Proposal to Drop Type 1 and Type 2 Classification

de Fronzo was a mentor of Dr. Schwartz, one of the authors of the proposal. He mentioned him in one of the 7 videos in this series.

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The proposal is interesting, but how feasible will having 11 different “types” of diabetes be? I might be oversimplifying things, but I view all of diabetes as three different spectrums: beta cell function, autoimmunity, and insulin resistance. A classical “type 1 diabetic” might be low on beta cell function (very few functioning beta cells) and high on autoimmunity, but the degree of insulin resistance varies (some may be highly insulin sensitive, while others may be highly insulin resistant). A classical “type 2 diabetic” might be low-moderate on autoimmunity and high on insulin resistance but may vary on beta cell function (is there beta cell burnout from the high insulin resistance, or is there higher than normal beta cell function because of the insulin resistance?). The big thing that medical professionals need to remember is that if there is very little to zero beta cell function, supplemental insulin is vital for survival, whether it is from a “type 1 diabetic” who lost all beta cell function from an autoimmune attack or a “type 2 diabetic” whose beta cells are “burned out”.

We’re all diabetic, but trying to classify diabetes is like trying to classify every single organism on Earth into two categories: there’s going to be a ton of oversimplification. Not everyone is going to fit in the “type 1”/“type 2” molds, but I am not expecting the medical profession (or insurance) to stop trying to oversimplify everything.

Immune actions is one of the causes attributed for β-cell damage in the article. As for insulin resistance, the summary article mentions that “Only one-third of individuals with insulin resistance will go on to develop diabetes.” I took that to imply that the hyperglycemia in T2s does not appear to be caused solely by the resistance to insulin.

I still feel that viewing this primarily as a discussion about “classification” misses the point that it is a discussion among researchers. These folks are interested in treatment, yes. But mostly they want to try to understand the why and the how of diabetes.

Off to one side of that goal they also are suggesting that treatment goals may not be being reached because the treatment is not a good fit to counter the underlying cause. (Trying to fit round causations into square shaped diagnoses?) But mostly they just want to try to find and isolate those underlying causes.

Type 1 and Type 2 are already classified by cause, and some physicians are reluctant to prescribe insulin for people Dx’d as type 2. If your physician has labeled you type 2 just because you’re middle-aged and overweight, you should get a C-peptide test to see how much insulin you’re producing and a GAD test to see if you have antibodies.

Screencaps of two slides from the video interview series of Dr Stanley Schwarz on Vimeo which Brian posted a link to in his opening post. Apparently this is Dr Schwartz’s “11 interconnecting pathways that contribute to hyperglycemia”.




Oh, one more thing. Here is a link to a list of Dr. Schwartz’s Diabetes In Control articles and videos which I stumbled across today. Adding it to this post mostly as a note to myself for possible future reference. But perhaps it might also be of interest to others …

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They may be classified by general cause, but there are many other factors that are at play in addition to genetics, lifestyle and autoimmunity. Also he was saying in the video series that there are 11 mechanisms involved and each person can acquire diabetes from any one or combination of those. The major point is that all the different treatments available should be for anyone with diabetes regardless of the type or stage. I began seeing Schwartz a year ago in Februray after I had antibody testing and tested positive for GAD. He was the only one willing to treat me even though my numbers were in the pre-diabetic range. He has my diagnosis as abnormal glucose. I think he didn’t use pre-diabetes because he suspected I’m in the early stage of LADA.

What treatments is he using with you?

I agree totally with your idea, Brian. But insurance and health care take forever for significant changes to occur. Diabetes is more of a spectrum. Too much overlap occurring. :slight_smile:

It makes sense to me to drop the classifications (the numbers) and use more descriptive terms. I don’t know many other conditions that are divided so rigidly into classifications, especially with no actual tests being done. I was recently diagnsoed with hyperthyroidism, and even though the endocrinologist (not my own) said she was 99% sure it’s caused by an autoimmune disease (Graves’ disease), she still did blood tests for antibodies and an ultrasound and mentioned another test being done if the antibodies are negative, just to make sure. I understand why tests like antibodies and c-peptide aren’t done in totally straightforward cases of Type 1 like mine (plus, I don’t think the tests were even available back when I was diagnosed), but for adults diagnosed with diabetes it makes no sense to me to just assume they are one type or the other.

I recently read an article about how they are dividing Type 1 into three “stages”, so if anything it seems they’re going the other direction of subdividing things even further.

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I believe that the present classification system is lacking, but I don’t think that there is a point in “pooling” Type 1 and Type 2 diabetes. Diseases are defined by disease process, and Type 1 and Type 2 are completely different disease processes that share the symptom of hyperglycemia. Type 1 diabetes is autoimmune (immune-mediated destruction of the beta cells) and requires insulin for survival. Type 2 diabetes is a garbage can diagnosis, and it would certainly benefit all people with Type 2 to have a work-up that can then be used for defining optimal treatment. My concern about lumping autoimmune diabetes with non-autoimmune diabetes is that the consequences of misdiagnosis for a person with Type 1 autoimmune diabetes are so drastic–death due to DKA, rapid onset of complications, etc.

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bmj2363 I agree it’s a lot more complex than just IR vs autoimmune. My point was that in the past we started with classification by treatment (insulin dependent or not) and then changed to classification by cause (autoimmune or not), and both approaches had problems. It would be nice if each patient had a personalized treatment on the basis of tons of tests that would be performed to determine exactly where one’s defect was, but this is simply not going to happen in the near future. So we need to figure out how to deal with this using the tools we have. Lots of patients never even have a GAD test. Some don’t get C-peptide. When I was Dx’d I asked my doctor for a C-peptide and he refused because he said, “I’d treat you the same way regardless of the result.” So if physicians won’t order a relatively simple test like that (because they want to save money), what are the chances that they’d order a battery of more complex tests?

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Physicians often don’t order tests that we know our patient’s health insurance won’t cover and will cost high 3 to 4 figures (at least). Believe me, I’d like to order a lot more tests than I currently do. But few of my patients can afford the out-of-pocket expense…

The real issue is that 95% of people with diabetes are simply given the diagnosis of Type 2 which as I have said before means “diabetes of unknown cause.” And until the medical field changes the understanding of diabetes and accepts that diabetes is in fact a complex and heterogeneous condition we are unlikely to make progress in more individualized and effective treatment. Until diabetes diagnosis is made more specific there won’t be a relevance to more specific diagnostic tests and treatments. Insurance coverage comes afterwards. That is simply the way the system “medicalizes” things.

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Even if they can’t afford cost of some test, it never hurts to offer it, explaining that it will be expensive. When I had $10,000-deductible insurance and had to pay for lab tests, I always asked what something would cost before agreeing to have it done. C-peptide costs $32 today, according to Lab Tests Direct. What I did was to enroll in a clinical study at Joslin that did a lot of tests, including C-peptide.

But I agree that doing all the tests to determine exactly where each patient’s defect was would probably be prohibitively expensive.

Since I am normal weight and exercise regularly we discussed my diet, which actually was more carb limited then what he recommended so I didn’t need to make changes there. He asked me if I wanted to try an incretin and that I would be using it off-label since it’s a treatment for type 2. I asked him about Metformin and he explained that it would not do much for the inflammation or my lacking first phase insulin response. He went on to explain that in some people with prediabetes it had delayed onset and improved insulin response. Because I have autoimmune diabetes there is no guarantee that it will halt or slow down the beta cell destruction. His goal is to always get the patient glucose levels the closest to normal without causing hypoglycemia. I know incretins are controversial, but I trust him and he is taking them himself. I do feel my treatment is being individualized to my particular circumstances and needs. My husband sees him too for other issues and in the past 6 months has tested with elevated fasting glucose. It will be interesting to see how he is treated since he is overweight with high blood pressure, cholesterol and a family history of type 2. Right now he is in the making the recommended lifestyle changes before meds will be introduced.

To repeat myself, my understanding is that Schwartz is saying that T1 & T2 are not completely different. Different, yes. Completely different, no. He is suggesting that the one common factor in most expressions of diabetes mellitus is problems with the β-cells, hence his use of the phrase “β-cell centric”.

If T2 is only about insulin resistance, then is the claim that “Only one-third of individuals with insulin resistance will go on to develop diabetes” simply wrong? Bad research? Or perhaps it is just inconvenient? :blush:

Again, I think Schwartz disagrees. I think the thinking behind his “Egregious Eleven” is to try to move the focus away from a knee jerk diagnosis and instead try to find out what is causing a person’s hyperglycemia and treat that. To treat the cause(s) of the problem rather than just start throwing stuff up against the wall to see if any of it seems to moderate the hyperglycemia.

As for cost … if something is impossible to do then it obviously never does get done. The first and hardest step tends to always be just getting people to consider the possibility of doing things differently. As long as people are stuck on “it’ll never work”, then not surprisingly it never does work. Funny how that works, eh? :confounded:

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I think the names and numbers are okay, they mean something. I also do believe that it is important to have a proper diagnosis so that the necessary treatment can be applied. There are more kinds of diabetes than are being considered here, and they are recognized and have a different name than 1 or 2. And they sure don’t belong in a pool. Here are the types:

Type 1 Diabetes - which include Maturity-onset Diabetes of the Young (MODY) and Latent autoimmune diabetes in adults (LADA)
Type 2 Diabetes
Gestational Diabetes
Neonatal Diabetes (which include transient and permanent)

In the research and medical institutions and even the NIH and WHO, these defined types matter for very important reasons.

I find the constant recurrence of proposals and petitions to change names or re-define/classify the conditions is just silly. In my involvement and experience in the social networks and diabetes communities it seems the diabetics are the folks who want to change redefine the name/number. And then I read perpetual posts from diabetics who say “Type 1 and Type 2 are not the same”!

I don’t want or need to have my tribe name/number changed, not only because there is no question of how to manage it but because when the cure is found for my type I think it will be found for all types as well. I don’t want to be declassified or dropped :worried:

“You miss 100 percent of the shots you don’t take,” Wayne Gretzky.

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It seems like the discussion is focused more on dropping the labels type 1 and type 2 when I believe the focus of his proposal is on treating the disease based on etiology rather than the category. Maybe I look at it differently since in my field of special education we have gone from treating the label and having a “one fits all” intervention to a non-categorical approach that focuses on interventions based on individual needs instead. I don’t have a strong opinion one way or another on whether we do away with the two main category labels, what I find most important is treating the person based on the factors that are impacting the beta cell dysfunctionality and preventing or halting the progression of the disease. The major hurdle I foresee is finding the markers and using the correct tests to evaluate the individual.

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Wasn’t there a slide that showed this chart and the recommended treatments under each area ?