I don't twitter. I just never have. But Ellen Ullman (a huge source of information on type-1 diabetes) pointed out that many twitterers (twitteri? what is the plural of people-who-twitter?) at the American Diabetes Association meeting had the tag #ADA2012 or #ADA12. So by searching for those tags, you could see what people were saying about the meeting. That sounded interesting to me, so I looked through about 1000 tweets and found the following ones that I thought were worth commenting on. Many of them have nothing to do with my normal topic of clinical trials aimed at a cure, but all were interesting. Below each tweet, I have included some commentary.
Obviously, the tweets (in green) are not my work, but the commentary (in black) is. Also, I often saw the same tweet many times, and sometimes by different people. So I'm sorry if I'm listing a retweet rather than an original tweet, and some tweeter is not getting the credit they deserve. Finally, I don't know if I was viewing all tweets that had the right hash tag, or just some of them, so I'm also sorry if I completely missed some tweets I should have seen.
Here are some tweets and my comments on them:
kellyrawlings Kelly / Diabetes
Fonseca: 98% of young researchers supported by ADA have remained in diabetes rsrch. (Enhance/support careers for future breakthrus)
This is an important point. A lot of people think of research in a linear way: more money leads to more research. But I think research is more of a "chicken and egg" circle. More money leads to more research, and more research leads to more researchers, and more researchers leads to more money, and the circle rolls along.
Sure, money encourages research and that means there are more people researching type-1. But then those people write more grant requests, and if more are written, more will be approved and funded. If more researchers are focusing on type-1, then more editors and peer reviewers will be familiar with type-1, so more papers will be published, and so on. If more researchers are focusing on type-1, then they will need to hire more post-docs, grad students, and even undergrads, and that means more people researching type-1 in the next generation, and so on.
diatribenews diaTribe
At ADA 2012 ORIGIN results out ~ no difference in CV outcomes or cancer w/ @Sanofi_Diabetes's Lantus. Omega-3 fatty acids also neutral.
About three years ago, some research was published which suggested that use of Lantus insulin was associated with cancer in type-2 patients. That created quite a stir. I reviewed the research available then (from a type-1 point of view), and thought the Lantus-cancer connection was probably wrong. If you are a member of the Brave Buddies group, you can read by previous discussion here:
Here are some tweets and my comments on them:
kellyrawlings Kelly / Diabetes
Fonseca: 98% of young researchers supported by ADA have remained in diabetes rsrch. (Enhance/support careers for future breakthrus)
This is an important point. A lot of people think of research in a linear way: more money leads to more research. But I think research is more of a "chicken and egg" circle. More money leads to more research, and more research leads to more researchers, and more researchers leads to more money, and the circle rolls along.
Sure, money encourages research and that means there are more people researching type-1. But then those people write more grant requests, and if more are written, more will be approved and funded. If more researchers are focusing on type-1, then more editors and peer reviewers will be familiar with type-1, so more papers will be published, and so on. If more researchers are focusing on type-1, then they will need to hire more post-docs, grad students, and even undergrads, and that means more people researching type-1 in the next generation, and so on.
diatribenews diaTribe
At ADA 2012 ORIGIN results out ~ no difference in CV outcomes or cancer w/ @Sanofi_Diabetes's Lantus. Omega-3 fatty acids also neutral.
About three years ago, some research was published which suggested that use of Lantus insulin was associated with cancer in type-2 patients. That created quite a stir. I reviewed the research available then (from a type-1 point of view), and thought the Lantus-cancer connection was probably wrong. If you are a member of the Brave Buddies group, you can read by previous discussion here:
Anyway, the ORIGIN study was a huge study specifically focused on checking out if there was a Lantus / cancer link. It found there was no link, and also no link to cardiovascular problems, either. Several people tweeted this news. They also looked at Omega-3 fatty acids, and found no good effect from those.
Lantus appears to be safe. From a research point of view, I suspect the matter is closed and no one will bother starting any more research on this point. The ORIGIN study was very large, and focused specifically at this particular question.
amdiabetesassn Amer. Diabetes Assn.
Vitamin D deficiency risk factor for diabetes, but researchers found high doses had no impact on development of diabetes.
I'll try to find the actual paper on this, but it fits with the previous research that I know about, and which I've blogged about here:
http://cureresearch4type1diabetes.blogspot.com/search/label/Vitamin%20D
http://cureresearch4type1diabetes.blogspot.com/2010/08/cinnamon-and-vitamin-d.html
Considering the following tweets together, as one issue:
amdiabetesassn Amer. Diabetes Assn.
Vitamin D deficiency risk factor for diabetes, but researchers found high doses had no impact on development of diabetes.
I'll try to find the actual paper on this, but it fits with the previous research that I know about, and which I've blogged about here:
http://cureresearch4type1diabetes.blogspot.com/search/label/Vitamin%20D
http://cureresearch4type1diabetes.blogspot.com/2010/08/cinnamon-and-vitamin-d.html
Considering the following tweets together, as one issue:
diabetesmine DiabetesMine
There was a 23% increase in type 1 diabetes between 2001 and 2009. http://t.co/bg26kTED - AB
sixuntilme Kerri / Diabetes
V. uncomfortable discussion about the rise in T1 dx. PWD finally living to reproductive age cited as a potential "cause." !?!?!!!!
diabetesmine DiabetesMine
Rosenstock responds, D-camp to blame for type 1 epidemic because campers marry each other. Ah, so THAT explains it!
That 23% number doesn't surprise me, and I don't understand why some people do find it suprising/alarming/unexpected. It is well known that type-1 has a large genetic component, and that up until 1920 almost all of the people who were diagnosed with type-1 died before having children. So of course the genetic component of type-1 is growing in the population. That's a good thing, because the alternative is dying young, which is much worse. As people who have type-1 diabetes continue to live longer, more healthy, and more normal lives, the genes for type-1 will continue to become more common in the population.
The real question is this: is that 23% growth expected based on the genetics, or is there some environmental factor which is also causing it to go up. That's important, because it might point to something that can be avoided, which might be a cheap and easy way to prevent type-1 diabetes. Also, it might point to new treatments to prevent or cure type-1 diabetes.
So which is it? We don't know. We can't know, because we don't know the exact genetics of type-1 diabetes. We know several genes that make it more likely, and a few that make it less likely, but we have no idea the exact genetics or the exact rate of type-1 given the genes in the population. So anyone who says "the rate is so high that there must be an environmental factor" is just peddling fear.
The next time somebody tells you that the growth of type-1 diabetes is so high that it MUST be (at least partly) caused by an increase of an environmental factor, ask them a simple question: How much should type-1 diabetes grow, based on the the increased type-1 genes in the population? If they can't answer the question about genetic contribution, then they can't be sure about the environmental contribution.
diabetesmine DiabetesMine
Study shows that pumpers who took more than 12 boluses a day had avg A1c of 7.3%. 7-12 boluses was 7.7%. - AB
Put another way: people who do more testing and more boluses with their pump, have A1cs that are .4 better than those who do less testing and less bolusing. Doesn't sound surprising to me at all. I do have two thoughts:
There was a 23% increase in type 1 diabetes between 2001 and 2009. http://t.co/bg26kTED - AB
sixuntilme Kerri / Diabetes
V. uncomfortable discussion about the rise in T1 dx. PWD finally living to reproductive age cited as a potential "cause." !?!?!!!!
diabetesmine DiabetesMine
Rosenstock responds, D-camp to blame for type 1 epidemic because campers marry each other. Ah, so THAT explains it!
That 23% number doesn't surprise me, and I don't understand why some people do find it suprising/alarming/unexpected. It is well known that type-1 has a large genetic component, and that up until 1920 almost all of the people who were diagnosed with type-1 died before having children. So of course the genetic component of type-1 is growing in the population. That's a good thing, because the alternative is dying young, which is much worse. As people who have type-1 diabetes continue to live longer, more healthy, and more normal lives, the genes for type-1 will continue to become more common in the population.
The real question is this: is that 23% growth expected based on the genetics, or is there some environmental factor which is also causing it to go up. That's important, because it might point to something that can be avoided, which might be a cheap and easy way to prevent type-1 diabetes. Also, it might point to new treatments to prevent or cure type-1 diabetes.
So which is it? We don't know. We can't know, because we don't know the exact genetics of type-1 diabetes. We know several genes that make it more likely, and a few that make it less likely, but we have no idea the exact genetics or the exact rate of type-1 given the genes in the population. So anyone who says "the rate is so high that there must be an environmental factor" is just peddling fear.
The next time somebody tells you that the growth of type-1 diabetes is so high that it MUST be (at least partly) caused by an increase of an environmental factor, ask them a simple question: How much should type-1 diabetes grow, based on the the increased type-1 genes in the population? If they can't answer the question about genetic contribution, then they can't be sure about the environmental contribution.
diabetesmine DiabetesMine
Study shows that pumpers who took more than 12 boluses a day had avg A1c of 7.3%. 7-12 boluses was 7.7%. - AB
Put another way: people who do more testing and more boluses with their pump, have A1cs that are .4 better than those who do less testing and less bolusing. Doesn't sound surprising to me at all. I do have two thoughts:
- Many people think that a drug is successful if it lowers A1cs by .5 (this is usually in type-2 diabetics). However, this data suggests that anyone who is currently using they pump 6 times a day or less, can get that same improvement just by using their pump more. Some people will think it is easier/better to just take the drug, others will want to use the pump more, while still others will want to do both.
- This also suggests to me that clinical trials that don't have a placebo group, need to show more than .5 A1c improvement to be taken seriously. Because someone newly enrollowed in a trial may take better care of themselves than previously. Now that someone is following them, they might be more careful to do more tests and boluses, so their A1c will naturally go down no matter what is being studied. If there is no placebo group to compare to, we might see headlines like "Stinging nettles lower A1c by .4!" when it is really just the diabetic paying more attention that is having this effect.
kellyrawlings Kelly / Diabetes
Berg: Adherence seems best when parents remain involved in adolescent d care even while "training" child to assume responsibility
Makes sense to me. (Although I don't like the the term "adherence". Couldn't they say something like "care seems best" or "care is most effective".)
adamagerika Erika Gebel
Artificial pancreas keeps kids under 7 w/ T1D in target BG overnight 5.3 hours vs. 3.2 w/ usual care, less hypo too(A. Dauber)
birdwingpress Haidee Soule Merritt
I might buy a podcast of Ed Damiano's presentation on closed-loops; I find his voice very reassuring
This is good news for artificial pancreas watchers, especially since that is a large difference. I'll try to find both of these papers paper for an update on AP work in general.
adamagerika Erika Gebel
Treatment for new onset T1D (abatacept)slows decline of beta cells, lowers A1Cs. Benefits persist 1 yr after treatment. (T. Orban)
This is right up my ally, and I'll find the paper and blog on it. My last update on this is here:
http://cureresearch4type1diabetes.blogspot.com/search/label/Abatacept
kellyrawlings Kelly / Diabetes
Patients typicly blame selves 4 not reachng trtmnt goals and may use self-deprecatng language. Such guilt harms self problem solving
A good thing to remember. (I feel like I'm retweeting this, but in a blog. Is there a world for that? Am I blogtweeting it?)
diabetesmine DiabetesMine
1 in 10 kids have DKA each year, 1 in 15 has a seizure. -
My first thought was: Wow! that seems high, but perhaps not. A lot of people did not like the JDRF ad about "dead in bed", and many did not like my analysis of the data they used, which is here:
http://cureresearch4type1diabetes.blogspot.com/2011/12/dead-in-bed-what-is-chance.html
but if the 1 year seizure rate is 1 in 15, then I think that supports a higher-than-we-want-to-admit "dead in bed" rate.
diabetesmine DiabetesMine
Day 2 at ADA 2012- new smaller OmniPod looks awesome! Already submitted to FDA. Can't wait -AT
I'm including this because I know there are a lot of OmniPod users out there who are waiting for this.
diabetesmine DiabetesMine
Not surprising to c up to 50% decline of CGM use in 1st months bcuz of frustrations like lags, inaccuracy, cost, too much info. MH
Sounds to be like the "early acceptors" (the people who are willing/eager to use new technology) are willing to use CGMs as they exist now, but there is a large mass of people who want something smoother and more thought out. My guess is that we will need another generation of CGM improvements before we can entice more people into using them. Remember, that 50% return rate, is for people who like the concept; people who think they needed or wanted a CGM, but then stopped using it when they actually had experience of how it works. That's a high return rate, for any gizmo.
carissa94 Carissa Jones
Novanex, a new company exhibiting at ADA 2012, has developed a non-invasive glucose monitoring technique that works by measuring body temp!
Here's the company's web page: http://novanexinc.com/index2.html and you might want to look here as well: http://novanexinc.com/products.html.
I would be interesting for someone to track how long it takes to get this approved, and what sort of testing is required. (I don't have the time myself: it's not a cure, but I am curious about it, and I bet others are as well.) I will say that over the years I have heard about many non-invasive BG tests, and somehow none of them have actually made it to market.
kellyrawlings Kelly / Diabetes
Change the research vocab: partners not subjects: http://t.co/xqOnFD1Z
I agree with this completely! My blog stopped using the term "subjects" years ago. (At least I hope I did!) Although I don't use "partners"; I think that goes too far. In my mind, clinical trials are done on people; maybe patients, but certainly not subjects. The whole relationship between researchers and patients is changing, but that is way too big a subject to cover here.
a_sweet_life ASweetLife
ADA 2012 update - Dr. Kevan Herold (now at Yale) giving an update on teplizumab, an anti-CD3 monoclonal antibody..
catherine_price Catherine Price
Question: What dose of anti-CD3 did you use? Answer: The right dose.
related tweet:
disclosure: I'm totally biased in favor of anti-CD3 b/c I got it, and it worked.
And here I thought Teplizumab was dead as a cure for type-1, I'll have to see find out more details about what Dr. Herold said.
marimacia Mari Maciá
Esperanza“@diabeticnews: Type 1 Diabetes Stem Cell Treatment Shows Promisehttp://t.co/HxFyPooA”
This is a confirmation of the "Burt" trial which I have blogged on before. People went insulin free for years, but there is a real danger of death (although no one has died in the trials to date). So far, three different groups have run similar protocols and gotten similar results, one in Brazil, one in Poland, and now these guys in China.
You can see my previous blogging on this research here:
http://cureresearch4type1diabetes.blogspot.com/search/label/Burt
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/
Thanks for the shout-outs! There were some interesting tidbits scattered throughout the Sessions!
ReplyDeleteJoshua,
ReplyDeletedid you see this one yet?
http://www.sciencedaily.com/releases/2012/07/120706013709.htm
Please review this when you are able,
Thanks
devi
pdx_dc: that research was done on NOD mice, so I'll list it in my "cured in mice" blog. But it hasn't started clinical (human) trials yet, so it is a long way from general availability.
ReplyDeleteJoshua
Joshua, thanks. Yes, it was done on NOD mice, but is this a new concept that has worked?
ReplyDeleteI couldn't judge how new this idea is..
When I googled "non-depleting antibodies" many drug names popped up - so I am wondering has this already been studied in human trials?
And it looks like it worked very well..in mice.
Thanks
devi
It would seem that there is a new paper out on dr. Faustmans research: http://www.faustmanlab.org/docs/academic/JournalPone0041756.pdf
ReplyDelete