Latent Autoimmune Diabetes in Adults – LADA – The Other (but more prevalent form of) Autoimmune Diabetes…

Latent Autoimmune Diabetes in Adults – LADA – The Other (but more prevalent form of) Autoimmune Diabetes…
Latent Autoimmune Diabetes in Adults – LADA – The Other (but more prevalent form of) Autoimmune Diabetes…

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
The first one of these is very obvious, and it is my belief that anyone presenting at a GP with a BMI that is normal and no weight gain but complaining of diabetes symptoms should be immediately tested for GAD and ICAs. 
But what of those who are overweight? Who, for want of a better term, look like a type 2? Should all diagnoses of Type 2 be accompanied by a c-peptide test of some description? Why? Well, LADAs typically produce less insulin than T2s. Even at diagnosis, as the below chart shows (Grey is T1, White is T2 without ICAs, Black is T2 with ICAs):
In response to glucose, the LADA doesn’t show enough of a difference in c-peptide release to be picked up effectively, so an oral glucose test is unlikely to show anything up. At T0, however, the LADA shows an almost identical insulin response to glucagon as a T1. 
This would suggest that on receipt of a glucagon shot, as used to bring a T1 out of a hypo coma, the LADA would see a dramatic blood glucose jump that the T2 may not have to the same extent, although insulin resistance may affect that. or looked at in a different way, if a blood sample was taken post a glucagon shot, the LADA should show very low c-peptide levels, unlike a T2. 
Could this be a more effective way to test for LADA amongst the T2 population at diagnosis and potentially save a lot more beta cells, which is believed to be an important part of making long term T1 easier to manage? Has anyone taken a serious look at it?
However you look at it, as it stands we are doing our LADA brethren no favours by treating them as T2s. To all intents and purposes, they are a variant of T1, and it’s my belief that they should be treated that way. This means we need to work out how to diagnose them properly as a first step, instead of simply saying, “Well, it will show up in six to twelve months time”. We are damning what looks like 10%-20% of the diabetic population to a more difficult life in the long term, as we often seem to do in regard to treating diabetes in the UK. 
It all comes down to cost. If it looks like a T2, smells like a T2, then it must be a T2, regardless of whether it is or isn’t, so why waste money now on undertaking an unnecessary test? 
Because in the long term, that test is a drop in the ocean compared with dealing with the implications of misdiagnosis and complications from running too high for too long. So let’s get it right first time, and give this group a fair crack of the whip. Treat them like T1s rather than T2s. As a fellow T1, I think they deserve it!

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