990’s, they began classifying the two major types of diabetes by their underlying metabolic problems and called them Type 1 and Type 2. Type 1 diabetes is characterized by autoimmune destruction of pancreatic beta cells (and the resulting production of little or no insulin), and the presence of certain autoantibodies against insulin or other components of the insulin-producing system such as glutamic acid decarboxylase (GAD), tyrosine phosphatase, and/or islet cells. It often develops in children (although it can occur at any age) and requires insulin treatment for survival. Type 2 diabetes is characterized by insulin resistance and beta-cell dysfunction, usually develops in adults (although it is now occurring with alarming frequency in children), does not show signs of autoimmune disease, and usually does not require insulin to maintain survival (at least in its early stages).
The medical professionals who study and treat diabetes noticed, however, that among the people who do not require insulin at diagnosis (most of whom were assumed to have Type 2 diabetes), a significant number showed autoantibodies, especially antibodies against islet cells and GAD. In other words, these people could be treated initially with diet therapy and oral medicines like people with Type 2 diabetes, but they also had an ongoing autoimmune process like people with Type 1 diabetes. The term “latent autoimmune diabetes of adults” (LADA) was originally applied to this subset of people with diabetes. It has also been dubbed “slow-progressing Type 1 diabetes,” and, in the late 1990’s, some researchers coined the term “Type 1.5 diabetes,” because it had features of both the major types.
Further study of these people who at least initially do not require insulin yet have autoantibodies has revealed some distinct variations, leading some researchers to subdivide those placed under the umbrella term LADA into three groups: Type 1–LADA, Type 1.5 or “double” diabetes, and Type 2 diabetes with autoantibodies. Under this scheme, people with Type 1–LADA are thought to have a more slowly progressing form of Type 1 diabetes. Like people with Type 1 diabetes, people with Type 1–LADA have autoantibodies and are usually not obese. Although they may initially be able to get by with diet therapy and oral diabetes medicines, they usually need to use insulin within about five years of diagnosis because of the destruction of their beta cells.
People with Type 1.5 diabetes are said to have “double” diabetes because they show both the autoimmune destruction of beta cells of Type 1 diabetes and the insulin resistance characteristic of Type 2 diabetes. People with Type 1.5 have autoantibodies and gradually lose their insulin-producing capability, requiring insulin within 5–10 years of diagnosis. As their insulin resistance suggests, many people with Type 1.5 diabetes are obese or overweight.
People in the third group are obese or overweight with insulin resistance like most people with Type 2 diabetes, and they also have autoantibodies. However, they still manage to produce insulin for more than five years after diagnosis and can continue to manage their diabetes with diet, exercise, and oral medicines. It is suspected that the autoimmunity in these people is very mild.
Some researchers suggest screening anyone newly diagnosed with Type 2 diabetes for GAD antibodies. In the United Kingdom Prospective Diabetes Study (UKPDS), most study subjects with Type 2 diabetes between 35 and 45 years old who tested positive for antibodies against both GAD and islet cells progressed rapidly to insulin dependency. Some researchers have also suggested that anyone who tests positive for GAD antibodies be screened for autoantibodies to thyroid and adrenal cells, because like people with Type 1 diabetes, people with Type 1.5 diabetes seem to be at higher risk of having other autoimmune diseases.
The jury is still out on the best way to treat Type 1.5 diabetes. Maintaining tight blood glucose control may help to slow the destruction of the beta cells (and delay insulin dependency) as well as reduce the risk of diabetic complications. A few small studies suggest that insulin therapy or insulin combined with rosiglitazone (brand name Avandia) may help to preserve beta-cell function, but these results need to be confirmed in larger trials. (Using insulin in combination with rosiglitazone may increase risks for people with heart failure.)
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