I am trying to get a definitive answer as to whether my daughter has type 1 or type 2 diabetes. Her endocrinologist response is “She has type 1 diabetes as certainly as any of our other 600 children. Sometimes it can be difficult to decide for a particular child because features are mixed, but she had all the major features of type 1 (weight loss, DKA [diabetic ketoacidosis]), full insulin requirement within a year, normal sensitivity to insulin, associated autoimmune thyroiditis, and highly positive GAD antibody. The older islet cell antibody was negative, as is the case in many otherwise typical type 1 children, and it doesn’t disprove type 1”.

I contacted another expert in the field who stated, “Many people, endocrinologists included, mistakenly conclude that any patient with diabetes and significant insulin deficiency have type 1 diabetes. In fact, the definition of type 1 diabetes is based on evidence of immunological cause of beta cell destruction, such as presence of islet antibodies. Type 2 diabetes may eventuate in significant insulin deficiency, but this does not mean it has become type 1.” Everywhere else I’ve turned to identifies people with type 1 diabetes as those who do not produce any, not a drop, of insulin.

During the most recent conversation I had with my daughter’s endocrinologist, he stated that she was still producing insulin (about 2% of her needs). How can she be identified as having type 1 diabetes, if nearly three years later, she is still producing insulin?

You ask a difficult medical and scientific question. The information you have received from her endocrinologists seems to be correct. We now know about several types of type�1 diabetes, and there is some movement to rename this autoimmune type 1 diabetes. This might be different from, for example, the type of diabetes that would occur if the pancreas needed to be removed surgically (after trauma or severe pancreatitis or after discovering a tumor).

There isn’t must difference known for long term complications with any of these types of type 1 diabetes, and the key clinical fact is that all of these would likely be associated with near total insulin deficiency rather quickly. Most, but not all, of people with type�1A (autoimmune) diabetes would be antibody positive. The problem is that the tests used to make such a diagnosis are not nearly as good as we would like them to be so there are significant false negatives.

For research purposes and epidemiological purposes, it is important to have good classification. For day to day management purposes, there is not much benefit for you or your daughter since insulin treatment decisions are made based upon glucose control parameters and not on antibody levels. Same thing for how much insulin production remains. For the individual family or patients, neither has much utility while they are extremely important research questions.

This would be distinguished from classical type�2 diabetes in which there is significant insulin resistance and much slower demise of pancreatic insulin output. Some would need insulin after a longer period of time.

To make matters more confusing, there are probably those who have insulin resistance because they are overweight/obese as well as autoimmune type 1 diabetes. This may be in certain ethnic groups (such as African-Americans, those from Asian groups, American Indians, etc.), but may also apply to Caucasians as well. We debate a great deal about this at our research meetings and do not have clear answers yet.

SB