About 3 years ago I was diagnosed as Type 2 by my PCP. I have been able to control my BS (A1C 6.0-6.1) with diet and excercise. I am normal weight 185 at 6’1". The past few months I have had a horrible time controlling my BS. I went to my PCP to have my A1C tested and it was 6.1. Lately (within the past month) I have been getting fasting BG of 150’s and post meals anywhere from 200-400. My PCP is confused because I do not show the typical type 1 or type 2. I finally convinced my PCP to do an insulin, cpeptide, and GAD. My insulin was 6 (0-17 range), cpeptide was 1.8 (0.8-3.8 range), and my GAD is 3.7 (<1 range). To throw another item into the mixture my son was diagnosed with Type 1 (GAD of 9) early this year. Genetically speaking then if my son is Type 1 and the information provided above wouldn’t one conclude that I am Type 1.5 and not Type 2? If the American Diabetes Association wraps Type 1.5 up wiht Type 1 then how do you approach your PCP with this information so you can be properly diagnosed?
As far as I know, a positive GAD test is always indicative of autoimmune (type 1) diabetes. What you’re describing sounds exactly like Latent Autoimmune Diabetes in Adults (LADA). Although it’s been given the moniker Type 1.5, it really is just Type 1 with a long honeymoon period and found exclusively in adults.
My best guess is that you’ve been doing well with diet and exercise while your pancreas was still working, but slowly dying. However, it’s likely that your beta cells are finally burning out and you’re moving towards insulin dependency.
At this stage, I would highly recommend seeing an Endocrinologist instead of a PCP. You need more specialized care, and a PCP might not be as familiar type 1 diabetes as you need.
Go to an endo & don’t mess with trying to convince your PCP of anything. He/she is uninformed. Doctors see so many Type 2s that they assume any adult is T2. I was diagnosed T1 at 53 with no history of diabetes in my family.
My endo said I must have had slowly creeping up BG for about 5 years before my pancreas crashed & burned. I ended up in the ER near comatose & near death.
Good for you for insisting on getting the proper testing done.
Yes, go to an endo as soon as possible. This sounds like a clear case of LADA. Some endos do not recognize LADA – so they may diagnose you as type 1. Either way, the treatment is similar. Are you currently taking insulin?
See an endo. Many PCPs treat all adult onset diabetics as "Type 2"s, who are 75 to 80% of the diabetic population, and the grand majority of the adult patients that they see. Though some have information and experience, many PCPs and medical personnel have not heard of LADA. Both you and your son should be treated by endocrinologists, who have far more experience with autoimmunity and insulin treatment paradigms.
A PCP is not generally an expert in diabetes, they have had a minimal education and in general do not keep up with things. This is really dissappointing because they are the first line defense and huge proportions of their patients suffer from diabetes. In general, the way that PCPs handle diagnosis is to see if you present as a type 1 (in the ER with DKA) and if you are not a type 1, then you must be a type 2. As a type 2, you get put on medications and then when you get worse (which obviously happens to all diabetics), then you will go on insulin. But you only go on to insulin when it gets bad. My GP felt bad meant repeated HbA1c > 8-9% or DKA.
In your case, you have come back with a positive GAD test, which in itself can’t diagnose you as any type. GAD is one markers for autoimmune diabetes (although not the only one). What you don’t know is the progression. Most T1s are autoimmune, some T 1.5s are autoimmune (LADA, but not MODY), and it is thought that about 10-15% T2s are autoimmune. The only difference is the rate of progression. In your case, you seem to have normal insulin levels and production, so could probably say you still have some significant remaining pancreatic function. However, from what you describe, your blood sugar has gotten markedly worse.
Given that your PCP is confused and does not know what to do, your best option would be to consult an expert (an endo). A reasonable treatment would to have been to immediately give you an oral medication like metformin to see if that could improve your blood sugar. The real concern is that if you actually are LADA, there is significant thinking that using insulin early as a treatment can actually help your pancreas functionally better and longer (avoiding burnout). A PCP would not be aware of this, only an endo.
Given that your son is a T1, you should already have an endo for him. I would just call that endo up or demand a referral from your PCP to that endo and just take all your test results and see the endo.
I just want to clarify a few points here.
According to my endo, a positive GAD test (combined with an elevated A1c or fasting BG) ALWAYS indicates type 1. There are other antibodies that also indicate type 1, but ALL type 1s are autoimmune. If antibody tests are negative, a diagnosis of type 2 is usually given. Genetic testing can look for MODY, but it is very different from LADA. LADA has been given the label type 1.5, but this seems to indicate that it has characteristics of both type 1 and type 2. Since most LADAs are actually insulin sensitive, the type 1 connection is clear. However, it doesn’t share any characteristics with type 2 (other than the typical age at diagnosis for type 2s). I believe that the type 1.5 label is not accurate. LADA is type 1.
Without knowing the fasting glucose at the time of the c-peptide test, it is impossible to say that the 1.8 c-peptide is normal. For example, if the fasting BG was 170, 1.8 would actually be considered a low c-peptide value. On the other hand, if the fasting BG was 170, and the c-peptide was greater than 3.8, this would be a strong indication of type 2. It seems likely that Mitchell’s beta cells are giving out.
As a LADA diabetic, metformin would be completely useless. Metformin helps to increase insulin sensitivity, which won’t help if there is not enough insulin present. Often, LADA’s were given a Sulfonylurea, which is an oral med that increases insulin production. However, studies have found that this causes the remaining beta cells to die faster. Now, many endos recommend insulin as the primary course of treatment for LADAs because it helps to preserve the remaining beta cells, and it provides better control.
I hope this helps clear up some of the common misconceptions about LADA.
Thank you all for your comments. As with any situation knowledge is power.
I went to visit with my PCP and was finally referred to an endo. I will be waiting to hear back from the endo clinic with an appointment and hopefully a confirmed diagnosis. My PCP basically told me that in order for him to classify me as type 1 (has know clue of type 1.5 or LADA) then DKA must be present. I have been with this PCP for about 16 years and he over medicated me one time where I actually passed out and spent 3 days in a telemetry floor at the hospital, he missed diagnosed my son’s type 1 because he was not DKA, and now the same for me. I finally have had enough and it is time for a new PCP.
So with that said does anyone recommend finding a PCP that has a good background in diabetes? How do you even find a PCP that has a good background in diabetic care?
I am just so amazed that we rely on these PCP for our first line of defense and how uninformed they actually are. My hats off to you Gerri for being so observent.
Oh… by the way he was pissed off that I had him run the GAD65 AB. His words were being positive for GAD65 was no indication of an autoimmune condition. Many things can cause GAD65 AB to be positive. If I remember right my son’s endo said that GAD65 was the most significant marker for autoimmune.
Thanks for letting me vent.
Because of earlier detection of Type 1, only about 25% of new onset Type 1 children are in DKA at diagnosis. And Shannon is correct–if you are GAD antibody positive, you have Type 1 autoimmune diabetes. The Expert Committee on the Diagnosis and Classification of Diabetes says that Type 2 diabetes is NEVER autoimmune. So the 10-15% of “Type 2s” who are antibody positive are misdiagnosed.
The Expert Committee came out with their results in 1997 and it was a negotiated definition between medical people, the ADA, the WHO and others. The newest AACE guidelines in 2007 defines type 1 as “an absolute deficiency of insulin secretion due to a cellular-mediated autoimmune destruction of the pancreatic β-cells” and then goes on to note that the “Markers of β-cell destruction include islet cell autoantibodies, autoantibodies to insulin, autoantibodies to glutamic acid decarboxylase (GAD65), and autoantibodies to the tyrosine phosphatases IA-2 and IA-2β.” I really don’t expect the “Expert Committee” to have much of any effect on medical diagnosis in the US, it is mostly an attempt to harmonize the statistical data collection, the US had traditionally used very different definitions in categorization from the WHO.
I would expect most endos to utilize the AACE guidelines. Unfortunately, these guidelines don’t have particularly good guidance for type 1.5 leading to great confusion for those patients. My attempts to get the GAD and other antibody tests have met with various forms of resistance ranging from a scolding to suggestions that I need a referal to a psychiatrist.
If the presence of antibodies were indicative of Type 2 diabetes then AACE would state that. Instead, they state that the presence of antibodies is indicative of Type 1 diabetes. LADA and Type 1.5 are just names used for people with adult onset Type 1 diabetes. Type 2 diabetes is not autoimmune in nature. Who knows how AACE is defining absolute deficiency of insulin secretion, but recent studies have shown that people with Type 1 diabetes for 50+ years have some insulin production.
The problem as I see it is not with the definition of Type 1–AACE makes it clear that autoantibodies are markers for Type 1 and that Type 1 occurs in adults (albeit with sometimes slower beta cell destruction). The problem is that the medical community does not recognize the prevalence of Type 1 diabetes in adults, and assumes that if you get diabetes as an adult it must be Type 2. As so many of us here at TuDiabetes know, including founder Manny H, Type 1 is quite common in adults.
I don’t necessarily disagree with any of your logic on this, but the situation is that the AACE diagnoses T1 based on absolute (or near absolute) insufficiency of insulin. The AACE further defines T2 as a diagnosis of exclusion (i.e. you have diabetes, but not T1). I myself suffer from insulin deficiency, did not present as insulin resistant, did not respond to metformin and yet have never been successful in convincing any medical professional that I am anything other than T2. We can argue all we want, but the vast majority of the US medical establishment works on this basic diagnostic critera.
ps. I agree with you on residual insulin production, Richard Bernstein says that he has only seen two patients in his entire career with no remaining insulin production.
Hi, I’ve been reading this discussion and it seems that the problem is that there is far too much variability in diabetics for these basic classifications. My endo dx’d me as a LADA. I presented initially with DKA, I’m in my fifties, I have a BMI of 21 and I didn’t initially respond to oral meds. Later it was found that my c-pep was 1.5 and I have no antibodies. My endo says that some T1’s never show antibodies and that I’m on the honeymoon. I believe I would be better classified a Ketosis Prone T2, which is an odd beast in itself. What is the actual difference between these two classifications? If I’m a LADA my c-pep should decline. If I’m a KP T2 my c-pep will rise, nearly double in the next 6 months. However, in 10 years I’ll probably be a T1 anyway.
LADA stands for Latent Autoimmune Diabetes in Adults. If you tested negative for antibodies, then that would presumably indicate that you DO NOT have an autoimmune condition. Note that you need to be tested for all the antibodies and testing negative for antibodies only means that you are not currently having an autoimmune reaction. If you had previously had an attack, but recovered, then you may actually show no antibodies, you just had an attack some time in the past. It is true that a range of currently diagnosed T1s don’t test positive for antibodies either because their β-cells were destroyed by some other than an autoimmune attack or their autoimmune attack has subsided enough that they test negative.
You can read the detailed findings of the "Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (http://care.diabetesjournals.org/content/25/suppl_1/s5.full). In the case of “Ketosis Prone.” The Committee basically categorized Ketosis Prone as Type IB, “Idiopathic” as opposed to autoimmune. A discussion of that categorization can be found in http://care.diabetesjournals.org/content/29/12/2755.full
I don’t know a whole lot about Ketosis Prone Diabetes, but I’d encourage you to consider yourself to be a different beast and to be optomistic about things. Why can’t you honeymoon forever?
Hi Michael. BSC briefly touched on what I think is your type of diabetes. You seem to exhibit all of the classic indicators for type 1B or Idiopathic Diabetes. I found a pretty good definition of Type 1B, which states:
Type 1 B diabetes is also referred to as idiopathic diabetes, or diabetes of unknown origin. This form of type 1 diabetes is not autoimmune in nature, and tests for islet cell antibodies will come up negative. People with type 1 B have an insulin deficiency and can experience ketoacidosis (a high blood sugar emergency), but their need for insulin injections typically waxes and wanes over time. Patients of African, Hispanic, or Asian descent are more likely to develop type 1 B diabetes.
You should definitely talk to your endo about this, as there may come a time when you no longer need insulin.
I’m not a doctor or CDE, just someone who has done lots of research on the different types of diabetes (in my quest to learn what my own type was - incidentally, I’m a confirmed LADA with GAD antibodies).
So here is my 2 cents. I was misdiagnosed by my endo at age 43. I had a fasting blood glucose around 350. I was sent home with Janumet. After a week of staying sick, my wife made an endo appointment. I was given the GAD and scored a 12. My dad was diagnosed with T2 just 4 months prior. I switched PCP’s immediately (had that one for about 20 years). My new PCP follows my diabetes treatment, but only treats my other issues. She leaves the diabetes to my endo. If she has concerns or questions, she speaks with my endo. Trick is to get a PCP who doesn’t feel like they have to be in charge of everything. When all your doctors are working together, it sure does take a lot of pressure off you.
Actually I’m not on insulin. I’m on an Actos-Met combo. You are right I would be considered idiopathic under the old classification. T1b was basically a catchall classification that’s been pretty much superceded. Note the “T1” part of it. Because the presentation was often DKA that had to be dealt with by insulin is was classed as a type of T1. The truth is that after the emergency passed, patients usually go to oral meds and in some cases just diet and exercise. Which would make them T2s. It is also considered another type of MODY by many. I am the weirdest form of this type, antibody negative, beta cell function-normal. Its called A-B+ for short.
Just an update… I finally was able to get scheduled for an Endo appointment and low and behold it will not be until Feb 1, 2010. So I am finally excited about getting into someone who I have heard good things about (that is why it is taking so long because this Endo has a excellent reputation). I did switch to another PCP and re-drew my labs. My A1C is up from 6.1 to 6.9 just over the past month (roughly). My GAD went from 3.7 to 5.9 so it is on the increase. What perplexes me now is that my Insulin and cpeptide were in better range then they were before (as he put it normal range). Outside of the GAD coming back positive you would think I was type 2 (ugh). FYI… my BMI is 25…hhhhmmmm perplexing.
I’m glad you are starting to get to see a specialist. If you are in a hurry to get in to see your endo and have some flexibility, tell them to call you if they have a last minute opening. Many endos fill their schedules far ahead with regular appointments, and often patients need to cancel leaving openings. So although you have been told the next opening is not till 2/1, if they will put you on the waiting list, you may see him much earlier. I know that the insulin and c-peptide may be confusing, but these will vary and can go up and down based on what you ate, your blood sugar level or whether you are “honeymooning” or not. In either case, a positive GAD indicates autoimmune and getting an appropriate diagnosis and treatment is important. And remember what you have been told here, there is a lot of thought that early insulin use can preserve your poor pooped out pancreas. Since you have gone through some of this with your son, I am sure that will help. Do let us know how it goes.
The adventure continues.
It’s great that you’re finally getting in to see an endo. I think you’ll get your BG under control much faster once you’ve started down that path.
But, you are definitely not a type 2 (I’d bet my next paycheck). I can’t stress that enough! The fact that your c-peptide was in a better range doesn’t mean much unless we also know what your BG was at the time. IF you were a T2, your c-peptide would have been elevated above the normal range. That’s one of the defining characteristics of T2.
Before my first c-peptide, my endo told me to eat a candy bar. That way, my body would be in a situation where it would have to pump out extra insulin (if it was making any). Despite the sugar rush, my c-peptide was 0.8.
Also, the fact that your GAD antibody is rising indicates a pretty “active” attack on those beta cells. I hope your new endo gets you on insulin ASAP. It should help extend your honeymoon even longer.
Please keep us posted!