Type 1 diabetes is an autoimmune condition in which your body’s own antibodies, for some unknown reason, attack your beta cells, destroying them and your ability to produce insulin. Insulin resistance (IR) is not involved.
Type 2 diabetes is a condition in which, for some unknown reason, you have IR coupled with defective beta cells that aren’t able to overcome the increased demand for insulin caused by the IR. Autoimmunity is not involved.
This is the current dogma about the two main forms of diabetes (there are also other types that affect fewer people). But is it correct?
Perhaps not, according to a recent study published in the Journal of Clinical Endocrinology and Metabolism. These researchers found that adolescents with type 1 diabetes have more IR than matched nondiabetic adolescents, as well as reduced cardiovascular fitness.
However, the type 1 patients were not overweight, did not have abnormal lipid levels, and did not have fat in their muscles.
Clearly, people with type 1 diabetes have less IR than people with type 2 diabetes, because they need much smaller amounts of insulin to keep their BG levels in normal ranges. But if the cardiovascular fitness of these adolescents was reduced with only a little IR, and with normal lipid levels, it suggests that the increase in cardiovascular events in people with diabetes may be caused by the IR itself, rather than by other factors, including lipid levels.
This idea that people with type 1 diabetes have some IR is consistent with a fascinating study from Toronto in 2006, in which researchers were able to reverse a type-1-like diabetes in mice by injecting capsaicin, the compound that causes heat in hot peppers, into the sensory nerves of the mice.
The Toronto authors said their treatment also reduced the IR in these mice. They suggested that IR is a factor in type 1 diabetes and the IR contributes to beta cell stress that enhances the autoimmune attack. The researchers also performed experiments to mice that have a type of diabetes analogous to type 2. They got similar results.
Of course, these results were in mice, not humans. The mouse that is used to model type 1, the NOD mouse, has some similarities with both types of diabetes, according to a research group at Stanford. The Toronto researchers are now trying to extend their research to humans with both types of diabetes, but so far no results have been published.
So what does all this mean for us? Clearly, the research hasn’t progressed far enough that we can apply capsaicin to our pancreas and hope to be cured.
What both these studies suggest, however, is that people with type 1 and people with type 2 probably have a lot more in common than is currently thought. The Stanford researchers wrote, “Our results suggest that there is a common etiology between type 1 and type 2 diabetes.” They also note that type 1 diabetes often develops in families with a strong history of type 2 diabetes, suggesting some common underlying cause.
They point out that up to 20% of type 2 patients do have autoantibodies. Perhaps even more have low levels not detected by the methods used. And the recent study in adolescents suggests that people with type 1 diabetes do have some insulin resistance, which is consistent with the studies in mice.
Perhaps in type 1, a little IR is masked by the large autoimmune component, and in type 2, a little autoimmune attack is masked by the large amount of IR.
Hence, as a type 2, I shouldn’t ignore the research that concerns type 1. And similarly, a type 1 shouldn’t ignore the research that concerns type 2.
We may all have the same underlying disease, and we need to listen to each other and support each other as we all seek the answers that none of us yet have.