According to work by Massimo Pietropaolo, in a study of first-degree relatives to T1s, those who tested positive for GAD and IA-2 had a 14% chance of developing T1 after 10 years. Those that had GAD, IA-2 and ICA had an 80% chance of developing T1 after just 10 years. Despite that, overt signs of diabetes, elevated fasting, high HbA1c and/or bad postprandials given any one of the antibody tests is probably enough evidence to predict continued progression towards insulin deficiency. If anyone has other data on the predictive ability of antibodies towards progression to insulin depdendence, I would be very interested.
In my case, I appear to have a steadily degrading fasting (average over a few years). I’ve not seen an average fasting below 100 since a good time I had back in fall of '08. My postprandial response can be highly variable, at times being quite poor and at other times showing seemingly “normal” response. This is consistent with things that I have heard about “honeymooning.”
T1s as opposed to LADA, don’t have a slow onset, and yes, any one of the antibodies is a diagnosis. On the other hand, GAD is specific for LADA and slow onset (i.e. not in a week or two).Apparently no other antibodies are associated (yet) with LADA.
Some T1s are even antibody negative for all tests. GAD antibodies, however, apparently never go away (correct me if I’m wrong). The others can disappear, especially once they’ve done their job of destroying the insulin producing mechanism.
shannon -
May I add to what you are saying. LADA can be associated with any of the antibodies for T1. It’s just GAD65 is found more often than others and yes, from what I have read also, they don’t seem to go away. Also I wonder if they are found more often since they are searched for more often??
ICA’s are more associated with HLA DQ8 and can be transient in nature as Libby (another poster) has seen in her case (however, I do not know if she is DQ8 - my case profile is close to hers and I am DQB1*0302 which is DQ8). LADA will more typically have only one positive antibody and have a greater percentage of protective HLA associated with it. (like DQ8 - high risk + DQ6 - protective) You get one from each parent. LADA will also have more of a genetic connection to high risk genes for T2. All of this is compared to classic T1.
I read a case study where the child was African American (which more often than caucasions come up neg for antibodies) this girl had features of T2 also and was classified as such. After a while - over a year I believe, the antibodies did show up and she was reclassified.
Coming to a point…many people are only screened for T1 one time and then classified as T2 forever or until DKA (that is what happened to that case study child). The one time screening process is not a catch all. There is someone on another board who was neg. and 3 years? into the process he showed up positive.
Someone said the antibody test is the ‘gold standard’ unfortunately, this standard isn’t perfect at all. And I question why doctors are more than willing to state in thyroid disease the antibodies don’t always show up at first. It could be later for thyroid disease but antibodies for T1 are there from the get go (interesting since they don’t even know what the antibodies exactly do for autoimmune process). If you think of it…we are searching for antibodies in blood…not at the source organ they are assoicated with.
I know much of this isn’t a comment to your post.
I highly suggest anyone to get all antibodies checked if they feel their treatment path isn’t working or even if they are curious to see what it might be. In the end, it’s your life and doctors make judgement calls based upon past experiences - whatever those experiences might have been. And not all doctors are willing to look for zebras (LADA) - many don’t know what to do with a zebra when they catch one - so why look?
My GP looked over my labs and saw I had all tests done (I was neg) and said, ‘good, we don’t have to have that done again’. I will get it done again…I can’t for the life of me figure out how I am showing up to have autoimmune diseases assoicated with the genetics for T1 and my diabetes (mild as it is) to be a form of T2 without my T1 associated genes affecting my disease process.
The whole you are x or you are y thing is a mess since diabetes is a mix of genes that interact and T1 and T2 are not caused by a single gene like MODY.
Many people are classic T1 and class T2, however…many isn’t everyone. And many isn’t a percentage.
I actually think separating T1 and LADA is a misconception. LADA is T1, it is just slow onset and for most adult T1s, things are slow onset. LADA is identified by exactly the same antibodies as T1, because (in my view) it is T1. All the antibodies, GAD, ICA, IAA, and IA2 are all highly predictive of T1, whether you think you are LADA or T1, if you have high levels of antibodies, you are problably T1. There are certainly genetic markers that indicate you may be a more susceptible to autoimmune attacks. But make no mistake, if you have an autoimmune attack which destroys your beta cells, you have t1, whether you are called t1, LADA or t2. The only thing which confuses the matter is that there are people who are undergoing autoummune problems, test postive for antibodies, but are not diabetic, and may never be diabetic.
Both articles are interesting. Thank you for posting this information. Even though David is a T1 I was particularly interested in the information on the enteroviral relationship to T2. It seems a lot of people tend to link T2 with a fault in the T2 diabetics lifestyle and I find this unfair particularly on reading how many of the T2’s on this site work, day in and day out, to improve their health. You should post your science daily webpage in the section that Manny used to post his acceptance video.
I disagree that LADA and T1 are the same. There are differences between the two on a genetic basis. Or shall I say there are factors that play into the onset and disease process of LADA that are not factors (due to genetics) of classic T1. That said…you would need a genetic panel and knowledge of what genes are at play for classic T1 and T2. There’s the issue…there is NO such thing at this time. Science is still trying to figure it all out.
I do agree, the whole thing of you can have antibodies and not be diabetic is odd. To me, it proves they really don’t know what the antibodies do.
Case in point - a small study in Canada of gluten sensitivity - this study found antibody neg. DQ8 T1’s were reactive to gluten 50% of the time. Antibodies show up in the much more often diagnosed DQ2’s. SO…really what do these antibodies do??? And are we fooling ourselves by calling them the ‘gold standard’ where you have people like myself at almost every turn I am the opposite of a classic T2 on my lab work but yet I am called T2 and offered T2 drugs that have not much to do with my disease process?
Getting back to each and everyone of us has to be seen as an individual patient.
I really don’t see how a properties of a certain genotype at risk for t1 proves or disproves anything about the relationship of LADA to T1. Both T1 and LADA are characterized by autoimmune attacks leading to insulin deficiency. The autoimmune attacks are characterized by the same antibodies and are indistriguishable.
I don’t disagree with you about misdiagnosis, that is the whole point of this discussion… I’ve been told at every turn that I am t2, that I am insulin resistant and I am fat despite not being insulin restitant nor fat.
I share the same story as everyone here. Was told I was Type 2 even though from everything I had read I did not fit the profile. Further I am an autoimmune person with Grave’s Disease. When I broached my doctor with my suspicions he told me there was “no way you could be a Type 1…and don’t ever ask me again.” I switched doctors to an endo who said that I had a 20 percent chance of being Type 1. I knew right then and there I was correct. Of course the GAD came back positive and at that point I had dropped 15 pounds in two weeks. I was happy and sad all at the same time. Happy that I was right and would now be treated correctly…sad that I would be insulin dependent the rest of my life. It can be a lonely and isolating disease.
Only time will tell. And autoimmunity is autoimmunity - I do agree with that. However, when it comes to treatment there are people with LADA and bloodwork that would point to a T2 process also. My point is and will always be patient first, label second.
I am so not a believer in the antibodies tell all. I was reading on another site and someone was telling a parent of a caucasian child, diagnosed as T1 & was antibody neg. at diagnosis that the antibodies could show up later. This person spoke to an endo about this case specifically before posting. So…if children can be neg at diagnosis why are we so strict about this for adults???
I have TSI’s for Graves (right under diagnostic numbers) but my labs support hypothyroidism without antibodies for Hashi.
So what does that mean? Also had/have a small goiter that is going down since I have stopped eating gluten. Gluten is known or suspected (don’t know exactly were science is at with this) of being a big player in organ specific autoimmune attacks besides Celiac. The grass is greener on the GF side It’s been a good thing to cut gluten out - really good.
My story of misdiagnosis continues. For me, I probably never will get a full answer of what ‘type’ I am. Personally, I will not use another T2 medication. Done with that and I’m starting insulin with or without my doctors help.
Everyone is different and certainly any diabetic t2 or t1 could have some insulin resistance. You are certainly right that you can be a type 1 without having antibodies, but the point is that apparently “signficant” numbers of diabetics test positive for antibodies, are actually t1 but are misdiagnosied as t2 and not getting appropriate treatment. Certainly everyone is different as I am sure you can attest, sometimes a patient can have a complex autoimmune condition that just totally defies categorization. I do hope that you can have more success.
The important point here, and why Kelly started this thread, is that there is a huge number of people with adult-onset Type 1 diabetes who are misdiagnosed as having Type 2 diabetes and given inappropriate and substandard treatment that is detrimental to their health. Kelly is gathering testimonials so she can raise awareness of this problem within the diabetes medical community (you go girl!). A child with new-onset T1 has a high probability of getting correct medical treatment; conversely, an adult with new-onset T1 has a low probability of getting a correct diagnosis and treatment. That is why the antibody test (GADA, ICA, IA-2) is so important for adults, because it is a definitive diagnosis. If a person is diagnosed with diabetes and is antibody positive, he/she has Type 1 diabetes. There is no other test that definitively distinguishes between T1 and T2.
<<May I add to what you are saying. LADA can be associated with any of the antibodies for T1. It’s just GAD65 is found more often than others’>>
Would love to know where you read that LADA can be associated with any of the antibodies for T1. From all I’ve read, it’s only GAD that is specific for LADA, so for me, this is new info. So are you saying that LADA can be diagnosed without GAD? Or are you just saying that if you have GAD, you could also have other antibodies?
T2 doesn’t have any antibodies associated with it, as far as I know. If someone has been diagnosed as T2, then T1/LADA antibodies show up, then it follows they’re a T1, in whichever form you have diabetes. But yes, some LADA patients have features of T2 (so do classic T1s, diagnosed as children or teens, as they get older), especially insulin resistance.
This is often where the term T1.5 comes in - it’s if you have some of the features of T2 with insulin resistance along with the slow onset LADA. Not all with LADA have features of T2 - in fact most thin LADA people won’t have any insulin resistance at all. But some do.
Thanks for sharing this. I know that you have started a similar discussion over on DD (http://www.diabetesdaily.com/forum/type-1-diabetes/40067-how-many-t…). You have an interesting perspective on this being a medical professsional yourself. Conservate estimates of diabetes suggests that at least 10% of the adult US population is diabetic, and with that rate one would reasonably expect even the front line family physicians would be competent to diagnose and treat diabetes, just as most of your patients depend on you for common dental problems. But apparently that assumption is too optimistic. I’d like to think that could be changed.
Yes…it seems logical that any doctor treating someone for diabetes should be familiar with the different types and possibilities. It perplexes me that so many do not. I don’t expect the lay person to know anything about diabetes but medical professionals should. It is epidemic in the US…the third leading cause of death. There must be a solution to this lack of education. I am just not sure how to go about it.
It’s been a good thing to cut gluten out - really good.