What are C peptide levels like in LADA/ adult T1?

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Vectian said:
Mainly avoiding pasta, white bread, rice, sugar & processed rubbish etc. But most diabetics do that don't they?
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Most Type 1s eat a normal diet the same as anyone else who is not diabetic and they adjust their insulin to match what they eat, just like a non-diabetic's pancreas will release insulin to match what they ate. So they can have white bread and pasta and rice and chips and cakes and biscuits and puddings and chocolate bars if they wish, although in moderation is advised. It is as important for people with Type 1 to have a healthy diet as it is for anyone else, but compared to Type 2 diabetes, Type 1 is all about learning to match your insulin doses to what you want to eat, rather than modifying your diet.

As regards you managing better without insulin than with, the very short time that you were on insulin was really not long enough to assess anything. It takes months to get doses right and figure out what needs what dose and especially in the honeymoon period. It could be that your basal dose was not enough and so the bolus insulin was being increased to cover that shortfall, which made it look like you were becoming insulin resistant. If my basal insulin dose is just 2-3 units too little, I may need twice as much bolus insulin to cover that shortfall, so I really don't think you can draw any serious conclusions from your short spell on insulin..... and there definitely are people who start on insulin and then manage with none for a while during their honeymoon period before needing to start it again. It may happen suddenly after an illness or maybe even a vaccination... Anything which stirs up the immune system to fight an infection or potential pathogen could trigger it.

I am not saying you are definitely not Type 2 either, but just that it really isn't as simple and straightforward as you might hope to diagnose one or the other and some cases are much less clear cut than others..... and going low carb can definitely muddy the waters during the diagnostic process if Type 1 is a possibility.
 
Inka said:
Did they test for other Type 1 antibodies apart from GAD @Vectian ? My consultant says two (or more) antibodies are indicative of Type 1.
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Negative for IA2, the 3rd beginning with z has been delayed. There was also a "triple antibody test" which was normal, nobody has been able to tell me what that relates to, including the Exeter lab. What does it mean if you have only GAD positive? I've not been allowed to see a consultant, the nurse just said the GAD means you are t1, many things I have read say it's not that black and white.
 
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rebrascora said:
Most Type 1s eat a normal diet the same as anyone else who is not diabetic and they adjust their insulin to match what they eat, just like a non-diabetic's pancreas will release insulin to match what they ate. So they can have white bread and pasta and rice and chips and cakes and biscuits and puddings and chocolate bars if they wish, although in moderation is advised. It is as important for people with Type 1 to have a healthy diet as it is for anyone else, but compared to Type 2 diabetes, Type 1 is all about learning to match your insulin doses to what you want to eat, rather than modifying your diet.

As regards you managing better without insulin than with, the very short time that you were on insulin was really not long enough to assess anything. It takes months to get doses right and figure out what needs what dose and especially in the honeymoon period. It could be that your basal dose was not enough and so the bolus insulin was being increased to cover that shortfall, which made it look like you were becoming insulin resistant. If my basal insulin dose is just 2-3 units too little, I may need twice as much bolus insulin to cover that shortfall, so I really don't think you can draw any serious conclusions from your short spell on insulin..... and there definitely are people who start on insulin and then manage with none for a while during their honeymoon period before needing to start it again. It may happen suddenly after an illness or maybe even a vaccination... Anything which stirs up the immune system to fight an infection or potential pathogen could trigger it.

I am not saying you are definitely not Type 2 either, but just that it really isn't as simple and straightforward as you might hope to diagnose one or the other and some cases are much less clear cut than others..... and going low carb can definitely muddy the waters during the diagnostic process if Type 1 is a possibility.
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I had no basal insulin apart from the first week when I was having hypos overnight. I was eating the same kind of diet and by the end of the 4 weeks I needed almost twice the bolus than at the start, and I was getting lots of peaks 10 or above. Since stopping insulin I get less peaks and a lower average. It just doesn't add up.
 
I have Type 1 and have GAD and IA2 antibodies. Somewhere online I’ve seen percentages of how many Type 1s have which antibodies. I believe IA2 is a common one.

My consultant said that my two antibodies proved my Type 1 whereas just having GAD wouldn’t have (although that along with my very low C Peptide would have led her to conclude T1 for me). I don’t remember exactly what she said about having only GAD but I think it was that some people without diabetes have it. She mentioned other auto-immune conditions (not just Stiff Person).

Your high C Peptide clearly doesn’t fit, but it might be that things will become clearer as time goes by, eg your C Peptide might decline.
 
Inka said:
I have Type 1 and have GAD and IA2 antibodies. Somewhere online I’ve seen percentages of how many Type 1s have which antibodies. I believe IA2 is a common one.

My consultant said that my two antibodies proved my Type 1 whereas just having GAD wouldn’t have (although that along with my very low C Peptide would have led her to conclude T1 for me). I don’t remember exactly what she said about having only GAD but I think it was that some people without diabetes have it. She mentioned other auto-immune conditions (not just Stiff Person).

Your high C Peptide clearly doesn’t fit, but it might be that things will become clearer as time goes by, eg your C Peptide might decline.
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Glad you have seen a consultant, I've not been allowed to see one. I read a study that said it's just as likely that you are t2 with positive gad (alone) as t1, and the reason that LADA seems to have features of both t1 and t2 isn't because it's some other hybrid form, but because some people categorised as LADA because of positive gad are actually t2. I know it's often misdiagnosed the other way around as well. Especially in older onset where something like 95% of new diabetes cases are t2. The thing is being a completely different cause and mechanism, the treatment is very different as well so not knowing puts you a bit in limbo as to what the right thing to do is.
 
What’s your latest HbA1C @Vectian ? If it’s high yet you have a high C Peptide, that suggests you’re more like a Type 2 to me, a non-medical person.
 
Inka said:
What’s your latest HbA1C @Vectian ? If it’s high yet you have a high C Peptide, that suggests you’re more like a Type 2 to me, a non-medical person.
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I haven't had one, about 7 weeks ago it was 97, now according to the Libre GMI estimated A1C around 41, although less than that with some other calculators. Everything else fits more with T2, except the GAD result which is the only thing they are basing the T1 diagnosis on. I have been doing a lot of reading of research papers etc. Seems that the GAD antibodies prevent the creation of an amino acid called GABA, which is needed for normal pancreas function (and also has a role in controlling anxiety, which is very interesting). So people with GAD antibodies have low levels of GABA, but you can buy GABA as a supplement, so why can't you just top up what your body isn't making, at least to an extent? Some new trials seem to be doing basically that, and it seems to work in mouse models. I have just ordered some so will give it a go.
 
Inka said:
Have you seen this study @Vectian ? It looks interesting from a quick skim:

www.ncbi.nlm.nih.gov

Presence of anti-GAD in a non-diabetic population of adults; time dynamics and clinical influence: results from the HUNT study

It is well known that anti-GAD (glutamic acid decarboxylase) serves as a marker for development of autoimmune diabetes in adults. On the other hand, the clinical implications of anti-GAD positivity in persistently non-diabetic (PND) adults are poorly ...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov

.
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No I hadn't, but thanks. Seems their GAD levels were quite low. I found this one really interesting

https://www.ncbi.nlm.nih.gov/pmc/ar...8 islet antibody,have a false-positive result.

Messenger_creation_2d33e4a4-6806-48d9-9399-7e1af5400d29.jpeg
Basically in an older onset where way more people are Type 2, it's actually more likely that you are GAD positive but t2 than t1 (6 vs 4) and that explains why LADA seems to have some features of t2, because some of those people actually are t2, not because LADA is something fundamentally different.
 
My consultant hardly uses the term LADA @Vectian but does use Type 1.5. Not for people with LADA though. She uses it to differentiate between LADA (later onset T1) and a form of diabetes that shares both features of T1 and T2. I didn’t ask anymore about that because I was busy squeezing all my questions in but I wonder if GAD would be part of that? So, T2 but with some ‘T1’ auto-immunity?
 
Inka said:
She uses it to differentiate between LADA (later onset T1) and a form of diabetes that shares both features of T1 and T2.
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My nurse gives it a different name as well (just to be contrary), but in all the literature LADA is the one that supposedly has features of t1 and t2, otherwise it's classic t1 that appears in adulthood which I believe is not very common.
 
I think the jury’s out on that @Vectian More adults are diagnosed with Type 1 than children. Lots of Type 1s are diagnosed in adulthood. There seems to be a little peak in the 30s if I’m remembering correctly.

My consultant only uses LADA for those diagnosed T1 over 55 or so and uses T1.5 for people who share T1 and T2 features. She said LADA is T1 later in life. I remember that because I asked her if LADA was anyone diagnosed T1 as an adult. She said No, and when I asked if she meant over 40s then (I was thinking that in the old days when they said T1 was usually diagnosed under 40), she said No, LADA was more like Over 55s and came on more slowly, as 20s, 30s, 40s were a normal age to be diagnosed T1.

I agree the literature tends to mix/muddle/replace the two terms. There were a few articles about that some years ago with people saying there was no official definition of LADA.

Could you ask to see a private endo or are you happy going along as you are for now?
 
Inka said:
Could you ask to see a private endo or are you happy going along as you are for now?
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Starting to think that, especially as I've not even been allowed to see an NHS consultant. I live on the Isle of Wight so ferry is quite expensive to add to private fees but may have to. On the other hand if I continue doing what I am doing and the BS gets gradually worse then it's T1 of some kind, if it gradually improves then it's T2 going into remission. Seems impossible that it would improve longer term with T1
 
I was one of the lay members on the NICE guideline update for T1 in adults that published in 2015 @Vectian - and it was something of a surprise to me how inconclusive the antibody (and cPeptide) checks were in indicating diabetes type.

You can have antibodies and not be T1, and you can have no antibodies (if all your beta cells have been splatted, and they’ve disappeared) and be a classic case of T1.

GAD and cPeptide can be helpful pieces of the puzzle, but the results do need to be carefully interpreted by a specialist.

The experienced clinical brains on the panel said that it was the clinical factors in the presentation which were the primary indicators, and that these tests helped to add some clues where there was doubt or uncertainty.

We’ve had a fair few members of the forum over the years whose diabetes seems determined not to be shoehorned into any of those neat little ‘type’ boxes. 🙂
 
everydayupsanddowns said:
I was one of the lay members on the NICE guideline update for T1 in adults that published in 2015 @Vectian - and it was something of a surprise to me how inconclusive the antibody (and cPeptide) checks were in indicating diabetes type.

You can have antibodies and not be T1, and you can have no antibodies (if all your beta cells have been splatted, and they’ve disappeared) and be a classic case of T1.

GAD and cPeptide can be helpful pieces of the puzzle, but the results do need to be carefully interpreted by a specialist.

The experienced clinical brains on the panel said that it was the clinical factors in the presentation which were the primary indicators, and that these tests helped to add some clues where there was doubt or uncertainty.

We’ve had a fair few members of the forum over the years whose diabetes seems determined not to be shoehorned into any of those neat little ‘type’ boxes. 🙂
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I'm one of those that no one is able to define. The .Gov article appears to say that most LADAs show up with typical T2 symptoms which I don't agree with. From many posts, those defining themselves as LADA show up as typical T1 i.e. sudden weight loss etc implying lack of insulin and needing beta cell stimulants such as Gliclazide or insulin. So we continue to have no clear definition for LADA. Bearing in mind it's known but largely ignored that viruses can result in beta cell damage why does the profession continue to use the team 'autoimmune'. For late onset is it merely guess-work? How many other diseases are described as autoimmune? I have no typical autoimmune issues and although I fit T1 characteristics, in my case the cause is not 'autoimmunity'. Let's stop talking about T1 as an 'autoimmune' disease as such and open our eyes to the wider range of causes of low insulin particularly in later life. My wife suffered kidney failure and does have autoimmune conditions but the kidney failure was not defined as an 'autoimmune' condition. The most likely cause in her case was a drug she was taking for one of the autoimmune conditions.
 
everydayupsanddowns said:
I was one of the lay members on the NICE guideline update for T1 in adults that published in 2015 @Vectian - and it was something of a surprise to me how inconclusive the antibody (and cPeptide) checks were in indicating diabetes type.

You can have antibodies and not be T1, and you can have no antibodies (if all your beta cells have been splatted, and they’ve disappeared) and be a classic case of T1.

GAD and cPeptide can be helpful pieces of the puzzle, but the results do need to be carefully interpreted by a specialist.

The experienced clinical brains on the panel said that it was the clinical factors in the presentation which were the primary indicators, and that these tests helped to add some clues where there was doubt or uncertainty.

We’ve had a fair few members of the forum over the years whose diabetes seems determined not to be shoehorned into any of those neat little ‘type’ boxes. 🙂
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Thanks that is very interesting that it was said officially that you can have antibodies and not be T1, are there notes of that available anywhere? Someone else said their consultant told them you have to be positive for more than one antibody to have a secure T1 diagnosis.

The blurred lines are challenging as it's obviously quite a different disease from T1 to T2. The treatment if BS is high because of insulin resistance is quite different that if it's high due to insufficient insulin production. That's why surely C Peptide is an important measure as it tells you that?
 
DaveB said:
I'm one of those that no one is able to define. The .Gov article appears to say that most LADAs show up with typical T2 symptoms which I don't agree with. From many posts, those defining themselves as LADA show up as typical T1 i.e. sudden weight loss etc implying lack of insulin and needing beta cell stimulants such as Gliclazide or insulin. So we continue to have no clear definition for LADA. Bearing in mind it's known but largely ignored that viruses can result in beta cell damage why does the profession continue to use the team 'autoimmune'. For late onset is it merely guess-work? How many other diseases are described as autoimmune? I have no typical autoimmune issues and although I fit T1 characteristics, in my case the cause is not 'autoimmunity'. Let's stop talking about T1 as an 'autoimmune' disease as such and open our eyes to the wider range of causes of low insulin particularly in later life. My wife suffered kidney failure and does have autoimmune conditions but the kidney failure was not defined as an 'autoimmune' condition. The most likely cause in her case was a drug she was taking for one of the autoimmune conditions.
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It is very frustrating. Do you know what your C peptide was at diagnosis? Which antibodies were you positive for? Read this, it is very interesting:

www.ncbi.nlm.nih.gov

Latent Autoimmune Diabetes of Adults (LADA) Is Likely to Represent a Mixed Population of Autoimmune (Type 1) and Nonautoimmune (Type 2) Diabetes

Latent autoimmune diabetes of adults (LADA) is typically defined as a new diabetes diagnosis after 35 years of age, presenting with clinical features of type 2 diabetes, in whom a type 1 diabetes–associated islet autoantibody is detected. Identifying ...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov

Saying that LADA appears to have features of T2 not because it is some separate and different condition, but because some people who are classified as LADA actually are T2 and are false positives. It often happens the other way around of course, people who are T1/LADA being told at least initially that they are T2.
 
DaveB said:
I'm one of those that no one is able to define. The .Gov article appears to say that most LADAs show up with typical T2 symptoms which I don't agree with. From many posts, those defining themselves as LADA show up as typical T1 i.e. sudden weight loss etc implying lack of insulin and needing beta cell stimulants such as Gliclazide or insulin. So we continue to have no clear definition for LADA. Bearing in mind it's known but largely ignored that viruses can result in beta cell damage why does the profession continue to use the team 'autoimmune'. For late onset is it merely guess-work? How many other diseases are described as autoimmune? I have no typical autoimmune issues and although I fit T1 characteristics, in my case the cause is not 'autoimmunity'. Let's stop talking about T1 as an 'autoimmune' disease as such and open our eyes to the wider range of causes of low insulin particularly in later life. My wife suffered kidney failure and does have autoimmune conditions but the kidney failure was not defined as an 'autoimmune' condition. The most likely cause in her case was a drug she was taking for one of the autoimmune conditions.
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Dave, what do you mean when you say you have "no typical autoimmune issues"?

Did you have a C-peptide and/or antibody tests and if so how long post diagnosis?

Viruses are believed to be one of the "triggers" of the autoimmune attack, so rather than the virus doing the damage to the beta cells itself, the virus stirs up the immune system and it mistakenly kills them as it is fighting the virus. Perhaps a case of mistaken identity if you like or getting trigger happy.
 
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