I'm experimenting with a second blog, which I'm calling:
Cured In Mice! you can read it here: http://t1dcuredinmice.blogspot.com/
Although the formatting will change a little over the next few months.
My goal is to have one blog entry for every treatment reported to have cured or prevented type-1 diabetes in NOD mice, or any other animal.
Each entry will have the date the cure was reported, one or more links to news reports, press releases, or research papers, and maybe a paragraph on the cure, or quotes from the articles. But I don't plan to put in analysis or discussion in those blog entries. I'm leaving comments open for now, but I really only want comments to note when one of these cures moves to a later stage of research. I may close comments entirely in the future.
Each title will be of the form TREATMENT by DOCTOR at RESEARCH INSTITUTION. Two examples:
Glyphosine by Michels at Barbara Davis Centre for Childhood Diabetes
Escapsulated Beta Cells by Nuvilex at SG Austria
I will use tags to keep track of the basic type of cure being reported. For example, the tags "cure", "honeymoon", and "prevention" will describe when the intervention is effective. There will be tags for the basic types of cure "encapsulation", "immune modulation" etc. And tags for the animal involved (such as "BB rat", "NOD mice" or just "mice" if the exact type is not known.
Why a "Cured in Mice" Blog?
This blog exists because of frustration. My frustration at constantly hearing that type-1 diabetes had been cured in mice (again), but never hearing that it was cured in people. My way of dealing with this frustration is to try to keep track of the number of times people cure type-1 diabetes in animals. After all, the first step to understanding something, is to catalog it.
At the very least, this blog will help readers keep track of how many mice cures are developed each year, what happens to them, and how long it takes to happen. I hope that the data found will fuel other types of "research into research" on type-1 diabetes. It will also help track how long it takes to move from animal to human trials. Whenever a human trial starts, I'll be able to go back to this blog, and see when the same thing was first successful in animals. You can think of this blog as raw material for future research into type-1 cures in mice.
How You Can Help
If you hear of a cure for type-1 diabetes in any animal, then please shoot me a quick email. All you need to do is put "Cured in Mice" in the subject line and put the URL where the news was reported in the email. I can get all the information I need from there. Don't worry if you think others have already sent it in. I'd rather get extra emails than not enough. I'm especially interested in research done outside the USA or reported in languages besides English. (Because I don't read any other language, and get most of my news from USA-centric news sources, I'm much more likely to miss research that is reported on in another language or country.)
Getting Either Blog Emailed to You
If you're reading this on my blog web site, you can easily sign up to get these blog posts sent to you (either this "Cure Research" blog or the new "Cured in Mice" one). Just enter your email address in the "FOLLOW BY EMAIL" box on the right. In the past, I had to have a Google email group for this, but that's a lot of work that I don't need to do any more.
If you are getting this as part of the Google group, please add your email (as above) and unsubscribe to the Google group. I plan to shut down the Google group sometime in 2012.
Reminder About The Blog
There three ways you can help with this blog:
First, tell other people about it! Heartfelt testimonials are the best advertising.
Second, tell me about any clinical trials you know about that are not already covered here.
Third, ask me questions that you have. This tells me what I'm not explaining well, and where I need to put more information into my posts.
Joshua Levy
All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions. My blog contains a more complete non-conflict of interest statement.
Clinical Trials Blog: http://cureresearch4type1diabetes.blogspot.com
Cured in Mice Blog: http://t1dcuredinmice.blogspot.com/
13 comments:
I love your commitment to research and helping people understand what's happening. I always feel incredibly informed after reading your posts. Thank you so much!
This doesn't have to do with mice...and probably isn't considered "true cure" stuff, but there's been a lot of hype about managing T1 and eliminating the need for insulin with diet therapies...Bernstein, Paleo, Diabetic Alkaline. I'd really like to know what the differences are, and any studies out there that have shown long term effectiveness.
I'm not interested in a restrictive diet lifestyle for my family, but I am interested in an article that lines them up with a frank discussion.
I love this blog, love sharing it, and will definitely keep up with you and the mice :)
Maybe it's worth noting the problems with the NOD mouse and other models:
"A further problem is the lack of an appropriate animal model. There are many successful treatments and prevention methods using NOD mice, but those failed to yield the same results in humans [Serreze and Chen, 2005]. The pathogenesis of T1DM is different in humans and NOD mice. In NOD mice the genetic factor is much stronger, there is a female predominance, and the inflammation of the islets is different and more profound than in humans. The T1DM rat model is the BioBreeding (BB) rat, and in this animal the diabetes develops with the lack of CD8+ cells, thus its pathomechanism is rather different [Serreze and Chen, 2005]. Using other animals, such as dogs or monkeys, is not feasible for ethical and financial reasons."
http://www.medscape.com/viewarticle/741510_9
Also it's often been pointed out that since you can "live" without a functioning pancreas, with insulin being so successful, the bar for a "cure" in T1D is that much higher. Suppose T1D were autoimmune juvenile Rheumatoid Arthritis: monoclonal antibodies would likely be the norm in treatment. And very likely some cocktail of mostly existing and already approved monoclonal antibodies, vaccines and small molecules would be improving lives, preserving islet function and we'd be moving incrementally towards insulin independence - my definition of cure - trading a couple of pills a day or injections a week would be a massive improvement over the complications of insulin therapy.
Case in point: teplizumab in phase III had 5% insulin free at one year in the treatment group vs 0% in placebo (P=0.03). Yet for some reason the Phase III trial used a dose ten times lower dose than earlier trials. Any surprise it did not meet its endpoints and criteria for success? I'm sure at one point many cancers had 0% survival rates, and 5% would have been considered a breakthrough.
Maybe it's worth noting the problems with the NOD mouse and other models:
"A further problem is the lack of an appropriate animal model. There are many successful treatments and prevention methods using NOD mice, but those failed to yield the same results in humans [Serreze and Chen, 2005]. The pathogenesis of T1DM is different in humans and NOD mice. In NOD mice the genetic factor is much stronger, there is a female predominance, and the inflammation of the islets is different and more profound than in humans. The T1DM rat model is the BioBreeding (BB) rat, and in this animal the diabetes develops with the lack of CD8+ cells, thus its pathomechanism is rather different [Serreze and Chen, 2005]. Using other animals, such as dogs or monkeys, is not feasible for ethical and financial reasons."
http://www.medscape.com/viewarticle/741510_9
Also it's often been pointed out that since you can "live" without a functioning pancreas, with insulin being so successful, the bar for a "cure" in T1D is that much higher. Suppose T1D were autoimmune juvenile Rheumatoid Arthritis: monoclonal antibodies would likely be the norm in treatment. And very likely some cocktail of mostly existing and already approved monoclonal antibodies, vaccines and small molecules would be improving lives, preserving islet function and we'd be moving incrementally towards insulin independence - my definition of cure - trading a couple of pills a day or injections a week would be a massive improvement over the complications of insulin therapy.
Case in point: teplizumab in phase III had 5% insulin free at one year in the treatment group vs 0% in placebo (P=0.03). Yet for some reason the Phase III trial used a dose ten times lower dose than earlier trials. Any surprise it did not meet its endpoints and criteria for success? I'm sure at one point many cancers had 0% survival rates, and 5% would have been considered a breakthrough.
Hi Joshua - I can't find your email id anywhere (easily), so maybe add that prominently on your blogs? :-)
Anyhow, the reason for trying to reach you is - have you read this? http://www.biomedcentral.com/1741-7015/10/3/abstract
What do you think? even has peptide numbers in the actual paper... how does this compare to.. for example Dr. Faustman's C-peptide improvements among others... thanks.
pdx_dc: I hope to have a blog on that ready by Thursday. Blog will not include direct comparison with Dr. Faustman's results, although I have thought about it. (for one thing, Dr. Faustman used pmol/l, while Dr. Zhao ng/ml). Maybe in another blog.
Joshua
Josh, very notable effort, you have a big thank you from me and I'm sure to represent millions of parents out there.
Not mice:
http://www.eurekalert.org/pub_releases/2012-01/ljif-lji011112.php
A Reply to the blog about Dr. Faustman is on its way. I have simply asked her to address each point brought up in the blog. She is busy, but will email me a reply to Josh's blog regarding her research. I will then, with her permission, post it on Brave Buddies. Her research is exciting and I believe that she will be the one to CURE Type 1. Stay tuned.... Tammy Taylor
Tammy, while I'm sure Dr. Faustman's reply will be interesting, the important important thing she could do would be to publish the results from her BCG trial. Another important item would be the paper work from the FDA limiting her trial to 3 people. She says they did that, so she should be able to show the materials they sent her. Another useful thing would be the ADA page where it said that she could not distribute her poster after the ADA convention. I looked for this, but could not find it. Finally, a specific explanation for why the phase-I trial has taken so long (month by month, year by year) would be nice, as would a specific explanation of why they are not distributing the poster. -- Joshua
I deleted the comment by Charles Weber just before this. It was a link to some of his own pet theories as to what causes diabetes. For a number of reasons, I did not want it on my blog, so I removed it. --Joshua
Dear Joshua Levy,
I can only conclude that you think my “pet theories” have no chance at all of being valid. I assume you think that some or all of the information acquired by scientists in my dissertation was invalid, incorrect or corrupt. So which facts were invalid? You do agree that some poison or infective disease must be causing diabetes, do you not? You can not possibly believe it arises by magic, say the wicked witch of the west waving her magic wand, for instance, can you? What do you think causes diabetes?
Sincerely, Charles Weber
Actually, I don't know what the chances are that your pet theories are correct. I can't see the future. What I can see, is that there are no clinical trials suggesting that either chili peppers cause type-1 diabetes or a lack of copper causes it, or both together cause it (which is my summary of your theories). Since there are not clinical trials supporting it, I don't want it here.
As for the cause of type-1 diabetes, I think there is strong evidence of a genetic component of cause, and there is a strong evidence of an environmental component of cause. As for poison or infective disease: maybe. Those are both environmental issues, but it could some other environmental issue, also.
Joshua
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