I was diagnosed Type 2 in July 2007 and am now questioning whether I am, in fact 1.5 (LADA). I just got my C-Peptide back. It is 0.381 with a lab value of 0.90 to 4.00. I realize C-peptide isn’t conclusive because Type 2’s over time produce less insulin. I wasn’t able to get antibody tests where I live. Next week I will be going to the capital for my first endo visit and will hopefully get those then.
Meanwhile, I was curious as to the numbers of people who know their c-peptides. Please include whether you are Type 1, 1.5 or 2. Thanks!
Zoe
My c-peptide initially was 2.5 on a 1.1-5.0 scale. 18 months later it was 1.1 non fasting and 0.8 fasting. Both times I was negative for insulin antibodies. I’m going to ask about a re-test for antibodies next appointment since it’s been about 9 months. I’ve decided that it doesn’t really matter what type I am as long as the treatment is working and will work long term, and I think I’ve finally found it. I consider myself type 2 though.
Thanks, Candi. Since I posted this thread my endo has diagnosed me as Type 1. Technically I’m 1.5 but that diagnosis isn’t official yet so she didn’t use it.
Hi Zoe: Good for you for pursuing this. FYI, medically, a person is not diagnosed as having Type 1.5. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus does not recognize LADA/1.5, the Expert Committee includes those in the Type 1 category. So your doctor is correct to diagnose you as Type 1, not 1.5.
Also, you bring up a common myth regarding Type 2 in your first post, which is that in Type 2 insulin production by the beta cells declines over time. This is not true, according to “Latent Autoimmune Diabetes in Adults: Definition, Prevalence, Beta Cell Function and Treatment” in Diabetes Vol. 54, Supplement 2, December 2005. In that article, the authors point out that if you remove people with autoimmune markers for Type 1a diabetes (aka slow onset Type 1 diabetes in adults almost always misdiagnosed as Type 2) from studies of Type 2 diabetics, “beta cell function was unaffected and preserved 12 years after diagnosis among individuals without islet antibodies.” If patients with LADA/Type 1.5 are appropriately removed from studies looking at beta cell function in Type 2 diabetics, there is no decline in production of insulin in the true Type 2 diabetics.
I definitely appreciate your level of research, Melitta! I do respectfully disagree with the correctness of diagnosing Type 1, rather than Type 1.5. I think the ADA, The Expert Committee el al are extremely behind the facts in their lack of willingness to diagnosis LADA. Using Insulin by John Walsh was printed in 2003 (which means it was probably researched a in 2001-8 years ago) and clearly lays out the LADA distinction. I believe the reasons why the “powers that be” are so far behind in their approval of LADA. In the U.S. especially, is that much hinges on managed care, which means that doctors are rigidly bound to the established protocols even when their instincts and experience tell them otherwise. They are also afraid of getting “stuck for the bill” if they do a non-approved treatment or test. Insurance, not medical practice dictates care and this imho is very wrong. Likewise the fear of malpractice and exhorbitant premiums going even higher is a motivator for caution. Perhaps we are talking semantics here, and you are correctly telling me “how it is” , but I am more concerned with “how it should be”. I also have heard on here and elsewhere of diabetics whose endos or even PCPs were willing to buck those tides and correctly diagnose LADA and I say more power to them.If doctors continue to adhere rigidly to the Type 1/Type 2 dichotomy they will continue to ignore that significant 15-20% of people who appear to be Type 2 but are in fact Type 1.5
Ok, stepping down off my soapbox.
If there is no decline in production of insulin in the true Type 2 diabetic, than why over time (average 10+ years) does it become necessary for Type 2’s to go to insulin use?
Hi Zoe: I completely understand why you would disagree with what I said. We both want to see more recognition of LADA/Type 1.5/adult onset Type 1. So many of us are misdiagnosed as having Type 2 diabetes, a different disease altogether, and that is a travesty. My focus has been trying to push the medical/diabetes community to recognize that adult onset Type 1 is two to three times more common than childhood onset Type 1 (always has been, I have a book from the 1950’s that states that). Because in fact they are all autoimmune diabetes, so all the same disease. That is why I don’t see a need for LADA/1.5 versus 1. But I completely understand your point. I don’t actually fit the criteria for LADA–I had rapid onset (hospitalized in DKA) Type 1 at age 35, but yet I was still misdiagnosed as having Type 2.
I do disagree with your comments about “fear of malpractice.” If doctors truly had a fear of malpractice, they would do all the right tests (antibody testing, c-peptide). I am very surprised that no one yet (that I am aware of) has filed a medical malpractice claim when misdiagnosed as having Type 2, when in fact they have Type 1. The diagnostic tools are readily available (at least in the U.S.) to provide a correct diagnosis.
As for why it becomes necessary for Type 2s to go on insulin, I don’t know. I just study Type 1, with an emphasis on adult onset Type 1. Type 2 diabetes is certainly complicated, but it is a disease I don’t have so I haven’t focused on it. The article about no decline in insulin production in Type 2s (when you remove those pesky LADAs from the statistical pool) was an article about LADA.
Good for you for pursuing good care for yourself. We all have to be our own best advocates.
Sounds like we are just coming at similar ideas from a bit different perspective.
I believe I’ve read the LADA article you reference. I think it may be just referencing the much longer time it takes for insulin production to lessen in Type 2’s, not saying it never does.
As for suing the docs for misdiagnosis, unfortunately I think that won’t happen until something awful happens to someone because they were misdiagnosed.
i havent read the other replies yet to this, but i believe the reason that some type 2s over time need insulin is because they end up so resistant to their own, that they need even more then what their body can produce, this is also why so many type 2s use way over 5 times the insulin a type 1 needs when first started on insulin On average a total starting insulin dosing is 70 plus units a day for type 2, and 35 units average for type 1s
The reasons Type 2’s over time need insulin is because their body produces less and less and so they start to become insulin deficient (like Type 1’s) in addition to their problem with insulin resistance.
when your body produces less and less insulin, thats type 1. all true Type 2 wouldnt be called type 2 if you were like a type 1 in the end. I know 8 type 2s and all of them still make high levels of insulin but cant use it right, and 2 are on insulin after 10+ years and they still have high c peptides. Type 1s can develop insulin resistance, but type 2s generally dont lose insulin their body just cant keep up with the amount they need to control their blood sugar, whether because of weight, diet, or little to no exercise
I’m sorry Tiffany, I could see why you might think this, but it is incorrect. Here is a quote from Using Insulin by John Walsh, "Type 2 diabetes is a progressive disease. After a person has Type 2 for several years, insulin often becomes a necessary part of the treatment plan as production gradually declines. Some people may think that a Type 2 who is pout on insulin becomes a Type 1, but this is not true. The differences between Type 1 and Type 2 are more complicated than this."and “Determining when insulin is needed in Type 2 is complicated. The pace at which people lose their insulin production varies greatly. The oral agents used to treat Type 2 diabetes can delay and occasionally overcome the need for injected insulin. However they have not been found to stop the progressive loss of insulin production. Table 27.1 (p.298) shows the natural progression of Type 2 diabetes. Insulin resistance, glucose toxity from high readings and one or more gene defects cause less and less insulin to be produced over time. Since insulin is a critical hormone for good health, it must be injected when too little is produced internally.” Walsh clearly distinguishes Type 1.5/LADA in other parts of the book so he is not including them in this material.
This information is well known and you can easily research it elsewhere. If you choose for some reason not to believe it that is entirely up to you. There are similarities as well as differences between Type 1 and 2 and that’s what sometimes makes diagnosis complex.
Melitta, over time, high blood glucose levels have been shown to kill beta cells. So wouldn’t insulin production decline in T2s with poor control? Isn’t that one of the primary reasons T2s use insulin - to preserve beta cell function by doing some of the work and by keeping glucose levels normalized?
Hi Yvonne: I have never seen a single scientific study that shows that high glucose levels actually kill beta cells in those with Type 2. Big caveat, though, I just study Type 1, with an emphasis on adult onset Type 1. Type 2 diabetes is very complicated, but it is a disease I don’t have so I haven’t focused on it. I do also study the areas where those with adult-onset Type 1 are included in various statistics for Type 2. And John Walsh, author of “Pumping Insulin”, makes that error, too. For example, in the fourth edition of his book “Pumping Insulin”, Walsh uses a 1999 study by R.A. DeFronzo to say that in Type 2 insulin production falls about 4-5% per year. But that 1999 study did not use antibody testing to screen out those people with LADA (Type 1) who were misdiagnosed as having Type 2. The only study that I have seen that studied beta cell function in Type 2 diabetics that correctly screened out the misdiagnosed Type 1s is “Latent Autoimmune Diabetes in Adults: Definition, Prevalence, Beta Cell Function and Treatment” in Diabetes Vol. 54, Supplement 2, December 2005. In that article, the authors point out that if you remove people with autoimmune markers for Type 1a diabetes (aka slow onset Type 1 diabetes in adults almost always misdiagnosed as Type 2) from studies of Type 2 diabetics, “beta cell function was unaffected and preserved 12 years after diagnosis among individuals without islet antibodies.” If patients with LADA/Type 1.5 are appropriately removed from studies looking at beta cell function in Type 2 diabetics, there is no decline in production of insulin in the true Type 2 diabetics even after 12 years. Yes, John Walsh has long acknowledged the existance of LADA, but he is still including those with LADA in information that should strictly be for Type 2.
In Using Insulin which was published in 2003, John Walsh very much seperates LADA information from that of Type 2. I’m confused Melitta because you keep saying you don’t know anything about Type II but then you keep making authoritative statements about things that are basic science and well known facts… There may be minority studies to the contrary, and perhaps one day they will be shown to be correct as so many things have already been shown to change. However, I was trying to share what is currently commonly known which is that over time Type 2’s lose insulin production. I’m not a scientist so I couldn’t explain the technical process of how this occurs, but Type 2’s losing insulin production over time is well documented.
