(I'd actually recommend giving the paper a skim even if you're not trained in biology. The Introduction and Discussion should still be very comprehensible, and while the Results do suffer from the alphabet soup problem (as do most biological papers), the overall structure of the evidence should be clear - pay particularly close attention to Figure 5A and Figure 6A-C).
The key next challenge appears to be the creation and testing of appropriate delivery device that can enable persistent survival of the differentiated cells while still enabling them to sense blood glucose levels.
Sure wish there was some way that I could help fund this research. I don't know if kickstarter campaigns are cool at Harvard, but they would have no shortage of backers.
This does reinforce my idea that medical technology and research is advancing at an exponential pace, faster than the evolution of diseases can keep up. A treatment for type I diabetes seemed to be impossible. A diabetic's pancreas betrays them and begins killing the cells that produce insulin. There's no pill or surgery that can stop that, nothing short of reprogramming pancreatic cells. And yet, here is a promising sign of a cure! It's really amazing, and the future probably holds even more legitimate medical wonders. We might be the one of first generations to live to 100+ on average.
Type I diabetes is expensive, ~$5,000/yr without insurance. Anyone with this diabetes would probably be willing to pay any amount less than that every year for the rest of their lives in exchange for this treatment. Talk about customer lock-in! Most of the controversy over stem cells has been centered around federal funding, but treatments for chronic and costly diseases will pay for themselves several times over. For now I can only hope that this research advances fast enough to help everyone who is currently dependent on insulin.
If this is truly promising, I expect they'll have to beat a path through all the aspiring donors to get to work each day. The problem with biomedical research as I see it is not a lack of donations, it's that the typical case is that the results people are desperately seeking simply can't be bought for any amount of funding. If this succeeds in curing diabetes, it will be on par with the greatest achievements in medical history (what disease was the Salk vaccine for again? Polio?). Every foundation on earth will want a piece.
There are many causes worth donating to. I'd recommend taking a sober look at charitable options and give to one that's relatively underfunded.
Without insurance, blood glucose test strips cost $40 for 25. I test myself 8 times a day. That's nearly $5k/yr right there. It is really expensive... Thank God for health insurance
If before using a strip you make a prediction how accurate is it? I only ask because I know diabetics who say my blood sugar is low/high but I am guessing that's not enough information in your case?
Edit: I also know a diabetic that went blind, it's a serious disease and I am all for staying on top of it. I am simply curious in this case.
Not a diabetic, but I interact with folks who are on a regular basis.
You know if you are getting into extreme territory (up to a point... eventually the confusion that comes from hypo/hyperglycemia means you won't be aware of it).
The danger of diabetes is that you can end up perpetually a little high, which is what causes all the nasty osmotic side effects (blindness, slow healing (leading to infection and amputation), etc...). You won't be able to know that without testing.
For many diabetics, the amount of insulin they inject depends on their blood sugar. There's no way you could 'sense' it to the level necessary to control dosing.
You generally always have a running estimate in your head, "I ate two tacos, took three units of Humolog, needed to correct down an extra 50 points with the extra unit (because I undershot last meal), etc."
But there are factors that you have a more difficult time predicting your levels with, like exercise, illness, the type of carb your eating (some carbs take longer than others to hit your system, but if you treat all the same, you insulin will hit you faster than your carbs and you're now hypoglycemic).
Truly staying on top of your numbers and this disease means constantly checking. You can always make a guess, but when the risk of serious short-term and long-term complications hang in the balance, you tend to want to know for sure.
> Melton expressed gratitude to both JDRF and the Helmsley Charitable Trust, saying, “Their support has been, and continues to be, essential. I also need to thank [research supporters] Howard and Stella Heffron, whose faith in our vision got this work under way, and helped to get us where we are today.”
Seems like they certainly accept donations. Perhaps you can support the JDRF or Helmsley Trust. If not why not contact them directly to ask whether they accept donations directly?
Good point. There should be plenty of diabetes research foundations to donate to -- JDRF would top my list. If you donate to one of those, it's like buying a mutual fund. Your investment is diversified and has the best chance of doing some good. Give to JDRF.
I thought it was the immune system that betrayed type 1 diabetics, not the pancreas. I recall the leading theory (at least used to be) that insulin producing cells had the bad luck to look like a cold virus or some other malicious infection, and after the person contracted a similar looking infection, the body just cleaned up the beta cells, thinking they're also malicious.
You're right that type 1 diabetes has autoimmune origin. The presence of autoantibodies can be used clinically to distinguish it from the other types of diabetes mellitus[1].
Can anyone with knowledge about the topic shed some light on it and tell if it's really a big breakthrough or just like another PR post by labs to attract and justify more funding?
Not only are islet cells able to be mass produced (one transplant means 150 million cells need to be created), but the challenge of the body not simply killing off these cells too through the device created at MIT really seals the deal.
Without the implatable device, this would not be as big of a breakthrough, but having both the challenge of mass producing these cells and ensuring they are able to survive after transplant without use of immunosuppressive drugs (read hardcore side effects) effectively solved makes this a real, viable solution to this problem.
Type 1 Diabetes is due to the total loss of insulin-producing pancreatic beta cells. The loss is a result of autoimmune destruction. This brings up the following questions:
1. Will the transplanted cells produce insulin in a human host?
2. Will the transplanted cells be targeted by the host's immune system and be destroyed just like the original beta cells?
3. Will the beta cells produce insulin in response to the same regulatory pathways as original system? One major problem with self-injected insulin administration is overdose.
Those are the questions I'd look to answer in the future.
I am Type 1 Diabetic. I have done some research, but am by no means an expert.
1. Yes
2. No. "Melton said that the device Anderson and his colleagues at Massachusetts Institute of Technology are testing has thus far protected beta cells implanted in mice from immune attack for many months. “They are still producing insulin,” Melton said."
There are two breakthroughs. The mass production AND the ability of the device to protect the cells from destruction.
3. Yes. It reacts ideally in pretty much all scenarios. When you eat, it produces insulin. When you fast, it doesn't lower you into hypoglycemia. When you're sick (like a cold) it regulates insulin as it should, as your body needs more or less as your insulin sensitivity is off.
The mice used in the protocol were SCID mice [1]. They do not produce B or T lymphocytes (and thus no Ig either). Pretty much no adaptive immune system to speak of. These are a mainstay of murine study.
The discussion section referred to the existing technique of islet transplantation [2]. This is sourced from cadaver tissue, and as such requires immunosuppressants. Obviously needed to counteract host v. graft, but I wouldn't be surprised if it masked the autoimmune recognition.
The discussion section alludes to several future hurdles: gene expression differences from primary cell sources, transduction response, local tissue effects (need for tissue engineering), need to produce alpha, gamma, delta, and epsilon cells (alpha and gamma may be important to precise beta function), questions regarding long-term maintenance of phenotype, ...
Nevertheless, this is very exciting! Stem cell researchers are truly hackers in every sense. The results here aren't only applicable to diabetes research, either. Patients aren't the only ones that need these cells.
I disagree. The fact they can now mass produce insulin producing islets and have a mechanism of ensuring the immune system doesn't attack them means it's very likely to be a long term cure.
The mice they have been testing have maintained their glucose at human levels for months (they generally run 60-80 points higher than humans). They've binged and fasted them, made them sick and everything and their levels have maintained.
This is definitely promising, don't be such a wet blanket before researching a little bit!
The mice were SCID mice. They have no adaptive immune system to speak of. I made another post in this thread and included some links.
This is a very incredible result though. Even if immunosuppressants are required, think of all the non-patient outcomes: easily sourced human SC-beta cells for research and high throughput study. This stuff can be grown at volume, and the techniques will only improve. The results will also inform research into other cell lines. Bottom line, this is yet another step forward for stem cell tech.
Yes, and I imagine that one possibility is to retransplant new cells as the existing ones are killed off by the immune system. Not an elegant solution to an engineer, but medicine is full of inelegant solutions.
Not to be a dick, but don't steal the limelight please.
For once, the focus is on T1 and not T1 lumped into the discussion as it usually is. Hey, I'm all for reporters putting out accurate facts(ie: knowing the differences between T1 & T2), but it's silly to act like this isn't "relevant".
T1 Diabetes is STILL extremely expensive to treat. Just because it's "only" ~10% of the total Diabetic population, doesn't equate to only ~10% of the costs incurred. T1 Diabetics account for FAR more costs(per person compared to T2) via: daily treatment, reoccurring, and emergency. Not to mention that for "most" T2 Diabetics, the disease can be easily managed via proper diet and exercise, something which CANNOT be done with T1 Diabetics.
source: someone who walks around daily with ~$8,000 worth of electronics strapped to their body everyday for the past 15 years.
I'd imagine the patents are owned by the institutions the research is being conducted at and a Big Pharma will company will buy or license those patents after trials.
Startups are too small for shouldering the financial load of developing/testing/insurance/lab facilities/high end staff. Plus, Big Pharma has established distribution channels that would get a Type 1 like me my cure faster, which one may consider ethical territory.
(I'd actually recommend giving the paper a skim even if you're not trained in biology. The Introduction and Discussion should still be very comprehensible, and while the Results do suffer from the alphabet soup problem (as do most biological papers), the overall structure of the evidence should be clear - pay particularly close attention to Figure 5A and Figure 6A-C).
Commentary from a very well regarded stem cell scientist (and prolific blogger, Paul Knoepfler) here: http://www.ipscell.com/2014/10/top-10-takeaways-from-harvard...
The key next challenge appears to be the creation and testing of appropriate delivery device that can enable persistent survival of the differentiated cells while still enabling them to sense blood glucose levels.