My latest lab results indicates that I tested negative to anti bodies. So my endo says that I am not Type 1. What the heck? I previously tested positive for GAD. This time GAD65 <5 IU/ml. Are there variabilities to these anti bodies tests?My c peptide is 2.4 (a year ago, the c peptide was 1.4) How does the c peptide increase?
He is pushing for Januvia or Glimepiride. I am uncomfortable with the lack of long history for Januvia. I’ve been using insulin (Levemir and Novolog). My recent A1C is 6.5. It is not great, it is not terrible.
Well the c-peptide is a very ambiguous lab and the level doesn’t mean much of anything (except that you’re still producing natural insulin) unless it’s taken before you start taking exogenous insulin and it’s compared to a simultaneous glucose level. The level varies. Just like the level of glucose in your body goes up and down, the level of c-peptide and insulin in a properly functioning metabolism will rise and fall to meet the need. It is not a static level.
I don’t know what to think about the gad 65 being positive before and negative now. That doesn’t make a lot of sense to me, but I don’t put near as much stock in antibody testing as some others here do or consider it the holy grail of diabetes diagnostics
GAD65 may come and go. You need to have your c-peptide taken fasting (like 8 hours) and it should not be measured with a high blood sugar (certainly not > 250 mg/dl).
maybe the insulin gave your pancreas a rest? it is current best practice for short term insulin with high BG for T2.
time will tell either way, I would go low carb higher fat, like a T2 would and see if you can just take metformin and get good BG levels. an introduction to low carb A Low Carb Diet Guide for Beginners – Diet Doctor
I have to tell you. From what I understand you have been living as a T1 on insulin for a while. Your last A1c was 6.5% and that was with insulin. Glimepride is a sulfonylurea a drug that while very cheap is also associated with burning out your pancreas. And Januvia is a DPP-4 which is considered a weak drug and inferior to the GLP-1 class of drugs. And most alarming of all, the implied suggestion that you can just stop insulin and be ok with these suggested drugs.
Personally I would push back. I would never use a sulfonylurea but I would accept trying some of the drugs normally associated with T2 (like GLP-1s or SGLTs). But I would refuse stopping insulin, instead I would suggest that if those drugs truly work then your blood sugar control should improve and you should be able to slowly reduce your insulin use down to zero. But I suspect that won’t happen. It is actually a bit crazy for the doctor to reverse a confirmed diagnosis on a hypothesis and then try to run a potentially dangerous experiment on you.
I am NOT a diabetes expert (spend most of my time researching celiac disease), but when I went gluten free after my celiac diagnosis three years ago, not only did my celiac antibodies go down to the normal range, but my thyroid antibodies decreased as well. In fact, I no longer have thyroid enlargement or nodules. They are gone (had them for over 15 years and it was the reason my MD initially caught my Hashimoto’s diagnosis – and verified by extremely high antibodies <2,000).
I have not been tested for GAD antibodies (for several reasons). I am insulin resistant and my doctor supports my LCHF diet and exercise plan.
Obviously, the known trigger for celiac disease is gluten. No one knows what triggers or flares other autoimmune disorders (lots of theories though).
Perhaps, your current diet has calmed down your autoimmune reaction. I can not recall, but are you gluten free?
There was a new study released about autoimmune disorders and wheat (not gluten). Could this be related to your reduction in antibodies? AI issues will never resolve, but like diabetes, it appears that they might calm down with a good diet.
The blood sample for c peptide and BG was not taken fasting. My BG at the time of blood test was 128 (Sept 2016).
I think if it isn’t broken, let’s not mess with it. I may be willing to try metformin. Maybe with Metformin I may only need basal insulin?
Typically, my 2 hour post meal with MDI hovers around 140 ish; sometimes lower and sometimes higher. After 3 to 4 hours, BG may be closer to 100. My carb count isn’t precise. That may explain the high 2 hr pp BG. If alot of the bolus insulin is used up by around 3 to 4 hours, what’s bringing the BG down? My basal is pretty decent because if I don’t eat for about 5 hours or more, BG is about 90 to about 100 ish. Is it the basal that brought down the BG after 3 or 4 hours?
If your c-peptide was not taken when fasting then it isn’t a meaningful reading. A stimulated (non-fasting) c-peptide is often 3-5 times higher than a fasting c-peptide. You may still have some residual insulin production, the majority of people with T1 do.
I agree with most of what people said. If you’re happy on insulin stay on it don’t allow your doc to change that. Redo the c peptide fasting if necessary but stay on insulin. It could be the antibody reaction is reducing from the treatments, hopefully for you. Or it could mean the test wasn’t accurate. You had antibodies so you’re type 1 whatever is going on, either way don’t let the doc change your diagnosis. Find a new one if necessary, I know this is easier said than done but in this case I think it’s needed. Over time antibody levels can reduce in type 1, many longterm type 1 don’t test positive for them but usually after many years I think.
I’m not sure why your doc retested for them, but it sounds like he/she was looking to change your diagnosis maybe? Many docs out there, even endos are VERY ignorant about diabetes and type 1. They think either you can’t have type one as an adult or it is very unusual. I have had many docs make such comments to me. An endo I saw recently after my hospital stay was questioning me about my symptoms at my diagnosis and I’m sure questioning if I was type one. These people need to be avoided like the plague since this could be very dangerous for you.
Um, no. Metformin does not deal with postprandial blood sugars. It’s more about fasting blood sugar levels background level, like a basal insulin is.
And I have to echo what others here have said. If it ain’t broke, it can be downright dangerous to start “fixing” it. And the discussion above about tests should be taken to heart.
Yup, I understand the concern about sulfonylurea burning out our pancreas. Does that occur over prolonged usage? or is it a dosage dependent scenario? The endo is recommending that I try 0.5 mg Glimepiride, once a day. If it doesn’t work, he will not increase it. 0.5 mg glimepiride seems like a small dose to me.
Most likely a combination. I used sulfonylureas for some years and gradually required larger and larger doses as it became less and less effective, until it reached the point where it just wasn’t doing the job any longer.
@David_dns- About sulfonylurea-- That makes a lot of sense – " I used sulfonylureas for some years and gradually required larger and larger doses as it became less and less effective," Do you recall approximately the dosage?
About insulin and BG management - The doctor said that because my body is likely producing some insulin, the MDI dosage is challenging. If my pancreas produced NO insulin, he said that the insulin dosing would be easier. My recent A1C of 6.5 (it has been generally around 6.5 for about 2 years) It seems like the doctor doesn’t know how to help me improve it using insulin. The CDE he recommended thought my A1C is terrific - so that’s no help.
My fasting BG is most often between 100 - high 120’s. My bedtime BG is often between 130-160. Any thoughts on how to improve my BG management? Thank you all so much in advance for your input.
I reserve the right to call bullhockey. Keeping some residual insulin production is beneficial as it will act as a buffer so you don’t have to as precisely dose insulin. Some doctors argue that when you have a LADA/T1 honeymoon that the variability is a problem. You have not suggested you have had a problem dosing insulin.
I am sure that most everything everyone else has said is right for some - or many. I agree with Brian about any insulin-production-encouraging meds – they feel “dangerous” to me. Diet (low carb, etc.) that helps you reduce insulin doses seems like a good idea to me - doing so myself (though I will probably always have to take some insulin) with good results.
As to the tests - taking insulin can help your pancreas “recover” beta cell performance, as some have said. Perhaps that is what happened? Alternately, like @Sam19 said, perhaps you just caught it at a different times in the produce/wane cycles? I have read that the GAD65 antibody test, though still considered an important indicator and used in LADA/T1 diagnosis, actually tends to be a rather unreliable test in many people - especially as they become older – the mature adult immune system can create both false positive and false negative results from the test - as antibodies get “lost” in the “noise.” I am not sure that this happened in your case, but it can explain differing results.
About the dosing, I don’t recall clearly, been too long now. I do remember that the dosage started small and grew steadily.
About insulin and BG management:
If your doctor is saying you can’t effectively use exogenous insulin because your body is still producing some—if that’s really an accurate transcription of what he said—then I must respectfully but strongly disagree, based on both logic and extensive personal experience.
When I started insulin, which by the way was at my own insistence, not the doctor’s recommendation, I was still producing modest but significant amounts of insulin. Aside from the usual and normal learning curve involved with starting something new, there was no difficulty in determining what to do, how to dose, etc. At the time my A1c was a few points higher than yours is now—hovering near 7.0 or thereabouts—and within a few months it was in the mid fives. My only regret is that I didn’t insist on it years earlier.
One of the greatest benefits of insulin for a T2 is to help preserve beta cell function by taking over part of the job and letting the beta cells rest and recuperate. The idea that insulin will be problematical because the cells are still working is just . . . well, silly.
Depending on how much beta cell function really remains, an insulin regime needn’t be permanent, either. A widely accepted protocol these days involves early intervention with insulin on a temporary basis until good control is reestablished. For many T2s, control can then be maintained with some combination of diet, exercise, and other meds.
As you’ve undoubtedly figured out by now, I am a true believer in insulin. It’s the most powerful weapon we have. Properly used, it can do immense good. If circumstances justify it, it’s something to be embraced, not avoided.
If your fasting BG is satisfactory but your postprandial readings aren’t, the obvious conclusion is that you are either (a) eating too much, or (b) not using enough fast acting insulin to cover what you do eat. That being said, there’s still some missing information:
You don’t indicate when those postprandial readings are being taken. That’s important. If it’s 30 minutes or an hour after eating, that’s a very different story than if it’s 2 or 3 hours later. Determining the right thing to do is going to depend in part on the timing.
You indicate that your fasting BG is under 100 but your bedtime BG is substantially higher. That seems contradictory at first glance. Do you eat right before going to bed?
If your fasting BG truly is good but your A1c is 6.5, it suggests that you are experiencing unmoderated postprandial spikes. A 6.5 A1c equates to an average BG somewhere around 145 mg/dl or 8.1 mmol/L. If you consider that to be too high—and you should, IMOP—then the answer, one way or another, is to correct the imbalance between food, exercise and medication.
