I was reading a handbook (I work in a medical library) and it stated outright that LADA is autoimmune, only, and 1.5 is autoimmune with insulin resistance!
Never seen that distinction anywhere else …
I was reading a handbook (I work in a medical library) and it stated outright that LADA is autoimmune, only, and 1.5 is autoimmune with insulin resistance!
Never seen that distinction anywhere else …
I have… however I’ve also seen the opposite stated. For a while I thought that 1.5/LADA was the same thing… apparently it’s not. LADA should just be classified as T1 IMO… not 1.5, since it just makes things confusing - and what is it, other than a slower developing form of T1. Maybe 1.5 should then also encompass anyone who is a typical T1 but also has some IR.
Wow, Linda, interesting! I’ve always seen them used interchangeably! I think it’s hard enough getting people to accept the differences of LADA/1.5 without a more narrow distinction! On the other paw, I actually feel there are enough differences, Sarah, that I gain a sense of clarity being classified as LADA rather than just Type 1, though for simplicity’s sake I just say “Type 1” to people I don’t feel like going into the whole explanation with. I also prefer LADA to “Type 1.5” because that sounds like it’s halfway between Type 1 and Type 2, which is just not the case.
Well in the sense that if you have IR and AI activity, 1.5 does make sense. Threw me the first time I saw it!
Then … I checked out a handbook to see “what the docs are reading,” keep in mind a small lab-coat-pocket handbook … in the first chapter I found FOUR things wrong. The worst of which referred to LADA as “Latent Autoimmune Diabetes of AGING” and went on to describe "these elderly patients … " I found it amusing b.c my internist actually used my AGE (51) in a different handbook to indicate I DID NOT have LADA and could not possibly need antibody testing.
Medical publishing has always been something of a racket – but how can we blame medical professionals when they are stuck reading CRAP!!!
I thought they were the same
Yeah, if something is listed in just one handbook not sure I would take it too seriously, especially in a field of medicine where new knowledge is happening all the time. Perhaps that is “head in the sand”, but at this point in my life I tend to ignore things like "oh and we have just discovered that this food that was previously considered bad is now the best thing since sliced bread (or maybe it IS sliced bread) or that Lantus causes cancer or that if the moon is in the second phase and jupiter aligns with mars…I’m sorry, sometimes I just get tired of new information!
I think this is more MIS-information, than new information, though.
That is for sure in this case. Other cases are less clear and I generally don’t get too invested in something that appears in one source until I hear a lot more information both “professional” and “anecdotal” .
I’ve also read literature, especially from the UK that makes this distinction.
However, 1.5 has to have the autoimmune component too, but also can have features of T2.
Lots of literature doesn’t make the distinction, but also talks about LADA having some features of T1 & T2, where I guess the T2 part comes in when you can still take oral meds and they do make a small difference for a short while. Some meds work directly on insulin resistance, and some work on making the body pump out more insulin. If you are thin, I’d expect only the second of those to have any measurable effect for a short while. If you do have insulin resistance, then both types of meds would work for a while.
The problem with this is that some people with LADA/T1.5 may only have GAD antibodies, whereas others have GAD another other antibodies, which apparently makes them insulin dependent sooner.
The distinction, if there is one to be made, in my humble opinion, isn’t clear. It depends entirely on what you’re reading and by whom it was written.
T1s can also develop insulin resistance after a certain age - do they then get called T.5? No!
The problem is that many LADA/T1.5 cases are diagnosed at an age where insulin resistance comes into play anyway.
LADA/T1.5, like T1s become insulin dependent because their beta cells are destroyed by antibodies. T2s have no antibodies (as far as we know at this point in the science) so if they become insulin dependent, it’s for other reasons.
LADA or T1.5, in Australia, is still classified as a variant of T1. It’s a slow onset T1 that may or may not have insulin resistance as well. At this point, I think some of the medical community makes the terms interchangeable.
Thanks, Susi, for a comprehensive response! I assumed an autoimmune component in 1.5 and LADA. But I also assumed that since onset is in adults, there would be some expected component of resistance, so did not understand why the distinction.
I am more used to reading peer-reviewed journal articles, where terminology is used more precisely. I tend to assume MDs are held to the same high standards (not sure why; guess I thought the literature vs. texts about autism for clin psychs was an exception!). Small wonder our book circulation is declining over the past decade, in my library. It must be terribly frustrating to be constantly contradicted after reading it in “your” book. Let alone, by patients! ;-D
Linda, these days, in the medical field, it’s like computer… soon as something comes out, it’s outdated. Some of what I’m reading is from 2006 and earlier. Some isn’t.
But even in peer-reviewed journals, the terms of LADA/1.5 is sometimes interchangeable.
Oh … Susi, that is just it – I have ONLY seen it as interchangeable, in peer-reviewed articles.
The books that are derived from the articles are not held to the same standards, clearly.
I was once a Medical Editor and I am no doctor. I could have made that same mistake in all the patient information (PI) and other literature I edited. It’s all paid for by the pharmaceutical industry and as long as it reads like you know what you are talking about, they will print it and bind it and sell their strips! I wrote a few PI’s, in fact. I even edited articles for doctors who could care less and just wanted to get paid by the drug lords. As long as it sounds good. It was a brilliant jumble of guesswork. And. I. Was. Clueless.
As is the NIH, apparently. One study that they “supposedly” did on Stiff Man Syndrome (for the purpose of studying an overpriced harmful drug, of course) stated in the Inclusion Criteria: only those with “elevated anti-GAD antibodies” and “Patients with Diabetes (Type II) will be allowed to participate because up to 40% of SPS [or SMS, same thing - Stiff Person v. Stiff Man] patients have Diabetes.” Crazy, huh? SMS’ers are LADA’s, mostly, which perhaps explains their gross mistake. I got LADA after SMS, but other SMS’ers got LADA first. That’s confusing. Sorry. I’m trying to say… If someone has SMS and happens to IR, there is no “link.” They would have 2 separate diseases. Then again, I always get sudden onset and SMS’ers could be dx’ed with IR before LADA. I know nothing. Unfortunately, the NIH knows less than nothing. They also wrote Apheresis instead of Plasmapheresis! High-larious!
But then, let’s not forget who pays for these studies. The things I made up… wow! I thought I was a genius. Swear. Oncology and endocrinology were my faves. I could never get my head around tardive dyskenesia, tho… It’s always in the list of side effects:-] Then again, maybe I was a genius b/c they printed my “sounds right” crap.
I’m loving Latent Autoimmune Diabetes “Aging”. Some poor temp med-editor was doing overtime that day!
Yes, most likely, Maureen … someone was doing overtime, and no one to follw behind. It is a sad state of affairs! But it must have been fun work, at times … I’d’ve loved it, I am sure!
Bill, yes, I spent 8 yrs working on NIH grants, in the 80’s. I have a friend whose work dovetails with Big Pharma, and he fully agrees with you – “lifestyle diseases” is where the profits are!
There is no official definition of “Type 1.5” anywhere. It is medical slang.
The official document defining diabetes lists classic Type 1, Type 2, genetic, gestational and diabetes caused by medications/surgery.
LADA turns out to have a genetic profile that has some Type 1 genes and some Type 2 genes, but almost all Type 2 genes cause insulin deficiency, not insulin resistance.
Interesting point on the genetics, Jenny.
I read this distinction in one of those handbooks – the ones medical students rely heavily upon, fits in a labcoat pocket, which might turn it into a sort of “folklore” that will become mainstream. I was just curious as to where it had originated – from a practitioner or an actual theorist!
It might not be “official” with the powers that be, but Joslin’s certainly refers to LADA, and there are certain practical considerations that set it apart – the need for more gradual – but early – use of an insulin regimen, for instance.
There may be no official definition of Type 1.5, but I do know that Professor Paul Zimmet of the International Diabetes Institutes (in Australia) coined and defined the term. I recently read what year that was, but my sieve of a brain can’t recall. Somewhere in the 1990s, I think.
I wonder which term, LADA or 1.5, will eventually stick. Or will we forever have to write and say “LADA/T1.5”?
Heck, I am still spelling out, “Slow onset type one of adulthood” to get my point across to non-D people!
Informative, Susi!
Thanks for clearing that up. I was certainly sure that the medical community would ever use something like Type 1.5. The disease is not like a version of some piece of software.