A Whole LADA Confusion

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I attended the American Association of Clinical Endocrinologists’ annual meeting yesterday, the same folks who recommend that people with diabetes maintain a HbA1c of less than 6.5%.  Held in the Pennsylvania Convention Center in downtown Philadelphia, it is an extravaganza of all things endocrinological — especially diabetes.

I got there just in time for a talk on a subject that has interested me for a while: LADA. Short for Latent Autoimmune Diabetes in Adults, it’s also known as Slow-Onset Type 1 Diabetes, Type 1.5 Diabetes or, occasionally, Late-Onset Autoimmune Diabetes of Adulthood. As I previously pointed out in a post on the topic, four names for one thing is never a good sign. 

I remember being confused while researching that post at how slippery the definition of LADA seemed to be – was it its own disease? A hybrid between Type 1 and Type 2? After speaking with people from JDRF, the key features of LADA that I was able to nail down were: 

1. Older age of onset (usually after 30)

2. Auto-antibodies (auto-antibodies are what trigger your body to attack its own cells, as is the case in Type 1 diabetes but not in Type 2). Interestingly, people with Type 1 tend to have more than one type of diabetes-related auto-antibody, whereas people with LADA tend to have only one.

3. An extended period of still being able to make some of your own insulin (indicated by positive c-peptide results — c-peptide is a byproduct of insulin production, so if you’ve got c-peptide in your blood, you’re still making insulin). Whereas people with classic Type 1 diabetes tend to be completely insulin-dependent within twelve months after diagnosis (usually less), people with LADA can sometimes survive without artificial insulin for years.

You can see why this would be confusing, given the current algorithms being used for diagnosis. You’ve got an older age of onset — usually (but not always!) associated with Type 2. You have autoantibodies, which are a sign of Type 1. But then you’ve still got an extended period of insulin production, which usually is only present in Type 2. You can imagine a primary care doctor reacting to her patient with a mental “WTF?”

Well, what I learned yesterday is that clinical endocrinologists — people who specialize in endocrine disorders — are confused about it, too. The talk was structured more as a discussion than a lecture, so after an initial introduction, the moderator posed the following questions and opened the floor to discussion (I’m paraphrasing here): 

1.  Are there enough similarities between Type 1 and LADA to think of LADA  just a variant of type 1?  Or is the clinical phenotype sufficiently distinct to make it a unique entity from Type 1?

2. How do you think we should manage the patient with LADA? 

What then ensued was kind of a real-life blog comment session, with endocrinologists lining up in the center aisle to offer their two cents. Often they just related stories of their own clinical practice — the types of symptoms they’d seen and the ways they’d treated their LADA patients.

That second part was particularly interesting. As someone with straight-up Type 1, there never was any question about my treatment: I needed insulin, fast. But with LADA patients, the situation isn’t as clear, partially because without explicitly testing for c-peptide levels, you might mistakenly think that their high blood sugars were being caused by insulin resistance rather than insulin deficiency. Consequently, many doctors put LADA patients on oral drugs for Type 2s, geared toward reducing insulin resistance/stimulating more insulin production, when that’s not actually what the problem is.  To put it in the words of one participant: ” If I see someone who’s thin without obesity and no metabolic syndrome, they don’t have insulin resistance. So why the hell would I start a treatment for insulin resistance if they don’t have it?”

The same person also put his point more subtly:  “As we approach the therapy for someone with LADA, we should approach it as  a disease in which the beta cell is failing. And we should think about that in the beginning rather than coming at it when the beta cell has failed totally. The data suggests that starting people on oral agents is not the way to go.  It’s nice because the patient doesn’t need injections for a few years, but it might mean [that by putting increased stress on beta cells] the disease progresses more rapidly.” 

Instead, he said, “It seems that when you have a diagnosis of LADA, what you want to do is to develop a treatment strategy that lowers stress on the beta cells, that lowers the amount of insulin they have to put out.”

I found this fascinating, logical, and scary: if the responses to my LADA post are any indication (not to mention the responses from the other endocrinologists), there are a LOT of people who potentially have LADA. And I’m going to guess that most of them are initially treated as Type 2s. Not only does this put them at risk of developing DKA if and when their beta cells conk out, but it also might speed up the progression of the disease by putting more stress on the beta cells than is necessary. 

Unfortunately, no one in the session, including the moderator, even had a concrete definition of LADA, let alone a definite, proven way to treat it. What was clear, though, was that most people in the room agreed that it should be classified as a unique condition, different from both Type 1 and Type 2 — and that the algorithms for diagnosis of diabetes need to change to account for the fact that there appear to be more than two variants of the disease. 

 “The phenotype of Type 2 diabetes might actually represent 10 to 15 different diseases,” said the moderator toward the end of the talk. “As we get smarter, the number of people we call ‘Type 2 diabetics’ will get smaller and smaller. My advice is to individualize treatment for the patient, and not to take the current algorithms too seriously.” 

An interesting comment from the audience: under current rules, Medicare will only pay for a pump if you have completely negative c-peptide results — which means it’s quite possible for someone with LADA who’s been happily pumping for years to suddenly find themselves without coverage. The moderator said that he would bring that up to the AACE board as something they should try to change. Something definitely worth pushing for. 

For more information about LADA, here’s a good article about it, despite its title — and you should also check out Jess’s previous post on the topic. 

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Thanks Catherine. This is great, there is so much confusion about this – doctors and patients alike. 

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