C-peptide test question

Any thoughts on what these c-peptide numbers mean in terms of my lada/ or type 1 or 2 status?
My fasting c-pep was 0.46 ng last year and later it was 0.53. I just did a post prandial c-peptide test which came back at 1.61 ng. This was about 90 min post meal. It shows within the “normal” range of the lab (which is .8 to 3.15). I am waiting for anti bodies, but one year ago I was mildly positive for GADA. - I am struggling with my BG control.
Yes I will ask my doctor but curious for other thoughts as I wait for the appointment. Thanks!!

Yes your numbers look pretty normal.
Usually if your fasting c peptide is low, it suggests type 1.
If your 2 hrs PP is high it strongly suggests type 2.

You are normal for both. But it’s not the whole story.

If you have positive antibodies then eventually you will lose beta cell function and need insulin.

Personally I didn’t get good control until my beta cell function was totally gone and I was getting zeros for my cpeptide.

The little bit of insulin production made it harder to control.

For me it took only about 6 months to be totally done.

The older you are the slower the cell loss is

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See what the tests say with your doctor. With the normal range c-pep, it’s a good bet you’re not T2. I would expect it to be raised, because of insulin resistance.

what was the BG with the post prandial c-pep? If you had high BG with it. it may mean your pancreas couldn’t put out anymore insulin

What BG issues do you have?

That’s true for us type 2 DMs who have diminished insulin secretion. Since I began MDI, I have had to do a lot of tweaking with the blessing of my doctor. The bolus rapid u:carb is steady, but basal is more of a problem.

I was having a real problem doing any kind of endurance exercise as 15 minutes of cycling or brisk walking would cause BG to dive.

My doctor suggested I cut the Metformin I take by half. This has improved morning diarrhea and I think allowed for a better glycogen response from the liver.

I’ve been able to do 4 rides of 2+ hours while staying in range, between 90 and 150mg/dl.

Gotta keep learning to keep the little gray cells happy.

The fasting c peptide numbers I noted earlier were below normals and with high sugars at the time. With mild GADA they said type 1 lada and prescribed multiple daily injection and bass. But another doc says “you are still making some insulin so you should be treated as type 2”.
My new tests shows no antibodies.
I am usually unable to bring down any high sugar (or it takes all day) without bolus.
My 1.6 ng c peptide result is likely the most I can make as it was after meal with 240 sugar. I read elsewhere that you should be over 3 ng after meal.

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Find another doctor !!


You are on insulin. Does a T1 have advantages, over T2? Given you had a positive antibody test before. It would be diagnosed LADA, late onset T1

One doc would put me back on type 2 meds. Maybe in addition to basal. I guess might as well try. Why not experiment

A GLP-1 and basal insulin may help in either case. LADA or T2. I wouldn’t take a Sulfonylurea and such.

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Thanks. Do you know , can you add a GLP-1 to both basal and bolus? Or is it just to be added to basal?

I meant as well as insulin basal/bolus. You take one injection a week of the new GLP-1’s, like Ozempic

I was 38 when I got chickenpox. A friend brought his daughter over and asked if I knew what the spots were. I didn’t, but I found out. At 39, I had polyuria and polydipsia. I moved, went to a new physician for a physical, and he asked, ‘Why didn’t you tell me you were diabetic?’ I said I was not. He showed me the strip from my urine that was green. So he diagnosed me as Adult Diabetes, and said diet and exercise were the best treatments, since (back then) every medication for Adult Diabetes made life expectancy shorter than untreated Adult Diabetes (this was before Metformin). He told me to check my sugars frequently. They went higher and higher. The Islets of Langerhans do not stop producing insulin instantly, their production goes down and down. And, since the GP had diagnosed me as Adult Diabetes, the Endocrinologist had to tell me I had an unusual form of Adult Diabetes where my body produced exactly half the insulin I needed, so I needed to double the amount of insulin. The amount of insulin I needed increased for about a year, then was stable for 30 years, then started going up again, and I had to add Metformin (family history of Type II, but the chicken pox gave my what used to be Type I, but is no longer since no antibodies, and the new and improved definition of Type 1 is presence of antibodies, not absence of insulin).
I moved again, and my new GP said he had to have a C-Peptide before he could refer me to an endocrinologist. I don’t have any C-Peptide, and probably haven’t had any for 30 years. So I got referred.
Net. Some physicians are very good. Some are not. All are told the First Law is to make sure no patient sues the establishment where they work. Like the 3 laws of robotics, the Second Law is that they must treat the patients for their illnesses if that does not violate the First Law.

Chicken pox has been known as a trigger for type 1.
And after your islets are all gone, it’s not unheard of that your antibodies are gone too. If you have no cpeptide you have no insulin production, so you are definitely type 1.


This was discussed in another thread, and I couldn’t find anything anywhere about this being true. Just a 2018 study that proposed introducing subtypes, and very specifically said they weren’t redefining how we diagnose/type diabetes. And I couldn’t find this proposal being adopted by any medical board. Just because it got published in a journal doesn’t mean it’s an adopted/accepted practice.

So can you please explain why you’re holding onto this idea that we somehow evolve from a Type 1 to a Type 2? Do you have a credible source that says this? Otherwise it’s just spreading false, and confusing!, information.

First, my endocrinologist told me my last visit in February 2021 that the new and improved definition of Type 1 was antibodies, not the absence of insulin. Then I read a newspaper article that gave the new and improved 5 types of diabetes, with Type 1 being the presence of antibodies, with or without insulin, and Type 2 the absence of both antibodies and insulin (obviously, Type 1 and Type 2 both used to be Type I, while Types 3, 4, and 5 were different variations of what used to be Type II).
My first complaint is that the word ‘diabetes’ is from the Greek and means ‘pass through’, i.e., polyuria and polydipsia. Today, Wikipedia says the word ‘diabetes’ means mellitus, and insipidus is not a kind of diabetes.
My second complaint is that lack of insulin is much more important than whether or not one has antibodies. And I have read in this forum that the only test to differentiate between Type I and Type II is antibodies, NOT insulin levels or C-Peptide.
Again, one endocrinologist and one newspaper article and several other posters said this is the new normal. I don’t like it, but there it is.

Except there is no “new and improved” definition of diabetes. Not since 1984! The World Health Organization publishes a statistical classification document called the ICD, which essentially serves to unify how we define and diagnose diseases worldwide, so we’re all speaking the same language. Our most recent version, the ICD-10, was published in 1984 and really shook things up in the medical world, and had not been significantly revised since then. There will be a new version published next year, in 2022. Only then might we find out that our types change.

Some countries do use a slightly modified version of the ICD-10, to better make it conform to their national healthcare system, but it’s still the worldwide criteria for diagnosis. A doctor can’t just defy this established protocol and start doing their own thing because they read an article! Just because it’s on the internet, doesn’t make it true. There aren’t even five types of diabetes mellitus according to the ICD-10. Just 4. Gestational diabetes and diabetes insipidus are classified separately.

As it stands, Type 1 (E10) includes all presentations of diabetes that are due to an immune process.

Unfortunately, the ICD-10 doesn’t actually say you must perform any specific tests to prove a diagnosis, it’s only based on how a patient presents… So there’s a little wiggle room for interpretation. EITHER the presence of antibodies OR the lack of producing any significant amount of insulin can be used to demonstrate auto-immune causation. Though in the latter case, no endogenous insulin, you have to exclude the last 2 types of diabetes which include medically/trauma induced diabetes. There are no new guidelines undoing this… Just a single scholarly article stating they were able to divide all their test subjects into five different subgroups. That doesn’t change the higher authority of the ICD-10. Can you show me a single government or medical organization (not merely “my doctor said…”, because man is fallible) who has disavowed lack of endogenous insulin production as a diagnosis guideline?

Next time you speak to your doctor, I would specifically ask what diagnosis code(s) they are using for you. If the code(s) starts with E10, then you are still Type 1, and they are just speaking in confusing terminology… Referring to the 5 SUB-TYPES or CLUSTERS of diabetes the article specifies.

If you’re diagnosis code(s) start with E11, Type 2, then they’re actually defying international protocol… Unless you actually are still making insulin and just can’t use it well.

Now come 2022, when they introduce the new ICD-11, we may all be disgruntled when they switch things up. Maybe the WHO read the same article in the Lancet, and decides to make it official… We won’t know until then.

Though I still have the same confusion as last time we talked about this. Autoimmune diabetes is still Cluster 1 in the article. I’m not sure how your doctor is jumping from lack of endogenous insulin to type 2. The study was for newly diagnosed individuals, who would still be making antibodies. There’s no jumping types later in life when the antibodies run out. That would be completely irrelevant to the study.


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Many thanks. I think this clears it up. The Lancet article has 5 clusters, not types, but the newspaper article and my endocrinologist used the wrong word, ‘Type’, when they should have used ‘Cluster’.
Unfortunately, your link only goes to the summary unless you have a paid account, so I read that my endocrinologist and the newspaper article were talking about the 5 clusters, but the summary did not say what, exactly, the 5 clusters are.
However, you are still partly wrong when you say nothing has changed since 1984. The official definition of diabetes had a major change in 1998.

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I hope this clears it up.
Blood test
High BG, High c-pep, go on a low carb diet
High BG, Low c-pep, go on insulin.
Normal range BG, keep doing what you are doing.

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Perfect. Sadly, a lot of primary care physicians use, 30 or over, Adult diabetes, under 30, Juvenile diabetes. Odds are about 90% that this is correct, but that’s 10% wrong, which causes a lot of problems for the 10%.
Some physicians say, no antibodies, Type II, give Metformin. Antibodies, Type I, give insulin. Only Cluster 2 has no antibodies and no insulin, so still not right for a minority of patients.
I prefer testing for either insulin or C-Peptide. Definition of diabetes mellitus: fasting blood sugar more than 126 mg/dL = 7 mmol/L ≡ HbA1c more than 6.5.
The best physicians then order either a C-Peptide test or a proper glucose tolerance test before starting treatment. Some physicians give an inadequate glucose tolerance test: measure blood sugar, give glucose. If blood sugar goes up, diagnose diabetes; if blood sugar does not go up, diagnose hypoglycaemia. In either case, the patient must see the physician regularly and have someone pay the physician. (We had one of these in my home town; the other physicians laughed at him and his patients, but were never allowed to say anything.)
The correct glucose tolerance test first measures fasting blood sugar and insulin, then gives glucose, then measures both blood sugar and insulin again at 1 and 2 hours. If no insulin, Type I. If both insulin and blood sugar spike, Type II. I watched some of these tests, and a Type II has both insulin and blood sugar go up a lot after the glucose.
If a physician has started insulin without testing and then later orders the glucose tolerance test, the insulin will be a horizontal line equal to whatever insulin has been administered (but it is wrong to start treatment without a proper test for insulin or C-Peptide).
The healthcare organisation I currently use starts with a blood test for fasting blood sugar, HbA1c and C-Peptide. If fasting blood sugar is above 126 mg/dL or 7 mmol/L and HbA1c is above 6.5, then diabetes mellitus. If no C-Peptide, endocrinologist and insulin. If C-Peptide normal, primary care physician who has some extra training in diabetes mellitus and who prescribes Metformin and, if HbA1c above 8, another oral medication, usually Sitagliptin.
Another organisation here that I used before gives the proper glucose tolerance test, so their diagnoses were perfect, but I was not happy with their treatment.
But at my prior location many years ago, my primary care physician tested my urine for sugar, found I had diabetes mellitus, figured I was over 30, so Adult diabetes and he started treating me for Type II.
Fortunately, I found a decent endocrinologist before I had any serious problems, and I’ve been on MDI ever since.

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I’d like to stir a bit of type 2 DM into the mix. I was diagnosed about 30 years ago and am definitely type 2. I was able to have normal or near normal BG for 10-12 years through diet and exercise. Then BG started rising without any changes in diet or exercise. Decreasing carbs to near zero grams and riding more miles did nothing.

That’s when I started Metformin. BG good for several more years and then started rising. Begin basal insulin. The last quarter of 2020 I was noticing my fBG and post postprandial were rising again. Come January I had a regular round of blood tests. HbA1c jumped a full percentage point.

My doctor started me on MDI adding Humalog to the mix. This has been tough to maintain BG without going high or too low as I do make some insulin, just no where enough.

What causes progressing in type 2 DMs is insulin resistance which wears the Beta cells out over time. That’s where I am.

As to doctors confused as to how to code patients, I think many of them are stuck in the old designations of Juvenile diabetes mellitus and adult onset diabetes mellitus. And heaven help the poor soul presenting symptoms of diabetes insipidus.

I go with type 1 DM which has subtypes including LADA, autoimmune and non-autoimmune. Type 2 DM has subtypes all marked by insulin resistance, MODY (mature onset of diabetes in youth), adult onset, gestational and geriatric (Beta cells just get old). Type 3c DM which is caused by damage by disease or injury damaging the pancreas, decreasing or eliminating both endocrine and exocrine functions.

There is nothing simple about diabetes mellitus even if some doctors would like it to be.

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