Here I am, a type 1, something which I’ve now written a great deal about on this blog, and instead of talking about Type 1, I’m raising the topic of another Diabetes. The other diabetes in question? Latent Autoimmune Diabetes in Adults. Why this one? Because it’s likely that this is a more prevalent type of diabetes than type 1 and yet it is routinely misdiagnosed and treated incorrectly.
Before we consider LADA (or type 1.5 as it’s also known) in terms of diagnosis, misdiagnosis, or any other fashion, let’s take a look at what it is.
Due to the nature of identification, the best way I can describe it is “slow onset type 1 diabetes during adulthood”. Why? Well it is an autoimmune condition that is generally accompanied by various Islet Cell Antibodies (ICAs) and GAD antibodies and generally leads, in the longer term, to a requirement to take insulin. As it is generally diagnosed in adulthood, it is often misdiagnosed as Type 2, until the symptoms become too much to bear. Then it gets re-diagnosed. To me i tlooks like a variant of T1 rather than a different condition. In December 2005, a paper describing characteristics of LADA was published in the American Diabetes Association Diabetes journal, which was clear in how LADA can be identified. It’s worth a read. It contains a number of disturbing statements:
- 10% of Type 2 diagnoses over the age of 35 are really LADA
- 25% of Type 2 diagnoses under the age of 35 are really LADA
I’m not going to list out the sources of these statements – they are all available in the linked paper. What’s far more disturbing about this is that by these statistics, LADA is a more prevalent form of diabetes than Type 1, and yet very few health care professionals seem to know anything at all about it!
Due to the slow onset of beta cell deterioration and the often similar characteristics to those of T2, many patients are diagnosed as T2 by GPs. They are then put on to T2 medication. This is where it starts to go wrong.
Type 2 medications typically are designed to reduce insulin resistance, reduce glucagon action and/or more disturbingly, stimulate insulin production. But why is stimulating insulin production an issue? In autoimmune diabetes candidates, proinsulin, a component of the creation of insulin is an autoantigen, in that it causes the body’s defence mechanisms to create antibodies that attack it, or in the case of diabetes, it and the beta cells. Stimulating insulin production requires more proinsulin. If you give these drugs to LADAs, it will encourage and enhance the damage to beta cells. Surely that’s the last thing we want? Surely we want to preserve the beta cells for as long as is humanly possible, by reducing the production of insulin?
There is only one way to do this. Stop the beta cells producing insulin. This is achievable through changing the diet of the patient to remove carbohydrate as much as possible, or by giving them exogenous insulin to manage the condition and “relieve the pressure”. Yet many aren’t receiving this level of treatment. Many are left to suffer as T2s until insulin is required without doubt. The worst thing about the situation? It is avoidable.
Woah, just a second. We are misdiagnosing diabetics and giving them the wrong treatments, and it’s avoidable? And they are likely to be the second most populace group of people with diabetes? What the hell is going on?
As I’ve already mentioned, they are regularly mistaken for T2. This is the problem. It should be fairly simple and routine to diagnose them as different, and yet we just don’t seem to be able to do it. The key differences between LADA and T2 are:
- The presence of Islet Cell Antibodies or GAD antibodies in one form or another – a simple test would identify this
- Differences in the way insulin is produced