When people talk about whether we need to clarify our type I always say yes because “they are two entirely different conditions” and I still believe this.
But I just had a totally random thought that may have no significance to the etiology of diabetes as a whole because it may just be my own unique path to Type 1 diabetes (LADA), but perhaps it does contain some clue to the connection between types. Just something to think about for you theoretical and scientific types (which I’m not).
A year before my diagnosis if you could have seen into a crystal ball and said I would be diabetic a year later you would say without a question of a doubt: Type 2. I was 57 years old, 40 pounds overweight, the heaviest I’d been but had struggled with some extra weight all my life as had my father and his mother who had diabetes (I’m assuming type 2, but don’t know for sure). I had Metabolic Syndrome: High blood pressure, high cholesterol and probably the third thing I can’t remember. I took meds for these. Heart disease ran in my family, my brother had had a quadruple bypass. So my misdiagnosis as Type 2 at age 58 wasn’t too hard to understand, even though by that point I had started to lose some of the weight (I lost all 40 pounds before and in the year after diagnosis), I had another autoimmune disorder (thyroid) and my blood pressure and cholesterol had normalized.
So what this leads me to wonder about is this: Was I, perhaps, on my way to being a type 2 who got derailed and became a type 1 (LADA) due to the autoimmune attack? Though I know not every type 1 (or even every LADA) has the same etiology could this perhaps show that types 1 & 2 are not all that separate but are like a train moving along that gets shunted (or whatever the word is) onto a side rail with a new destination?
Like I said, just a thought.
Even though some of the aspects of the causes are different, it’s not so obvious to me that they are different conditions in mindset or long-term-care (with the obvious exception that T1 always involves insulin). I read the DCCT (a T1 study with a cohort group that was in the teens or early adulthood at the start) and the UKPDS (a T2 study with a much older study group) and the conclusions reached are remarkably similar:
All diabetics are at great risk for complications.
Many of the risks are lowered (but not to zero) by good bg control. This is especially true for kidney disease and retinopathy.
Some risks (especially cardiovascular) seem to be vaguely related to bg control but not strongly related. High blood pressure is very common for both older T1’s and T2’s.
Intensive control for either group consists of medication plus diet plus exercise.
Sound remarkably similar to me in all but onset. I think personal issues related to onset become less important to me as time goes on (I’m now middle aged but was diagnosed as T1 in my early teens, many decades ago.)
I would say the key factor differentiating the types in the beginning would be insulin resistance. If you had metabolic syndrome pre diagnosis then you probably had insulin resistance. If so I would agree that you had T2 that was derailed by and autoimmune attack. I would think that these are 2 unrelated conditions and you just got hit with a double wammy.
The interesting question is do you still have Insulin resistance? If you don’t I suppose the insulin resistance could have disappeared with the weight loss. If that was true then your T2 was “cured” by regaining normal weight something that is not usually true. If you still have insulin resistance then you probably have both types.
I have a ton of family members with T2, so this is actually something that I think about as well:) It’s definitely possible to have double-diabetes. Sometimes people talk about them being mutually exclusive, but they aren’t entirely because they affect two separate sides of the equation (the insulin made and the response to insulin). Having a T1 diagnosis generally over-rules a T2 diagnosis because there’s no way to tell, but any underlying insulin resistance I think is a factor in disease outcome. Differences in insulin sensitivity can play a big role in how difficult it is to control bg levels, or even maintain a healthy body weight on insulin therapy for that matter.
I’ve also heard some musings that the inflammation and beta-cell stress that stem from T2 may tilt the balance in favor of autoimmunity in susceptible people. That’s from a well-regarded scientist that I won’t name. But, as far as I know, that’s just speculation. I think that if it is true that it will depend on where your autoimmunity ‘set-point’ is. Some people probably have a low set-point and looking at their T cells funny sets them off, whereas some people probably need that extra push to set things in motion. LOL, just rambling…
Nope, I don’t have any insulin resistance to speak of, BadMoon. I have maintained the weight loss,and am insulin sensitive. Whether I had it years ago when I battled weight, who knows, but once I was diagnosed my diabetes has followed classic a LADA/type 1 path. I had my other autoimmune condition (thyroid) 13 years before my diagnosis, so maybe that was the turning point. I don’t think I had type 2 but that maybe both conditions have some similar, as yet unknown etiology that then branches off in very different directions (even perhaps in people that for example get diagnosed type 1 in childhood where the branching just happened sooner)
Thanks, Tom. I wasn’t so much talking about the double diabetes thing as what you mentioned in your second paragraph. Very interesting; why don’t you want to mention the scientist? I not only have another autoimmune condition (which is very common) but have, all my life had an unusually strong immune system. All the other kids in my class passed around the usual childhood bugs and they passed me by. I rarely get colds let alone flu. I joke that I don’t get “sick” I just get “conditions”. I am one of about 10% of people who spontaneously cleared the HepC virus I was exposed to. I have no clue if there is a relationship between autoimmune conditions and a super immune system. Maybe said scientist wants to use me in a study…paid of course! Yeah, I’m just rambling too.
I think at least in Canada if you are older that 12 and are not DKA and in the hospital you will be diagnosed as insulin resistant type 2. I does not sem to occur to the Doctors that you can be insulin deficient. Possibly the same occurs in the USA see BSC saga. This causes grief as in these people prompt treatment with insulin is needed.
Well, I guess I think things are a muddle. We have autoimmune T1 where you have insulin deficiency, but of course T2 also has insulin deficiency. But of course autoimmune T1 has a hallmark of the autoimmune reaction which you can test for with antibody tests, right? Well, not perfectly. I believe 85-90% of T1s test positive for antibodies. So T1s that don’t test positive are what? Non-autoimmune T1s? And then there is T2. Apparently 20% of T2s test positive for antibodies, so are they really autoimmune T1s even if they are not insulin deficient? And what about all the non-diabetics who test antibody positive, they are not insulin deficient?
So many questions, so much confusion. In truth, diabetes is a bunch of diseases/defects which today are categorized mostly by symptoms not by cause. And because the symptoms of T1 and T2 overlap it is just a royal mess.
I wonder if during the “fade” (I just watched ‘Fellowship of the Ring’) into T1 it might present like T2 for a while? If you are sensitive enough to notice, you get the test and they come out T2 but then a few months down the road your pancreas burns out the rest of the way and your numbers segue into T1?
Acidrock23, possibly you just described the onset of LADA. Who knows?
I think it might depend on how you define “presents as T2” and how deeply the provider looks. LADA would present as type 2 in the sense of not needing insulin but not usually in the sense of being insulin resistant. If antibody testing and c-peptide were done it would become obvious it wasn’t type 2. Or are you saying that might not be the case if you caught it early enough?
To me the question is, what about earlier? As a LADA I was diagnosed with the usual symptoms and a fasting of 325. If I had been randomly tested a couple years before would my numbers have come out pre-diabetic? What about any other type 1? What about a type 2 diagnosed in middle age with metabolic syndrome, might they have had some type 1 signs earlier in life?
Damn, I knew I should have gone to medical school! I could have been a contenduh! LOL. Really, I think there’s probably a whole bunch of types? Hanging around message boards, i kind of get the idea that we (PWD) have tons of data and really have a much better idea of our diseases than the medical industry are able to describe since they feel the obligation to “type” us so strongly? Maybe it’s easier for me to say since I am pretty solidly type 1 but maybe I’m type 1a or 1d or 1π or whatever? The genetic diversity of humans is kind of known but I think that the implications are only being touched on with clinicians who encounter and researchers who research ghastly chronic diseases like diabetes of type ∞
But there’s a detectable genetic component too I thought? I just read these things and vaguely remember them but I think that’s the big thing? I think a lot of the confusion is because we have so many tests now that we didn’t have 30 or 40 years ago but the scripts doctors/ clinics/ insurance companies use are probably older than that?
Hey, my keyboard doesn’t have an infinity sign!!! Yeah, this genetic stuff is definitely beyond my understanding (and usually interest). What do you mean, acidrock, by “there’s a detectable genetic component”. To Type 2? I thought it was just the absence of antibodies, but I also remember hearing something about there being a way to actually test for insulin resistance, not just its manifestations?
Yep, I think all the variations seem to hint at a common genetic cause or at least precurser. It’s funny, I had to work so hard to establish that I was type 1 (lada) that I wouldn’t have even considered a connection two years ago. But then, those are my personal issues…lol
Thanks all for helping me entertain myself.
I thought that there was a gene involved in predisposing people to T2 too? I find it very interesting as, while it killed people for the first 4,499,900 years people were around, I wonder how the gene survived despite it’s generally fatal consequences?
Good question. It definitely hints at an environmental component or trigger (as does the rise in Type 1 as well as Type 2 cases!)
BSC comments are apropos. The macroworld is analog meaning there is a continuous spectrum of the disease. It would be nice if doctors were able to tell if you are insulin deficient or insulin resistant. It is not obvious that even this can be done easily.