Anybody hear about this yet? Thoughts?
Click on the word "Article" to go to the actual article. Sorry, it looks easy to miss. LOL
Very interesting... I hope they're right!
Very interesting. I just read an article about how cancer might trigger autoimmune T1, but i cannot find a version of the article in english… i love stuff like that, it just helps understand more how our bodies work and why we get diabetes.
I’ve never read about this line of research before. My understanding is that T1D is caused by an autoimmune system misfiring. I’m aware that in a healthy metabolism, amylin is co-packaged with insulin. Perhaps this amylin clumping described in this research is the cause of the immune response that kills off the beta cells.
I don’t understand their claim that T2D is caused by the same mechanism.
Thanks for posting this link. I only wish that I could be around when the first person ties all these disparate medical findings into a single unified theory about what causes diabetes.
Well the autoimmune theory has never really been proven to my knowledge, and really doesn’t undermine what they are saying here… The immune system could be attacking clumped amylin and beta cells are just caught in the crossfire…
If you google Lymphoma and Diabetes 2 you will find lots of sites concerning this link. When I was diagnosed T2 my doctor gave me a printout of a site relating to lymphoma and later T2. I can't find this page now.
Type 1 is immune-mediated destruction of the beta cells of the pancreas, and the autoantibodies (GAD, ICA, IA-2, IAA, ZnT8) are the evidence of autoimmunity. The autoantibodies are not present in Type 2. Phenotypically, they are quite different.
The article itself doesn't really go into why the researchers believe that the cause is the same.
The immune theory has been proven as far as I know.. they have identified specific T cells which attack the beta cells in addition to the auto antibodies that are found on testing although some individuals who do seem to have autoimmune diabetes don't produce them it seems, but not very many.
That doesn’t disprove their assertion by any means though— why couldn’t some people develop auto antibodies to this initial issue and not others? Something has to trigger that immune response and why can’t it be the same thing that’s the initial source of the issue with t2? Further explains why long term t2s often end up insulin dependent over a longer period of time and t1s generally are insulin dependent very rapidly (because an immune attack trying to clear the problem causes accelerated collateral damage) Makes perfect sense to me…
Autoimmune T1 is characterized by antibodies. T1 can result from a number of causes including autoimmne, all resulting in profound loss of beta cell function. The authors seem to only indicate that the mechanism can cause profound loss of beta cells, not about whether it is a suspected cause of any T1 let alone autoimmune T1.
They don't even suggest that it is suggested as a cause of T2, only that it could explain the beta cell loss.
Yes, but glucose is also known to be toxic to beta cells starting at 100 mg/dl and up. So how does their theory fit with glucose toxicity? It would be nice to have a testable all inclusive theory.
Wait a minute, all this type1 stuff was with mice! You know like mouses?? Last I checked I didn't have long whiskers or even like cheese. Cool if its true, but I seen a whole lot of mouse poop that didn't mean crap for us people. What about antibodies? I'll wait till they do some tests with us people.
I looked for the abstract from the original article but was unable to find it. This strikes me as just a theory, and maybe I am wrong (I'm not a scientist), but you have to be pretty careful when staying something causes something else. How do they know this amylin clumping is the cause of both types of diabetes rather than just a result of, say, high blood sugar or beta cell damage or something else that both types of diabetes have in common?
Here's the abstract and a link:
The aggregation of human amylin (hA) to form cytotoxic structures has been closely associated with the causation of type 2 diabetes. We sought to advance understanding of how altered expression and aggregation of hA might link β-cell degeneration with diabetes onset and progression, by comparing phenotypes between homozygous and hemizygous hA-transgenic mice. The homozygous mice displayed elevated islet hA that correlated positively with measures of oligomer formation (r=0.91; P<0.0001). They also developed hyperinsulinemia with transient insulin resistance during the prediabetes stage and then underwent rapid β-cell loss, culminating in severe juvenile-onset diabetes. The prediabetes stage was prolonged in the hemizygous mice, wherein β-cell dysfunction and extensive oligomer formation occurred in adulthood at a much later stage, when hA levels were lower (r=−0.60; P<0.0001). This is the first report to show that hA-evoked diabetes is associated with age, insulin resistance, progressive islet dysfunction, and β-cell apoptosis, which interact variably to cause the different diabetes syndromes. The various levels of hA elevation cause different extents of oligomer formation in the disease stages, thus eliciting early- or adult-onset diabetes syndromes, reminiscent of type 1 and 2 diabetes, respectively. Thus, the hA-evoked diabetes phenotypes differ substantively according to degree of amylin overproduction. These findings are relevant to the understanding of the pathogenesis and the development of experimental therapeutics for diabetes.—Zhang, S., Liu, H., Chuang, C. L., Li, X., Au, M., Zhang, L., Phillips, A R. J., Scott, D. W., Cooper, G. J. S. The pathogenic mechanism of diabetes varies with the degree of overexpression and oligomerization of human amylin in the pancreatic islet β cells.
Ah, okay. So it was with mice. Mice have been cured of Type 1 diabetes more than a hundred times. Obviously, they are not the same as humans. I'll pay more attention when they do a study revealing these types of findings in humans who actually have Type 1 and Type 2 diabetes.
Thanks for tracking down the abstract!
That article wasnt about T2, but T1 and other auto-immune diseases in particular, it stated that it could be that cancer triggers T1, since the immune system has to attack cancer cells that are similar to some of our body cells, and after the cancer is destroyed (we often dont seem to notice that kind of cancer) the immune cells attack other body cells, like beta cells.