I was diagnosed as type 2 6 years ago then shortly after told this was wrong and I was in fact a type 1 so have been living as a type 1 for 6 years. Now they have finally done the blood test to look for antibodies and found out I am type 2 for definate.
I write this blog http://onesizefitall.blogspot.com/ Some of you might find it an interesting read, some might not but you wont know till you read it lol.
I'd like to offer my help and support to both type 1 & type 2 as I have experience with both.
Why were you classified as Type-1? Many here have reported trouble getting the doctors to agree to test for antibodies to confirm either way and remain classified as Type-2 by default.
Also, you should be aware that once you lose all your beta cells after the honeymoon period, your antibody titer also falls and may go below the sensitivity levels of the tests. Did your C-peptide tests come back normal?
I don’t like the idea of type 2 being a default diagnosis. Especially due to the fact that most doctors will only test A1C (that is if he is competent enough). However the A1C does not tell the whole story, all it indicates is that there is a problem with handling sugar. This is way so many type 1 wind up in DKA. Just because type 1’s are a small percentage, doesn’t mean that, that possibility should be ignored. DKA is a VERY dangerous condition.
There are real problems diagnosing diabetics. And while certainly DKA is a great concern, even more alarming to me is that many diabetics are diagnosed with T2 and medications just don’t work. We all know what spending long periods of time with high blood sugars does. If medications don’t work, is that perhaps an indication that the diagnosis might be wrong?
In truth, we must also realize that LoubieLou lives in NHS land, where mixtard is the standard insulin treatment and socialized diabetic care is at perhaps even at a lower standard than even the US. We don’t know the story, and nobody can agree on diagnostic standards for T1 anyway. Some declare it to be about “absolute” insulin deficiency. But almost no T1 has Zero c-peptide. Some say it is about antibodies. But even testing for all four antibodies is not full conclusive, some 5% of T1s test negative for all four.
In the end, all the diagnosis and labelling does not matter, what matters is that you get appropriate treatment. If you are able to control your blood sugar without damaging your health, then that is what matters.
Where did you read that “almost no” type 1s have zero c-peptide?
The studies I’ve seen show that a small percentage (17%) of long-term type 1s had detectable levels of c-peptide. Detectable does not mean a lot. I believe the average was 0.2 in whatever units of measure are used, which is still far below the lower limit of normal.
If you’ve seen additional studies I’d be interested in reading them.
I was diagnosed with type 1 at age nine after a few weeks of intense symptoms. It seems us “classic” type 1s are becoming ever rarer (or maybe the less-classic types are just being better diagnosed).
Dr. B says that he has only observed two type 1s in his entire career with zero c-peptide. Joslin is currently researching why a signifcant number of long term type 1 diabetics still produce insulin (http://www.joslin.org/news/study_finds_individuals_with_long-term_t…). I beleive Richard157is taking part in the study.
NATURAL HISTORY OF C-PEPTIDE IN HUMAN TYPE 1 DIABETES
1–15 years after diagnosis of type 1 diabetes.
Although cross-sectional, the largest amount of data on C-peptide in the period 1–15 years postdiagnosis comes from the DCCT. Enrollment in the DCCT for patients with type 1 diabetes of 1–5 years’ duration required that mixed-meal (Sustacal)-stimulated C-peptide (90-min) be <0.50 nmol/l, whereas for patients with type 1 diabetes of 5–15 years’ duration, stimulated C-peptide had to be <0.2 nmol/l. To identify the 1,441 patients ultimately enrolled in the DCCT, Sustacal-stimulated C-peptide was evaluated in a total of 3,736 patients with type 1 diabetes. Much greater presentation of β-cell function, that is, higher C-peptide levels, was found than commonly expected. Figure 2 shows the stimulated C-peptide values upon initial evaluation for those 2,432 subjects who were at least 18 years of age at the time of diagnosis of type 1 diabetes. Among those with duration 1–5 years at the time of eligibility screening, stimulated C-peptide was >0.2 nmol/l in 48% and >0.5 nmol/l in 15%; for those with duration >5–15 years, stimulated C-peptide was ≥0.2 nmol/l in 8% and >0.5 nmol/l in 2%. As observed by many others, the stimulated C-peptide values at the time of DCCT screening were lower among those in whom the diagnosis of diabetes was made at <18 years of age (Fig. 3). Among these, 33% had stimulated C-peptide >0.2 nmol/l 1–5 years after diagnosis, but only 3% exceeded 0.2 nmol/l after 5–15 years of type 1 diabetes. These data were collected from 1983 to 1989. With the current emphasis on aggressive early glycemic control and since glycemic control reduces the decline in β-cell function in type 1 diabetes (8), β-cell function is now probably even more preserved in the years after diagnosis.
I do think T1 onset for children tends to be accelerated and abrupt. But still residual insulin production is common, if not typical in T1s, particularly for those with adult onset. And it may well be that with good blood sugar control residual insulin production may remain, potentially “forever.” One would expect that poor control would have a detrimental effect on ones poor pooped out pancreas.
I can’t tell you how many times I threw-up, uncontrollable diarrhea, stomach pain, etc., on Metformin, Actos, Jenuvia, glyburide, etc., etc… I had to demand insulin from my new doctor. I took out all my frustrations on him… LOL. But I explained what I went through and he understood… Now not only do I feel better, my sugars are good as well.
Thanks for the links, I found them really interesting to read. I do have problems with Dr. Bernstein’s statements (many of them, not just the one you referred to) as he doesn’t actually document and publish data on anything he says; he just says it’s based on his “experience” and “patients” and we are supposed to take it on faith that he’s reporting things accurately. I understand that in the past he probably didn’t have resources to conduct studies, but with a medical degree and more publicity in recent years I don’t see why he can’t publish empirical data like everyone else.
I do think type 1 in children and LADA is very different in terms of its speed and residual insulin production. I know of people with LADA who have been in the honeymoon phase for years, even if they also use insulin. As a kid my honeymoon only lasted about six weeks–and I don’t even know if it counts as a honeymoon, because I definitely still had highs, I just also had a lot of lows despite lowering my insulin TDD by 50%.
According to that study you posted, only 3% of people diagnosed with type 1 before age 18 had c-peptide levels above 0.2, compared to 10% for those diagnosed after age 18. If people with LADA (i.e., those diagnosed in their 30s and later) were tested after having diabetes for 5-15 years, I bet the percentage of those who still had c-peptide levels above 0.2 would be even higher. On the other hand, I have to wonder whether that “over age 18” category didn’t catch some people with LADA in there, since it doesn’t specify the actual ages.
It would be interesting to do another DCCT-type study today (a whole new one with people diagnosed in the 1990s and 2000s, not just a follow-up with the original cohort) and see how things have changed. I bet a lot of useful data could be collected just by following a new cohort of a few thousand people with type 1.
