In the comments of a recent post, I and a couple other people mentioned Type II, or insulin independent, diabetes. You might assume that the existence of a type II means there must be a type I and, well, you'd be right.

The difference between type I and type II is fairly straightforward: type II diabetes is characterized by a loss of sensitivity to the hormone insulin, while people with Type I diabetes don't make any insulin to begin with. The reason for this lack of insulin (in people with Type I) is, broadly speaking, that the cells that make it have been destroyed by their own immune system.

The genetic basis of type I diabetes is murky, but it's known that there are risk factors in genes involved in immunity and the production of insulin, as one might expect. But there's also evidence of a strong environmental role (these points are essentially copied from the abstract of this paper):
1. a pairwise concordance of type 1 diabetes of <40% among monozygotic twins
2. a several-fold increase in the incidence over the last 50 years
3. migration studies indicating that the disease incidence has increased in population groups who have moved from a low-incidence to a high-incidence region.

In this context, it's interesting that a new study looking for genetic susceptibility factors in type I diabetes fingered IFIH1, a gene coding for a protein the authors descibe as "a sensor or pathogen recognition receptor for viral infection"

The implication is thought-provoking: the environmental factor (or one of the environmental factors) that "pulls the trigger" on the autoimmune destruction of insulin-producing cells may be a virus, but genetic factors in the host determine whether the response is catastrophic or not.

See also: Agnostic on No Two Alike and developmental noise.

Labels: disease