I just got my blood work back...

[hazatude]

My C-Peptide was 73 pmol/L

Is this definitive proof that I am type 1.5 now?

I presented in 2005 as type 2. I was 275lbs and controlled for a couple of years with diet, excersise and pills. I was re-diagnosed in Oct./09 after losing 100lbs and losing control of my bgls. I'm currently on 15units Lantus at bed and a 1:6 of Humalog with meals.

I'm 39 years old, 5'10" 180lbs now.

[mortis505]

Is that 73.0, 7.3, or 0.73? Was a GAD, ICA, or IA2 test performed to look for the presence of antibodies? Sorry to say this but a diminishing C-peptide only indicates diminished Insulin production, which can happen in T2 due to ß-cell burnout, or just as a natural progression of Diabetes.

[mazea]

A low c peptide level does indicate type 1, or type 1.5. My endo said my c peptide was lowish as after a meal it was 1. ( after a meal the c peptide is higher). I have heard an increasing c peptide level indicates type 2. Get your antibodies checked, although they are not always present as I don't have them being type 1.5. You haven't really had type 2 that long have you?

Your c peptide level is lowish if is below 1 I think. Was it a fasting c peptide?

[hazatude]

I had less than 0.4 Anti Insulin Antibodies and the islet cell test isn't in yet. I haven't had the GAD done. At the time, my GP didn't even know what that was.

[mortis505]

A low c peptide level does indicate type 1, or type 1.5. My endo said my c peptide was lowish as after a meal it was 1. ( after a meal the c peptide is higher). I have heard an increasing c peptide level indicates type 2. Get your antibodies checked, although they are not always present as I don't have them being type 1.5. You haven't really had type 2 that long have you?

Your c peptide level is lowish if is below 1 I think. Was it a fasting c peptide?

C-peptide is produced along with insulin. Yes if the ß-cells are destroyed due to an autoimmune attack then there will be less c-peptide. However, if someone who has been DX'd as a T2 for a few years and their beta cells have burned out due to high insulin production from high BG levels, or the use of drugs designed to stimulate insulin production such as one of the Sulfonylureas, or the completely natural and total progression of the disease, will also have a low to nonexistent C-peptide value. This does not turn them from a T2 to a T1. They are still T2 but are now insulin dependent.

C-peptide levels are not a clear and simple indicator of type as there can be multiple reasons for diminished production.

Snippet from this article. Mechanisms of {beta}-Cell Death in Type 2 Diabetes -- Donath et al. 54 (Supplement 2): S108 -- Diabetes (http://diabetes.diabetesjournals.org/cgi/content/full/54/suppl_2/S108)

Understanding that decreased ß-cell mass is an important factor in the pathogenesis of type 2 diabetes raises a concern regarding the application of drugs potentially harmful to the remaining ß-cells. Conversely, protection of ß-cells from death presents itself as a new therapeutic target. In this context, modulation of the ß-cell ATP-sensitive K+ (KATP) channel (KATP channels are octamers composed of four inwardly rectifying K+ channels [Kir 6.2] and four sulfonylurea receptors [SUR1]) appears particularly interesting. Indeed, closure of the KATP channels by the sulfonylureas tolbutamide and glibenclamide may induce Ca2+-dependent ß-cell apoptosis in rodent and human islets. This effect was observed only in vitro and not consistently. However, in an important recent clinical study comparing insulin and sulfonylurea treatment of type 2 diabetes, it was shown that treatment with insulin preserved ß-cell function more effectively than glibenclamide. It remains to be established whether it is the beneficial effects of insulin per se or the possible ß-cell toxicity of glibenclamide that accounts for this observation. Whereas a deterioration of insulin secretion was seen in patients treated with sulfonylureas in the U.K. Prospective Diabetes Study, those treated with insulin were not evaluated in this regard. Given the possible deleterious effect of some sulfonylureas, alternatives to these as well as alternative insulin secretagogues may have to be considered. When applied for their respective circulating half-lives in vitro, repaglinide and nateglinide do not appear to have an apoptotic effect on human islets. In contrast to sulfonylureas, KATP channels’ channel openers may exert protective effects on ß-cells. In 1976, Greenwood et al. were the first to report an improvement in insulin secretion after administration of diazoxide to diabetic subjects for 7 days. Similar protective effects were observed more recently in patients classified with type 1 and type 2 diabetes. Finally, other antidiabetic drugs that have emerged as protectors of ß-cells from apoptotic stimuli include thiazolidinediones, glucagon-like peptide 1 analogs, and, last but not least, insulin.

[mazea]

That's good mortis. I agree with you to but the OP hasnt' had diabetes for long and is only 39. Hence my thought it would be unlikely he has had burnout. I guess it really depends on what his c peptide level was on diagnosis OP?Did you have a c peptide on diagnosis? Did you have a decrease in c peptide or has it always been that level. Because if there has been a decrease from a high c peptide I would think Mortis you may be right. But if the c peptide went from normal to low I would wonder if the diabetes is Type 1/ 1/5.

The Op's HBAC1 is a little high at 8.0. Would that cause burnout?

In any case it is better to use a range of tests to diagnose type 1.5 and I think a GAD antibody test would be helpful.

[hazatude]

I was diagnosed as type 2 in 2005 at the age of 35. There were no tests done at the time. I lost a lot of weight and my glucose went crazy all in the period of a couple of months culminating in a re-diagnoses in Oct./08. I tried glyburide and actos. Neither worked.

[mazea]

Were you overweight at the time of diagnosis hazatude? Never mind. I just realised you wrote it - I''ll go away and try to convert it into Australian measurements 125kg- that is overweight if your average height. And did any of the diabetes mediction besides the ones you mentioned help your blood sugar levels? It is my understanding that diabetes medications actually don't help a type 1 diabetic much.

I would go and get the GAD antibody test if I were you and get this mess with diagnosis sorted as it has been going on long enough. GAD antibody test picks up 95% of type 1 diabetics.

[Dan Gato]

Mazea,

Did you go from a 20.0 AIC to a 5.3? Wow!

[mortis505]

The glyburide is a classic second generation sulfonylurea. Did you experience lows while taking it? Sulfonylureas work by making the pancreas massively overproduce insulin which in turn has been known to be a contributing factor of ß-cell death.

Here are the tests that will be helpful.

Islet Cell Antibodies (ICA) tests
Islet Cell IgG Cytoplasmic Autoantibodies, IFA; Islet Cell Complement Fixing Autoantibodies, Indirect Fluorescent Antibody (IFA); Islet Cell Autoantibodies Evaluation; Islet Cell Complement Fixing Autoantibodies - Aids in a differential diagnosis between LADA and type 2 diabetes. Persons with LADA often test positive for ICA, whereas type 2 diabetics do not.

Glutamic Acid Decarboxylase (GAD) Antibodies tests
Microplate ELISA: Anti-GAD, Anti-IA2, Anti-GAD/IA2 Pool - In addition to being useful in making an early diagnosis for type 1 diabetes mellitus, GAD antibodies tests are used for differential diagnosis between LADA and type 2 diabetes[2][5][6] and may also be used for differential diagnosis of gestational diabetes, risk prediction in immediate family members for type 1, as well as a tool to monitor prognosis of the clinical progression of type 1 diabetes.

Or for the all in one.

Insulin Antibodies (IAA)tests

RIA: Anti-GAD, Anti-IA2, Anti-Insulin; Insulin Antibodies - These tests are also used in early diagnosis for type 1 diabetes mellitus, and for differential diagnosis between LADA and type 2 diabetes, as well as for differential diagnosis of gestational diabetes, risk prediction in immediate family members for type 1, and to monitor prognosis of the clinical progression of type 1 diabetes. Persons with LADA may test positive for insulin antibodies; persons with type 2 rarely do.

Other characteristics of LADA that may aid in differential diagnosis include:

* Onset usually at 25 years of age or older
* Initially mimics non-obese type 2 diabetes (patient is thin or of normal weight)
* Lack of family history of type 2 diabetes
* Persons with LADA are insulin resistant like Type 2 but at levels less than Type 2
* HLA genes associated with type 1 diabetes are seen in LADA but not in type 2 diabetes

A C-peptide test will only show level of insulin production, and will not be a clear and decisive indicator of type.

[hazatude]

When I was on the Glyburide and Humalin, I had a few lows.

The diabetes nurse and the dietician both said I was type 1 but that was re-diagnoses without any tests.

All I have back are Anti insulin antibodies (< 0.4) and the C-Peptide (73). An Islet cell antibody test was done but I don't have the results.

I'm off all oral meds now and and controlling a lot better with insulin.

[mazea]

Did you go from a 20.0 AIC to a 5.3? Wow!
Yes I didn't know I had diabetes then. I was pretty sick and so dehydrated they couldn't get blood out of me. But I feel a lot better now:) that's is why I love the insulin.

[hazatude]

Today was, "Diabetes Day" at the hospital for me and the team said that I was type 1 LADA. I still don't have the freakin' islet cell antibody result back from the endo though!