Not My Type?

Not My Type?

There is a terrific article in the May 2014 Diabetes Forecast titled “Not My Type?”. It examines some of the lesser known types of Diabetes that are not covered under the labels Type 1 or type 2. On March 6 of this year I wrote a previous blog on this topic:

So as you go through this writing it may be helpful to look in other areas of the site including my previous blog and the extensive work that Melitta has posted on LADA including but not at all limited too:

Taken together all this work is very important and deserves more readership if only because we as diabetics are often called on to provide education to our respective communities.

I hope you will not mind that I beat a dead horse to death once again, but this article in Forecast is worth a read and deserves to be in the TUDiabetes community of literature on the various forms of Diabetes.

Before I get into the article, the online edition of the Diabetes Forecast appears to not include this article. If you dive deeper however you find it is really an openly available article listed in the online index of the magazine and not credited as being written by a specific person. That is odd, but also a bit of good luck because in addition to referencing it, we also get to embed the article here since it is freely available. As an aside why the ADA is treating it like this is beyond me but oh well we will take our good fortunate where we find it.

So the link to the article is as follows:

It is a fine summary of the issue.

Here are some highlights:

LADA – Latent Autoimmune Diabetes – “an adult onset of diabetes caused by the body slowly developing autoimmune Type 1 diabetes” ("Not Your Type?," 2014, p. 52). According to Regina Castro, MD “it is the gradual destruction of beta cells that make diabetes’ ("Not Your Type?," 2014, p. 52). The article reports that the main difference between type 1 and LADA is the rate of destruction and the time of onset ("Not Your Type?," 2014). Obviously type 1 occurs more in childhood while LADA occurs more in adulthood however it is not clear the exact rate of destruction of Beta Cells. It varies by individual and is often treated as type 2 which morphs into type 1. On the other hand it can also have very rapid onset. That is one the mysteries of the disease ("Not Your Type?," 2014).

After reading this article it actually made me wonder if my mom who I always considered a type 1 might in fact have been a LADA. She developed gestational diabetes, and 5 years later was diagnosed as type 1 in 20’s. It matters little but since she had what appeared to be rapid onset she was considered a type 1 from the beginning. It is just something I never thought of the issue really.

As I said Melitta has developed a great library of material regarding LADA and she is our source person on this aspect of the disease. I will leave it to you to explore her blogs at:

It is great reading for all concerned.

MODY – I am not an expert on MODY so what I report is from this article in Diabetes Forecast. Given that, it is reported that “Various Genes contribute to type 1 and type 2 diabetes, but some forms of diabetes depend on a single gene. There are 12 known types of diabetes caused by a mutation of different single genes, all under the umbrella of MODY, maturity -onset of diabetes of the young” ("Not Your Type?," 2014, p. 53). (At first I thought this was my uncle Monty but that is different, he did not have diabetes and was not a very nice man but he was my uncle two different times, oh never mind I got off track sorry). “Because the different types of MODY are so diverse- and because the only way to be sure a patient has MODY is to do genetic testing –it’s hard to know how many people actually have MODY” ("Not Your Type?," 2014, p. 53). “Genetic testing for MODY may be prohibitively expensive; it’s not a typically covered by insurance” ("Not Your Type?," 2014, pp. 53-54) so many people wil treat itas type 1 and go forward.

Insulin Resistant type 1 – “Type 1 but taking metformin” ("Not Your Type?," 2014, p. 54). “People with such disease are at higher risk for developing cardiovascular and renal failure” ("Not Your Type?," 2014, p. 54). They often manage well with aggressive use of type 2 drugs and may never use insulin. However they may also have high cholesterol and triglycerides and a family history of type 2 ("Not Your Type?," 2014). In such patients the metformin controls liver enzymes that may drive blood sugar up ("Not Your Type?," 2014).

But in these patients some or all Beta Cells no longer produce insulin and they certainly do not produce insulin in sufficient quantities to control blood sugar alone. These people may also have double diabetes. That is insulin resistance and a lack of insulin production ("Not Your Type?," 2014). The treatment in this case might be a combination of metformin and insulin.

There is also a condition not often mentioned called PCOS (Polycystic Ovarian Syndrome) ("Not Your Type?," 2014). This is a completely new one that I have not heard about. “Patients have too much androgen which can lead to insulin resistance and weight gain” ("Not Your Type?," 2014, pp. 54-55). “More than half of all women diagnosed with PCOS will develop type 2 diabetes or prediabetes before age 40” ("Not Your Type?," 2014, p. 55). Often times these people also use metformin in addition to insulin for blood sugar control ("Not Your Type?," 2014). Just a note, the term prediabetes is going out of use pretty rapidly, I am merely quoting the source.

Cystic Fibrosis related diabetes – Cystic Fibrosis affects the body’s secretion of enzymes from the pancreases” ("Not Your Type?," 2014, p. 55). “More than half of the 30,000 patients with Cystic Fibrosis will also develop diabetes” ("Not Your Type?," 2014). That is not something I think most of us recognize.

Ok this is getting pretty long for a blog. The entire article is posted below. I need to acknowledge that this blog is Lloyd's idea so if you like it please acknowledge Lloyd, if not well feel to acknowledge me.


Not Your Type? (2014). Diabetes Forecast, 67(May 2014), 52-55.

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