We simply must not assume that autoimmunity will continue to occur without the presence of the trigger.

Even if a transplant is still needed, removing the trigger (and thus autoimmunity) will improve the success of a transplant. If one’s own stem cells are used, no anti-rejection drugs will be required (assuming the autoimmunity is removed with the trigger).

Have you considered that we will only have clinical reactions to any antibodies present only with the presence of the trigger, or that these antibodies will disappear if the trigger is removed?

Again, look at Celiac Disease, the only autoimmune disease in which the (second) trigger is known. Remove the trigger, remove the active disease process.

I am not sure why one would assume that autoimmunity is set in motion from only one event. New evidence suggests that it is constant, and many T1’s have constant beta cell turnover with constant autoimmunity (Joslin 50 Year Medalist Study). In other words, the body is trying to constantly heal itself.

Current human islet transplants are futile and will never be a cure. They fail for a number of reasons, including poor beta cell mass and health, toxic diabetogenic anti-rejection drugs, and yes, continued autoimmunity. Again, dumb career researchers in the lab are not thinking clearly. All Edmonton Protocol transplants do is add more fuel to the fire.

Once you have auto-antibodies (e.g. GAD65) on board, you’ve got trouble. As long as those antibodies are present, they will recognize islet cells as foreign. That’s one of the problems with transplanted islet cells, no?

There is much evidence that a virus may be ONE of the triggers involved for typical autoimmune diabetes. The food proteins gluten and casein are also implicated in many studies.The TRIGR study is under way right now. A lack of Omega 3 and Vitamin D may be the clincher in someone genetically prone and exposed to all of the triggers.

Too many people look at autoimmunity the wrong way. They are taught that is an “organic” misfiring of the immune system. That may be partially true in a sense, but the trigger may STILL be present and continuously causing the disease.

We *may* have to modulate the immune system, but we *may not* have to as well.

I have to use Celiac Disease again, which is genetically related to Type 1 and the only autoimmune disease in which the trigger is known (Celiac also seems to need an initial trigger such as a virus). Basically, in people prone to autoimmunity, anything that can increase the “leaky gut” and exposure to food proteins/viruses/factor x may bring on the disease onset. This may be stress, illness, trauma, etc.

In people with ACTIVE long standing Celiac, you take away the trigger (gluten), and the disease goes into remission and the body heals (in most cases). Not in all cases (Refractive Celiac), but most.

So I am not sure why med schools keep teaching the theory they do when all recent data says something otherwise.

I’m not saying all people can regenerate beta cells, most likely euglycemia from a temporary transplant/a permanent transplant/beta cell regenerating drugs will be needed.

But what I am saying is that many people are STILL looking at autoimmunity the wrong way. The way I once did.

This is why we have made so little progress until now. We were barking up the wrong tree.

I know memory T-cells are an issue…but with no trigger, they may not be…

All I’m saying is that the “old way” of seeing autoimmune diabetes is not helping the cause, and the track record for past research shows. New research is what people should be focusing on.

As for autoimmunity, once your body has antibodies to an antigen, it will continue to recognize it as foreign and rally the immune defenses each time it detects the antigen. (The efficacy of vaccines is due to this feature of the immune system.) So, even if the beta cells repopulate, they are doomed once the immune system gets a whiff of them.

It’s theorized that knocking out memory B cells (through immune modulation) will cause the immune system to stop recognizing beta cells as foreign. But again, that’s experimental, and it’s certainly no cure.

It’s true that I don’t find diabetes debilitating but I also don’t find it a cinch to manage. I am not a brittle diabetic, however. My BGs are responsive to my management. I’m grateful for that. As long as I can live complication-free I’ll count my blessings.

I personally think the AP is a pipe dream, a waste of money, and a load of crock (sorry to burst anyone’s bubble). Ditto on the first post. I’m not going to attack those who support JDRF. I’m sure the little guys at the bottom fundraising for little Johnny mean well. But if you look at the bigger picture, all JDRF has done was fund the DCCT, which:

-Was common sense.
-Found that some complications may be autoimmune or linked to genes or c-peptide levels in some cases (not attached to A1c levels at all).
-Gave Big Pharma a great platform to push more injections, test strips, and the like. Perhaps Big Pharma paid for the DCCT? So where does all of that JDRF millions in donations go?

I know I can’t get anything from them other than a letter asking me to organize a “Walk”. It’s like a perpetual scam.

Nevermind new technology, the old still is not perfected. My pump was recalled twice this year and died 3 times. I have a diabetes association newsletter talking about the “artificial pancreas”…in 1967. If we could do it, we would have by now.

I personally think that we have made such great strides in autoimmune diabetes that it simply doesn’t make any sense to focus on another piece of junk I have to buy to keep me alive. I think we’ll see a feasible “cure” before we ever seen an AP.

P.S. Lauren: You are looking at autoimmunity the wrong way. If the theory that beta cells regenerate is true, then removing the trigger (assuming it’s possible) should stop the autoimmunity. In Celiac Disease, the disease (generally) goes into remission with the removal of gluten from the diet. Simple as that. Modulating the immune response without removing the trigger is the most stupid thing scientists have ever tried to do. Doomed to fail. And Type 1 CAN be “debilitating”. Some of us can have very unstable BG’s and are prone to seizures. It’s not always as easy to manage as people have been brainwashed to think. We have new generations of people clueless about how hard it really is to live with T1, and thus, no incentive to understand why we need a cure.

Read the article (linked below) to understand that progress is being made in the field with tools that were designed based on human factors studies and behavioral psychology. The result is fewer hypos, less time spent hyperglycemic, less time managing, and efficiencies for the clinic staff and endos.

Diabetech’s technology (my company) is only part of the solution. Ultimately, superior results come from expert application of the tools and the easier the tool the easier it is to maximize results.

The story ran a few weeks ago and South Texas doesn’t seem to get its fair share of mainstream press:

http://diabetech.net/pdf/diabetech.business.journal.pdf

Any meter or CGM feeds the data warehouse. All pumps list too. Multiple ways and programs for using data need to be available.

Sadly those making the equipment see value in ‘proprietary.’ They invest in litigation of “their” systems over better products.

If MAC, PC and cell phones all speak internet, why can’t our meters, cgm, pumps and software speak a common diabetes language.

JDRF’s AP project will do a huge amount of good if it only helps bring standards to OUR data.

Your Diabetes May Vary, so should the tools you have to address it.