T1d or not?!

[ert]

C-peptide refers on producing proinsulin not insulin but yeah thank you guys so much I'm glad that you guys exists BCS there is no one around me who can understand or even help lots of love

C-peptide gives an interpretation of how much insulin you are producing so my comment was correct. This may be more helpful. Below is what the Exeter University diabetes team use to diagnose type 1's.

https://www.exeterlaboratory.com/test/c-peptide-plasma/

Edited: This article is one I read when I was first diagnosed and may be useful too.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5446389/

 

[david4503]

Some people just don't seem to fit into neat diabetic boxes (T1, T2, T3c , GD etc) and have to wait years for a proper diagnosis of diabetes type. Having read some of the stories from posters here, I also personally think that there are more diabetes types than the officially named ones. The most important thing (in my opinion) is that whatever treatment you get keeps your levels under control.

I'm sorry though, I appreciate your frustration. I know you wanted MODY testing but can't get it where you are but my understanding is that there are a lot of different types of MODY and so even if you got that as a diagnosis you wouldn't necessarily be better off, because the more obscure types are just so rare.

Lots of virtual hugs from New Zealand.

I’d say you’re right. The existing diabetes classifications seem to be only a vague approximation of the various ways diabetes raises blood sugar levels in the human body. What seems clear is that there is a classic, full-on version of Type 1 that strikes at an early age and presents very quickly, in weeks or months from initial symptoms to DKA, coma and death if insulin therapy is not begun. In this case, either all beta cells are destroyed or any remaining insulin production is insufficient to keep the patient alive. This would probably include most people labeled Type 1.

Then there are a range of cases which are diagnosed as Type 1 at some point but present differently from the classic version. This is a fascinating group because, for one thing, it may not have existed in the past to the extent it does today. Also, just from some of the reports here, which may or may not be reflected in the literature elsewhere, this group may be capable of achieving tighter control with lower A1c numbers than the classic group.

Then we have the classic Type 2s who get diabetes at an older age, are clearly still making insulin and can often manage with diet alone or combined with oral meds. (Those on insulin may just be more severe cases who don’t respond to other therapies.) This is the biggest group by far and the story here is about insulin resistance rather than insulin production. There also seem to be some sub-groups within Type 2 that have some unusual characteristics. Like the Type 2 cases in children and younger adults.

And last (maybe or maybe not), there’s kind of a hodgepodge of other types which occur due to some unusual genetics or other disease processes which affect the pancreas. MODY is a very interesting example.

This whole picture is made even fuzzier by the fact that the diagnostic tests being used are fairly recent, sometimes indirect measures of processes medicine doesn’t fully understand. Worse, they are open to interpretation by doctors who are trying to set standards at the same time that they are diagnosing patients. What could go wrong with that?

Anyway, I’m sure I left a bunch of things out and got other things wrong but that’s the point. There’s a lot we don’t know and we don’t even know what we don’t know. And with that, I’m out of breath writing this treatise or whatever it is.

 

[Awiiiiin]

I’d say you’re right. The existing diabetes classifications seem to be only a vague approximation of the various ways diabetes raises blood sugar levels in the human body. What seems clear is that there is a classic, full-on version of Type 1 that strikes at an early age and presents very quickly, in weeks or months from initial symptoms to DKA, coma and death if insulin therapy is not begun. In this case, either all beta cells are destroyed or any remaining insulin production is insufficient to keep the patient alive. This would probably include most people labeled Type 1.

Then there are a range of cases which are diagnosed as Type 1 at some point but present differently from the classic version. This is a fascinating group because, for one thing, it may not have existed in the past to the extent it does today. Also, just from some of the reports here, which may or may not be reflected in the literature elsewhere, this group may be capable of achieving tighter control with lower A1c numbers than the classic group.

Then we have the classic Type 2s who get diabetes at an older age, are clearly still making insulin and can often manage with diet alone or combined with oral meds. (Those on insulin may just be more severe cases who don’t respond to other therapies.) This is the biggest group by far and the story here is about insulin resistance rather than insulin production. There also seem to be some sub-groups within Type 2 that have some unusual characteristics. Like the Type 2 cases in children and younger adults.

And last (maybe or maybe not), there’s kind of a hodgepodge of other types which occur due to some unusual genetics or other disease processes which affect the pancreas. MODY is a very interesting example.

This whole picture is made even fuzzier by the fact that the diagnostic tests being used are fairly recent, sometimes indirect measures of processes medicine doesn’t fully understand. Worse, they are open to interpretation by doctors who are trying to set standards at the same time that they are diagnosing patients. What could go wrong with that?

Anyway, I’m sure I left a bunch of things out and got other things wrong but that’s the point. There’s a lot we don’t know and we don’t even know what we don’t know. And with that, I’m out of breath writing this treatise or whatever it is.

Thank you so much

 

[Awiiiiin]

I’d say you’re right. The existing diabetes classifications seem to be only a vague approximation of the various ways diabetes raises blood sugar levels in the human body. What seems clear is that there is a classic, full-on version of Type 1 that strikes at an early age and presents very quickly, in weeks or months from initial symptoms to DKA, coma and death if insulin therapy is not begun. In this case, either all beta cells are destroyed or any remaining insulin production is insufficient to keep the patient alive. This would probably include most people labeled Type 1.

Then there are a range of cases which are diagnosed as Type 1 at some point but present differently from the classic version. This is a fascinating group because, for one thing, it may not have existed in the past to the extent it does today. Also, just from some of the reports here, which may or may not be reflected in the literature elsewhere, this group may be capable of achieving tighter control with lower A1c numbers than the classic group.

Then we have the classic Type 2s who get diabetes at an older age, are clearly still making insulin and can often manage with diet alone or combined with oral meds. (Those on insulin may just be more severe cases who don’t respond to other therapies.) This is the biggest group by far and the story here is about insulin resistance rather than insulin production. There also seem to be some sub-groups within Type 2 that have some unusual characteristics. Like the Type 2 cases in children and younger adults.

And last (maybe or maybe not), there’s kind of a hodgepodge of other types which occur due to some unusual genetics or other disease processes which affect the pancreas. MODY is a very interesting example.

This whole picture is made even fuzzier by the fact that the diagnostic tests being used are fairly recent, sometimes indirect measures of processes medicine doesn’t fully understand. Worse, they are open to interpretation by doctors who are trying to set standards at the same time that they are diagnosing patients. What could go wrong with that?

Anyway, I’m sure I left a bunch of things out and got other things wrong but that’s the point. There’s a lot we don’t know and we don’t even know what we don’t know. And with that, I’m out of breath writing this treatise or whatever it is.

Do you guys know anyone like my case that their type hasn't been detected for a long time?!