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Change in Age of T1 Diagnosis in Recent Decades

david4503 said:
So then, with this being the 1.5/LADA type, were you and your doctor watching your insulin requirements steadily rise?
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They did for a couple of years but doses have been pretty stable for the past year now. Which may or may not indicate my honeymoon has passed.
david4503 said:
And were they rising to levels well beyond what the doctor should have known were abnormal for Type 2
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There is no abnormal level of insulin use for a T2 (or whatever other type). On average, T2's on insulin need higher doses than T1's because of insulin resistance. But on an individual basis you have diabetics of all types who need only 10 units a day, and others who need a couple 100 units a day. Dose doesn't give you any information on being fully insulin dependent or not.
david4503 said:
eventually to a point where they should have realized that this patient is now fully insulin-dependent?
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I have no idea, not willing to stop my insulin to see if I go into DKA or not.
I'm not even sure what 'fully insulin dependent' means. It can't mean producing zero insulin, because as you say, in classic T1 some people retain a slight amount of insulin production even years after onset.
So does it mean dying from DKA when stopping insulin? I'd say I'm insulin dependent, without insulin I'd have very high numbers and even if I wouldn't go into DKA I'd likely become very sick in a very short time.
david4503 said:
Could it be that with 1.5/LADA, a useful amount of production remains in some patients, which could help with their control?
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This could well be possible. Although for some, this honeymoon phase is not a blessing but a curse, where the pancreas splutters unpredictable amounts of insulin at random times, making dosing almost impossible. In others, correct dosing becomes harder after a couple of months or years, so it seems that whatever their pancreases were doing helped them.
 
 

First off, that’s a good article you posted. I wish it dealt a bit more with 1.5/LADA which is what’s driving a lot of the questions I have. I think the experts have a decent handle on what areas to explore in order to explain rising rates of Type 1 geographically. Different environmental factors and different genetics affecting different groups differently (say that five times fast!). But I don’t think they know much more critical information for certain today than they did 20 years ago.

As for the rising number of cases in older people, no I do not have a hypothesis, working or otherwise. I’m still in the information-gathering.stage, which is apparently also where the researchers are. Antje77’s last post did help me focus on one possible benefit of understanding this phenomenon, especially if it actually is something new. As regards full insulin dependence (which the article refers to as “absolute insulin deficiency”), we know what happens when a “classic” Type 1 stops taking insulin or takes much too little. They rapidly go into DKA and die unless treated. What happens in the same situation with 1.5/LADA, after any honeymoon period? Are they still making enough of their own insulin to stay alive? If so, why has the autoimmune attack left so many beta cells alive? Did the attack just stop for some reason?

If we knew what was going on with this, it might very well help us with preventing or stopping the autoimmune attack on the pancreas in all Type 1s. It might also help to make beta cell transplants work better. So that’s where I’m coming from. At the moment, anyway.
 
david4503 said:
What happens in the same situation with 1.5/LADA, after any honeymoon period? Are they still making enough of their own insulin to stay alive?
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No, they die just the same as the quick onset childhood T1s.
Lots of LADA's get rediagnosed because they end up in ICU with DKA after months or even years of struggling with their uncontrolled 'T2'.

The progression may be slower but the end result is the same. Negative or very low C-peptide.

I only said I have no idea if or how much insulin I produce at the moment.
After the honeymoon period insulin production is nil or close to it. LADA is T1.
 

That’s helpful to know. But then, what’s slowing down the attack during the honeymoon period? Basically, the same question I was asking in my last post. That would be good to understand. In some cases, it could well be the insulin (supposedly a benefit of early detection) but I’m not sure that explanation covers all 1.5/LADA.
 
I'm 5 years post T1 diagnosis at age 43. Positive antibodies on 2 of the tests and hba1c of 147

I was asked to go on a trial so I've had my c peptide tested a few times after a glucose drink. Unfortunately testing stopped in 2020 with covid but I was still producing some insulin but with a "sluggish" pancreas. Basically they'd give me the 60g glucose drink, take bloods every 15 mins and on the last blood test of the 2 hours my pancreas would wake up

My insulin requirements haven't really changed and I'm still struggling with mid afternoon hypos which suggests that my sluggish pancreas is still kicking out something. I'd rather it didn't because the glucose needed to sort the hypos is making me put on weight.

Oddly when I was diagnosed one of the nurses said they'd had a run of people in their 40s and were asking if we'd any memory of a virus in the 12 months before. I'd been as healthy as I'd ever been in the years prior to diagnosis which was depressing
 
Also I do wonder if there is a genetic susceptibility which is only really coming to light as general life expectancy improves. After all it's only 100 years since insulin was first extracted and prior to then T1 was a death sentence so genes weren't being passed on.

My blood sample disappeared off into a big data bank so no doubt that's being considered
 

This is exactly the kind of input I was hoping for. I’d be interested to know more about this trial you participated in. What was the purpose of it and what criteria did they use for selecting participants? I’ll read the article you posted. Getting positive reviews I see.
 
I have just read all the above comments ( except any links) and some of it is above my cerebral level
However I will say that my wife was misdiagnosed with Type 2 and only after I kept querying it they double checked and said it was Type 1, this was 6 months after the initial diagnosis. During those 6 months she lost several stones in weight and I did think that it was cancer, but it was not.
In the relatively short time I have known about this condition ( it was and still is a steep learning curve) I have discovered that you have to ask questions of the medical profession and not take everything at face value.
eg At the annual check up the doctor said we should reduce the basal insulin from 16 to 14 units each morning, we tried it for 2 to 3 weeks and the average level within range went down to 30 to 40%. So I made the decision to put it back up to 16 units and the level within range went up and is about 60 to 70% now and we are happy with that.
I will say that the nursing team at the local hospital are brilliant and always willing and ready to help and ALWAYS ring you back if you leave a message.
 
Apologies as I have not read all of the above comments. But I think autoimmune Type 1 (also LADA) is only now beginning to be more broadly diagnosed in adults and sadly many may have suffered trying insulin resistant Type 2 therapies for far to long. Personally, at age 51 I was lucky to have an endocrinologist at early diagnosis to test both GAD Abs and C-peptide levels so confirmed Type 1 early = endogenous insulin essential. But what makes my ongoing treatment difficult is that I also have Type 2 insulin resistant symptoms as soon as I have a few carbs and/or high protein. Fine-tuning my medication is a huge ongoing journey.
 
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