Hi, gang. I know this isn’t the most detailed article, but I found it interesting and thought of everyone here.
Will continue digging for more detailed abstract.
ETA: my apologies if this has already been discussed recently. Trying to play some looong-overdue catch-up.
The new classifications are interesting and perhaps applicable to lots of different people. My classification appears to have remained the same though… still in category 1.
I like this summary a little more:
I would be, too. But I think those of us diagnosed as kids, with rapid onset and DKA and a clear autoimmune cause are the most distinctive and straightforward type. We’ve never been a mystery.
@Irish, it is great to see you here! These were fascinating articles to read! I am going to look for the original paper if I can get it.
It makes sense that there would be considerably variability in T2 especially, since there could be multiple pathways to insulin resistance/metabolic dysfunction.
Yes, although I think there are likely distinctions within category 1, less regarding things having to do with diabetes per se and more whether the diabetes is part of a larger autoimmune syndrome or not (and that seems to be related somewhat to how heritable the diabetes is as well). Some T1 seems extremely heritable, with families with streaks of it throughout, and yet my understand is that it’s still more common to see cases like mine that are isolated. So even if the direct autoimmune mechanism is similar, I would guess the trigger for the autoimmune attack is variable.
Also, this still doesn’t seem to clearly distinguish LADA (also autoimmune) from “classic” T1, which do seem distinct on a number of levels.
Interesting. Not sure whether I’d be cluster 1 or 2… typical dka onset age 30 skinny, low c-peptide. Positive gad antibody but not sky high, just barely positive. Honeymoon is pretty much completly over now, lasted 6 months-ish. I don’t think anything there would have changed treatment, insulin and that’s it. Lada but faster than “typical lada” or just didn’t notice / get diagnosed for 3 years after first instance of sporadic symptoms since I attributed symptoms to running.
This seems more complicated than what the study looked at. I’m the only Type 1 in my family, but I do have multiple autoimmune conditions, and there are several members of my extended family who have autoimmune conditions. It’s hard to tell how much genetics versus environmental factors play into things, too. I definitely have a genetic predisposition, but I’ve also been exposed to environmental factors that no one else in my family has been exposed to and that likely had a profound impact on the development of my immune system. I think it’ll be years before they work the genetic/environmental stuff out enough to come up with any type of sub-classification of Type 1.
Yeah, I agree with this. I’ve read numerous studies that indicate that “classic” Type 1 and LADA, although both autoimmune in nature, are actually quite different even though they’re both “Type 1” under our current classification system. This new classification system dosn’t really seem to address LADA at all.
I think this is really fascinating but I hope this can be tied to actionable medical treatment. We know, for instance, that different types of patients tend to have different outcomes – how can we translate that into better treatment?
I also was wondering how they didn’t find a separate cluster for those with LADA. It’s my impression that there are a lot more of us than you’d think, so out of close to 15k people, you’d think there would have been a statistically significant number to report on.
This is the strangest outcome of the study in my book as well. To a degree, it is contradicting other studies that seem to show LADA as having attributes of a different disease.
If there was a LADA cluster, one interesting issue would be that some type 1s diagnosed early would be part of a “LADA cluster” while some types 1s diagnosed late would be part of a “juvenile onset diabetes” cluster.
It is always troubling to deal with “diseases” which really are a cluster of symptoms rather than a causal relationship. You can see it when you read this early literature on diabetes. I am sure that, 50 years down the road, people will think the same of diabetes papers in our time.
Once again the media (BBC in this case) simply misunderstood what they were writing about. Here’s a better summary https://www.scimex.org/newsfeed/type-2-diabetes-could-be-five-separate-diseases Apparently this paper was looking only at adult-onset diabetes which has traditionally been termed T2 diabetes, and found they could split these into five groups, but not the ones that the BBC reported. If you were diagnosed as a juvenile you are still a T1 and this doesn’t change, and the T1 group can be considered in addition to the ones they talk about that have traditionally been considered T2 (which includes LADA as group 5.):
Adult onset diabetes types:
The most common form of the disease was one of the more moderate forms of diabetes, which was seen in elderly people and affected 39-47% of patients (cluster 5, or mild age-related diabetes).
The other mild form of diabetes (cluster 4, or mild obesity-related diabetes) was mainly seen in obese individuals and affected 18-23% of patients.
Among the severe forms, there was one group with severe insulin resistance and a significantly higher risk of kidney disease than the other types (cluster 3/severe insulin-resistant diabetes, affecting 11-17% of patients)
Another severe form was a group of relatively young, insulin-deficient individuals with poor metabolic control but no auto-antibodies (cluster 2/severe insulin-deficient diabetes, affecting 9-20%).
The remaining severe group were insulin-deficient patients who had auto-antibodies associated with autoimmune diabetes (cluster 1/severe autoimmune diabetes, affecting around 6-15%), a form of diabetes formerly called type 1 diabetes, or latent autoimmune diabetes in adults (LADA).
Yeah, this kind of research all depends on what they were looking at and looking for—they clearly weren’t trying to understand T1/LADA better and were not setting up this study to do so.
And yes, definitely not the point of this study, was just saying that there probably are classification distinctions to be made within T1 if someone wanted to look for them. It likely could be done without identification of genetic factors even, just descriptively, but that wouldn’t be as conclusive in terms of what it means (but might well be useful for research into the underlying causes of those differences).
Okay, this is more in line what I’ve heard before --about their being 7 different kinds of diabetes.