Just missing the one-year anniversary of my initial Hypoinsulinism and Insulin Resistance Syndicate content post, which argues that we need to stop talking about "diabetes" and instead focus more on the causes of each individual's tendency towards elevated blood sugar, I've run across the posting SKEWED STATISTICS: The Inclusion of People with Type 1 Diabetes in the Statistics for Type 2 Diabetes which summarizes a few sources to paint a picture of type 2 diabetes behaving much more predictably than is commonly believed. According to this article's premise, much of the complexity attributed to the causes and progression of type 2 is actually due to the failure of researchers to properly distinguish slow-onset autoimmune (i.e., type 1) diabetes from type 2 diabetes in adults.

If the author is correct, removing autoimmune-mediated diabetes (regardless of age at onset or speed of progression) from studies of type 2 diabetes:

• Increases the proportion of type 1 diabetes from the often-stated 5-10% to as much as 15-25% of all diabetes cases.
• Strengthens the correlation between obesity and type 2 diabetes.
• Reduces the proportion of people with type 2 diabetes who will eventually require insulin to manage their blood glucose levels.
• If I'm reading correctly (she doesn't quite state this point clearly), non-autoimmune gestational diabetes rarely, if ever, develops into lasting type 2 diabetes. Cases of gestational diabetes ultimately becoming permanent are instead due to slow-onset autoimmune (type 1) diabetes discovered during prenatal screening, which may or may not be pregnancy-related.
• Finally, and most controversially, insulin-producing beta cells don't eventually "wear out" and die from overproduction of insulin as they attempt to overcome insulin resistance, but, rather, cases in which insulin production is lost over time are, in fact, due to autoimmune destruction of beta cells. According to the author's interpretation of the research she cites, there was no observed loss of insulin production or beta cell function in a 12-year study of people with type 2 diabetes who had been screened to verify that they did not have the autoimmune markers associated with type 1 diabetes.

Now, I haven't gone through all her sources, nor have I encountered anything like this anywhere else, but it does make intuitive sense to me, given the long history of the medical community as a whole assuming "young onset = type 1, older onset = type 2" and doing both research and treatment of undifferentiated "diabetes" without distinguishing between hypoinsulinism (type 1) and insulin resistance (type 2). Whether the article is entirely correct or not, even the possibility that it might be accurate makes a good case for the need to more thoroughly distinguish between the two common causes of diabetes so that we can properly determine which research findings apply to which people with diabetes.