For all who have been in the 'wars' please read :-)

First off…I loved Manny’s video from today. Very well said.

I’m someone who if I say something… I like research to back it up. Well here is (I was looking for another article but for the life of me I couldn’t find it in my favorites section) Regardless…this one is easy to read and only a couple of years old and has links to other papers. It proves my point that we are choosing sides that really only exist as a line in the sand drawn up to categorize us. If there was no cross over between the genetics of the two types I would be so happy - since I wouldn’t be diabetic.
PS…Please read last paragraph of the article. It sums it up for me :slight_smile:

Thank you

Thanks :slight_smile:
The article I couldn’t find states overlaps with people and all the different technical stuff - it’s quite interesting. I’ll look again for that tomorrow.
As the article basically states we are each an individual patient with our own situations and our treatment should be based upon our own needs.

This is very interesting, but it is also confusing. Does this article mean Type 1.5 has features of both Type 1 and Type 2 diabetes? Which I have heard. Type 1’s can suffer insulin resistance in the morning, and evening hours when a lot of cortisol is excreted. But treatment of Type 1 and 2 is very different. I think a lot can be learned from Type 2s (since they control blood sugars at first through diet and exercise, we can learn from this, particularly when endos tell us just to let her eat the foods she has always eaten). Yes and no. The main thing I see in common is that both types must keep blood sugar under control or they will suffer the same complications. I think of Type 1.5 as a cross-over of sorts between Type 1 and Type 2, though I think Type 1.5 has more in common with Type 1. Was told by the endo they are really two different diseases. We can still learn from each other, regardless of Type.

Thank you for posting this. I love ALL of you! No matter what Type! :slight_smile:


Unfortunately, the article cited is a classic example of bad science. The authors state that some with Type 2 diabetics have the autoantibodies characteristic of Type 1 diabetes. The authors fail to recognize that those “Type 2” diabetics have been misdiagnosed–autoantibodies are only present in Type 1 diabetes, according to the Expert Committee on the Diagnosis and Classification of Diabetes. The authors also state, “both diabetes types share similar characteristics, no single feature clearly discriminates the two.” Except that autoantibodies are the definitive discrimination between Type 1 and Type 2 diabetes. Just because people CAN get published doesn’t mean they are correct, especially when promoting bad science.

Are you refering to this statement? "Moreover, recent studies have shown immune-cell infiltration in islets of type 2 diabetic patients (our unpublished work)."
Since the article came out in 2006 and LADA was known at that point I gave it a pass (they stated it was unpublished - in 2006 with ICA, GAD etcs as being well documented in persons whom were first suspected as being T2 was common knowledge). Even I knew this from looking on the net and I was in the twilight zone for diagnosis of my own case). It’s unknown what immune cell infiltration they were speaking of IMO - BUT that’s an assumption I made that they might be something unknown.
I’m still looking for that other article and that one has more info that links the two diseases together (not for all but for others).
You see…I wouldn’t exist as a diabetic if there wasn’t some linkage. I did not put myself at risk for classic T2, nor does my blood work look like T2. I match up with LADA for other autoimmune disease, however, I do not have the antibodies for T1 to support this and my progression is slow. I can not solve my problems with diet and working out (and I’m considered mildly diabetic) Been there - didn’t happen. Not that I want to be T1 - whomever I am is ok with me. My hand isn’t that bad. Frustrating but I’ll keep the hand I was dealt.
The more I read the more I have come to the conclusion that science is still learning. And in the meantime we have been boxed with two classifications that don’t truely match everyone.
I’m not trying to start an arguement but rather pointing out we as patients are making judgements while the jury is still out (in fact for some aspects of this disease - they jury hasn’t even heard the evidence)

Yes, it’s been proven that T 1.5 has features of both.…

My point about all of this has been the more we think we are totally different the less we can learn from eachother and it’s dangerous for doctors to pigeon hole people - been there, DONE with that. It’s apparent that there are cross-overs with diabetes and it’s not limited to just LADA.

It appears that the T2’s who do the best at control are doing much the same as the T1’s who are also in control. Of course, each of us has different issues - so the technique is modified accordingly.

Or better said…eating a candy bar and a piece of pizza then washing it down with a coke is NEVER good for any one of us :slight_smile:

I’m probably as close to LADA as one can get without being it. If you were to meet me you would be so surprised that I’m diabetic. Give me just that piece of pizza and test me…results not good.

I think if the doctors who care for us see us for what we have (our specific case) rather than put us in a slot and look no further we would all be better off. I would have never discovered I had gluten sensitivities (celiacs) if I allowed that. Celiacs is commonly associated with T1 not T2.

Thanks Jill :slight_smile:

Jan, this statement misses the one point of the article, which is that the differences between T1 and T2 are only a matter of degree. The type of treatment should not be used to define the type of diabetes. Some Type 1’s might also control blood sugars with diet and exercise.

This articles argue for regarding diabetes as a continuum or a scale of overlapping components. A person may, for instance, simply be insulin resistant but producing all the insulin they could need. There are degrees of resistance. At the other end of the scale a person may be insulin deficient but be highly insulin receptive. There are degrees of insulin deficiency, from 0 to plenty. Each of us then falls somewhere along the scale of insulin resitance/insulin deficiency. The type of treatment we respond to should not be used to classify us at T1, T2, T3 nor should the classification define or narrow our treatment. We should each receive the treatment we need based on where we fall on the scale.

That’s how I read it.


Terry -
I couldn’t agree with you more. From my own experience I know how dangerous it is to assume and to treat. On GP nearly did me in my doing that. I would laugh about it but it’s too serious of an error. That’s what happened to me. I was lucky, my mom is an RN and she noticed things didn’t add up. Then I braved it and keep going until I got answers. I’m classified as T2 but I’m insulin sensitive. Classic T2 treatment options are not the best course of action for me. Neither is the classic T1 option - insulin. We all are a mix somewhere. Even with T1, not all have the same HLA risk factors.

Hi Kathy: I completely appreciate and agree that much remains unknown about diabetes. We don’t all fit in some box, and it is far more important to get appropriate treatment than figure out which box. I am just pointing out that Type 1 autoimmune diabetes has characteristics that do distinguish it from Type 2 diabetes. If autoantibodies are present (GADA, ICA, IA-2) the person has Type 1 diabetes; antibodies are not present in Type 2. Antibody testing is easy, relatively inexpensive, and conclusive. Then there is Type 1 idiopathic diabetes, where antibodies are not present. But in more than 90% of new onset Type 1 autoimmune diabetes, at any age of onset, antibodies are present. But good for you for persisting to get the right care for yourself, and yes the fact that you have celiac would make one suspect autoimmune diabetes, since they are closely linked.


She was diagnosed with Juvenile Diabetes at 8. I was told point blank it was a totally different disease by the endo. The diabetes clinic she goes to treats both Type 1 and Type 2 patients. I have to trust the endo, who is tops in her field, over one article. So I know where she falls on the scale. I think MODY, LADA, Type 1.5 (which I thought was LADA) do fall in the middle of the continuum, JD being on one end of the continuum and Type 2 on the other. I do read the Type 2 forums for information about controlling with diet or exercise as I think Type 1s may be able to use that information. The insulin resistance many Type 2s suffer from, she can also suffer from if she is high, always in the morning before breakfast and also from 6pm to 12 midnight. There is a lot to learn from Type 2s, I agree. Just because the types are different does not mean one type should discriminate against another type. Regardless of whether or not we have more or less in common. Yes, I do see some overlapping. I don’t see that much, in her case, though. Regarding diet, she can eat 70 grams of semi-crappy food without it having an effect on her BS (such as lasagna, potato chips or icecream); or she can eat a nice, healthy piece of fruit and go sky high. Not that she would ever have 70 grams of icecream or chips alone…I still think this article may be more useful to LADA, 1.5 or MODY. There is no confusion about whether you have Type 1 or not if you are diagnosed as a child in ketoacidosis.

I agree with this. I found the article very confusing and it did not mesh with what I had been told.

At the end of the day, the moniker you stick on your diabetes doesn’t really matter. Either you need (or probably should be on) exogenous insulin (IDDM), or your body is producing sufficient insulin for your needs, if you maintain proper diet and exercise (NIDDM). To some extent, any part of a treatment that works in IDDM to increase beta cell mass will help NIDDM patients, and, in theory (though it would probably be a piss-poor idea in practice) lowering insulin resistance in IDDM patients would be good as well, so that insulin dosages can be lowered. NIDDM can progress, for a number of reasons, to IDDM, though the reverse doesn’t seem to be the case.

The distinct separation into T1 and T2, classified based solely on antibodies, is a relatively meaningless distinction. As a very slowly progressing LADA/IDDM patient, I still have to worry about putting on weight and becoming insulin resistant; in fact, I postulate that my original dx was probably insulin resistance and stress, rather than solely autoimmune factors, based on duration of honeymoon. I’m almost a year into this ride, and if I go beyond 6-7 units of Lantus, I’ll get morning highs in the 140s that I absolutely can’t break and run higher sugars all day, as if though I’m dropping low and rebounding hard. My dx went from T1, to probable T2, to LADA/wtf? - and it hasn’t affected my treatment plan in the slightest.

The only time that there’s any reason to distinguish based on pancreatic function rather than on treatment is at diagnosis, since putting a T1 on oral meds won’t help, and, in the long run, can kill the honeymoon period but good and have long term deleterious effects.

The antibody/lack thereof distinction is important for research purposes, but for the “end user,” does it really matter? I’m still going to take those 5-6 units of Lantus either way. I’m still low carbing.

I guess my ultimate point is: treat the patient, not the disease. My lab numbers would indicate that my pancreas should be producing slightly less insulin than the sole of my shoe. A year later, it’s still sorta chugging along.

I also believe there have been some recent studies that show some other cross-over, but I may be misremembering.

Hi Dov: I really just advocate for antibody testing at diagnosis for exactly the reason you state, to get correct treatment. Type 1 and Type 2 are different diseases with different genetics, causes, treatments, and cures. For myself, I want to know which disease I have, and I advocate for antibody testing (and c-peptide testing) in newly diagnosed adults just so that the appropriate treatment, exogenous insulin, is given. So many adult-onset Type 1s (LADA/1.5) are misdignosed as Type 2 and undertreated. The result is poor control, which hastens the onset of complications and can result in death due to DKA. Preventable if the correct diagnosis and correct treatment occur.


Yes, T1 and T2 are different disease processes. The point of this article was to show that there are overlaps and that care should be patient based rather than category based.
Type 1.5 and LADA are generally considered the same thing.
We are on common ground with our thinking about things :slight_smile:

Melitta -
I’ve been researching more on my situtation and I’m coming up with people who are just like me who are antibody neg BUT they were given the LADA diagnosis. Not by GP’s either…by their endos, one doctor stated the antibodies could show up later. Now I do know ICA which is more common for DQ8’s can be transient (from what I have read). So I’m kind of questioning how much of a ‘gold standard’ the antibodies are. Research hasn’t proven what they do but I am seeing that there is some protien produced by insulin the T cells go after. Makes me think…studies have shown that DR4 / DQ8 is expressed more with T2 than controls but if you look further…family members of T1’s that are diabetic and have DQ8 lack insulin more than insulin resistant and tend to go to insulin use much sooner than classic T2 - however they are classified as T2 because they lack the antibody markers and they come from mixed T1 / T2 family backgrounds. Also there is another study of fathers with T2 passing on to their children who are T1 this DR4. Again, I’m questioning…the parent is neg. for the antibodies. Maybe with the DR4/DQB1*0302 it’s really always T1 / LADA if the diabetic patient has this gene? (of course given the correct extention of DR4 since I think one of them is not a high risk factor with the DQ8 but that’s really getting technical) Then…with certain ethnic groups…they are less likely to present with antibodies as children and they are classified T1 not T2. Lastly, very young children under the age of 2…there is a number of them who do not present with antibodies.
I have more than Celiacs as an autoimmune issue. Other isn’t big (psoriasis) and my subclinical hypothyroidism looks to be improving on the Celiacs diet (hope this is true). Psoriasis is another funky type of thing - it’s separated into T1 and T2 also. Imagine that! T1 has more of an HLA connection & tends to have other family members affected and T2 is more associated with enviromental factors and obesity. Same disease…different factors going into making it appear. Sound familiar?
There is so much yet to be learned. I’m just hoping they are on the right track.
With my own case if I am LADA it’s on the light side and I’m sure whatever genetics I probably have for T2 got me started but I think the T1 high risk genes are working on me now. For now I’ll still call myself T2 unless there is even more proof otherwise.
I know I’ve taken this to the extreme but I’m mad. I’m slowly getting worse and it doesn’t make sense at all. Oh well.
Best to you!