Adult Type 1 - full insulin - longer term issues?

[PD Oz]

A long story short. I was diagnosed type 1 about 18 months ago (age 55). Placed on Rapid and Lev - 4 shots daily Originally type 2 diagnosis for about 7 years prior and well managed on tablets. Have been going well to date with good HBA1c around 6.5-7. My question is, has anyone gone long term from adult type 1 diagnosis to indicate whether they have developed any problems beyond the initial 2-3 years? ie increased difficulty in control etc?

 

[noblehead]

There's quite a few on the forum, I'll tag one lady who was diagnosed around your age @pheonix

 

[LucySW]

Nearly two yrs since my T1 dx (after brief T2 dx) and the only issue is disappearing honeymoon. But thanks to 30g carb/day and low doses, my honeymoon's still going, if a bit thinner.

 

[PD Oz]

Nearly two yrs since my T1 dx (after brief T2 dx) and the only issue is disappearing honeymoon. But thanks to 30g carb/day and low doses, my honeymoon's still going, if a bit thinner.

Sounds good thanks. My concern is say at 10yrs on+. There are a lot of people on forum with like 20 yr plus who really have big issues with control. Surprisingly I look at how I am doing and wonder if this side of things will become progressive still, although I am apparently producing very little if any insulin now.

 

[tim2000s]

Sounds good thanks. My concern is say at 10yrs on+. There are a lot of people on forum with like 20 yr plus who really have big issues with control. Surprisingly I look at how I am doing and wonder if this side of things will become progressive still, although I am apparently producing very little if any insulin now.

Variability is majorly a consequence of life, food and insulin. The better preserved your beta cells are, the more stable you are likely to remain. Having said that, stability is not impossible, even with plenty of years under the belt. you just have to use the right tools to achieve it and these differ from person to person.

 

[PD Oz]

Variability is majorly a consequence of life, food and insulin. The better preserved your beta cells are, the more stable you are likely to remain. Having said that, stability is not impossible, even with plenty of years under the belt. you just have to use the right tools to achieve it and these differ from person to person.

Do you think that Beta cells would be more likely to be better protected by getting on to insulin earlier for those heading into T1 in mid adulthood?

 

[himtoo]

@LucySW has some great reading on that very subject
hopefully she will come along and post it by tomorrow with the tag

 

[LucySW]

Definitely, yes, though I don't have research evidence to support that. Maybe @phoenix does? It works though.

 

[TorqPenderloin]

There's a bit of relevant but indirect research available on the topic. Basically, it's about the potentially harmful effects of certain sulfonylureas causing cell apoptosis (the term for your beta cells dying).

With that said, it seems that Glibenclamide was the particular drug that caused issues as well as some of the 1st generation sulfonylureas. Gliclazide is considered to be much safer in terms of preserving beta cell function. Even still, we are talking about cell damage after 10+ years of taking the drug.

With that said, I personally believe what @LucySW believes and figure it certainly couldn't hurt to start on insulin earlier rather than later.

 

[tim2000s]

There's a bit of relevant but indirect research available on the topic. Basically, it's about the potentially harmful effects of certain sulfonylureas causing cell apoptosis (the term for your beta cells dying).

With that said, it seems that Glibenclamide was the particular drug that caused issues as well as some of the 1st generation sulfonylureas. Gliclazide is considered to be much safer in terms of preserving beta cell function. Even still, we are talking about cell damage after 10+ years of taking the drug.

With that said, I personally believe what @LucySW believes and figure it certainly couldn't hurt to start on insulin earlier rather than later.

The research that's of concern isn't so much related to the drug, it's the research that shows that Auto-Immune Antibodies latch on to Proinsulin, which is part of the production of insulin, in order to attack the beta cells. If you cause the beta cells to generate more insulin, you produce more proinsulin which provides more opportunity for the antibodies to act.

By reducing the need to produce insulin, you reduce proinsulin and the amount of attack that goes on and reduce the damage to the beta cells.

It's also linked to the vaccine development research story from nearly three years ago, which built up "immunity" to proinsulin whilst the treatment was being given.

That, at least, is the theory.

 

[LucySW]

Thanks Tim. I've been interested in seeing that proinsulin article since you first mentioned it. Why don't *all diabetes specialists* and in fact *all family doctors* know about that. Grrrr: so many late-onset people we see on here being made ill because they are assumed to be Type 2.

 

[tim2000s]

@LucySW I think this is surprisingly cutting edge! Being research belated and all...

 

[mibby]

I was diagnosed age 42 and put straight on Novorapid/Lantus. Now 54 and my HbA1c is 40.

 

[PD Oz]

There's a bit of relevant but indirect research available on the topic. Basically, it's about the potentially harmful effects of certain sulfonylureas causing cell apoptosis (the term for your beta cells dying).

With that said, it seems that Glibenclamide was the particular drug that caused issues as well as some of the 1st generation sulfonylureas. Gliclazide is considered to be much safer in terms of preserving beta cell function. Even still, we are talking about cell damage after 10+ years of taking the drug.

With that said, I personally believe what @LucySW believes and figure it certainly couldn't hurt to start on insulin earlier rather than later.

This is very helpful. While I had been on metformin and then on Januvia, I couldn't imagine that causing both liver and kidney function to uptake sugar faster than they otherwise would, could not potentially have side effects. Time will tell I suppose.

 

[Daibell]

HI. I went onto insulin late due to an ignorant diabetes GP but have been on Basal/Bolus for 3 years now. My control is good although I've gradually increased my Basal during that time by perhaps 30% and the Bolus ratio a bit.

 

[PD Oz]

Interesting about Diabell's situation of when the need to go onto insulin arises will vary markedly from person to person. Just what causes the trigger of our immune systems attacking the islets must somehow be delayed. Is it environmental, or dietary, or genetic or a combination? Targetted research may unlock the key as to why this happens. How this has taken decades with still no answer is amazing with all the discoveries in other immunology areas. Perhaps the answer may be staring researchers in the face, just that a more wholistic set of considerations may need to be considered.

 

[Daibell]

Interesting about Diabell's situation of when the need to go onto insulin arises will vary markedly from person to person. Just what causes the trigger of our immune systems attacking the islets must somehow be delayed. Is it environmental, or dietary, or genetic or a combination? Targetted research may unlock the key as to why this happens. How this has taken decades with still no answer is amazing with all the discoveries in other immunology areas. Perhaps the answer may be staring researchers in the face, just that a more wholistic set of considerations may need to be considered.

Yes, far more research is needed in this area and it's why so many GPs don't recognise the existence of Late onset T1. It took me around 8 years from 1st diagnosis as a 'T2' (stick thin) to needing insulin whereas others like my 22 yr old nephew went into DKA within months from no symptoms. I suspect the rate of anti-body destruction varies for many reasons and also there are non anti-body causes such as viruses, pancreatitis and so on. I'm always a bit suspicious of the term 'honeymoon period' as I suspect it may be more about continued destruction of the islet cells as in my case rather than short-term recovery of the cells after starting insulin(which I'm sure does happen for some). If more of the thin T2s i.e. around 15% were correctly diagnosed in many cases as Late onset T1 it would spur the research into non-childhood T1. I'm still listed as T2 so don't show up in the figures.

 

[PD Oz]

Adding to the sparse research into this area are the unknown factors.
If it is a virus which triggers the auto-immune response, thus what virus or viruses might be at play? Are they viruses or pathogens which thrive predominantly in high blood sugar environments and have evolved that way? Have they the ability to trick the immune response into attacking the islets and shutting down the insulin supply to create an environment suited to its survival? Another problem is, how are such viruses detected when they may have died off long after any researcher looks for clues? The strange thing in adult onset type 1, is it the case a pathogen is able to be resisted for longer? It may be that researchers will only be able to find the answers in research using a sample of individuals well before they develop type 1, in order to detect any tell tale viruses before their presence disappears after their damage has been done.

 

[Daibell]

Adding to the sparse research into this area are the unknown factors.
If it is a virus which triggers the auto-immune response, thus what virus or viruses might be at play? Are they viruses or pathogens which thrive predominantly in high blood sugar environments and have evolved that way? Have they the ability to trick the immune response into attacking the islets and shutting down the insulin supply to create an environment suited to its survival? Another problem is, how are such viruses detected when they may have died off long after any researcher looks for clues? The strange thing in adult onset type 1, is it the case a pathogen is able to be resisted for longer? It may be that researchers will only be able to find the answers in research using a sample of individuals well before they develop type 1, in order to detect any tell tale viruses before their presence disappears after their damage has been done.

Yes a wide open area for research. In my case I offered myself as a drug tester with the local international pharma company but was rejected as my white cell count was too high and they said I had inflammation going on. My blood sugar was OK. I felt fine apart from a background mild ache in the abdomen over the previous year. 1 year later I was diagnosed with diabetes 'T2' and very high blood sugar. I'll never know whether the events were related but it indicates that islet cell death can have a range of undetected causes. BTW I had a c-peptide and GAD done privately and the GAD was negative although taken 8 years after diagnosis so was less reliable. This also implies a GAD test isn't always the answer. My c-peptide showed quite low insulin.

 

[tim2000s]

Yes a wide open area for research. In my case I offered myself as a drug tester with the local international pharma company but was rejected as my white cell count was too high and they said I had inflammation going on. My blood sugar was OK. I felt fine apart from a background mild ache in the abdomen over the previous year. 1 year later I was diagnosed with diabetes 'T2' and very high blood sugar. I'll never know whether the events were related but it indicates that islet cell death can have a range of undetected causes. BTW I had a c-peptide and GAD done privately and the GAD was negative although taken 8 years after diagnosis so was less reliable. This also implies a GAD test isn't always the answer. My c-peptide showed quite low insulin.

When I was doing some research into this, it looks as though the best way of checking late onset T1 is the response to Glucagon. The graph below is revealing:

A LADA produces significantly more c-peptide in response to a glucose injection than they do to a glucagon injection, so a good test would be to give a potential T1.5/T2 query a glucagon shot and see what the induced blood glucose rise was over the next five - fifteen minutes.

With the new nasal Glucagon shot, this would be very easy to administer in a GP surgery and wouldn't involve and injections or invasive blood tests. Simply the inhalation, then three finger prick tests.