Type 1 diabetic here: you're right, it's a bad tradeoff. We already can do pancreas transplants for T1D, but the reason it's very uncommon is that immunosuppressants are a very bad tradeoff. Insulin treatment is preferred in the vast majority of cases.

Stuff like this will never be a breakthrough until it doesn't need immunosuppressants. The best advancements in diabetes treatment will most likely continue to be on closed loop artificial pancreas systems.

Insulin-specific immunotherapies are currently under development. We will soon be able to restore tolerance to insulin, and other pancreatic antigens such as GAD-65, without the need for broad immunosupressants. Ideally, this should stop β cell destruction and conversion to T1D from auto-antibody positive status, as well as facilitate islet transplants with minimal side effects for those that are already T1D patients.

I'm sorry for your plight and I genuinely hope there will be a much more tenable solution in the near future.

I wouldn't call closed loop systems much of an advancement... Sure, it doses insulin automatically based off of CGM data, but it's barely any better than just injecting yourself. Cons even outweight the pros for some - being constantly attached to a device is no fun. And the slugishness of exogenous insulin (both: the way it is injected and its time of action) diminishes any attempts to achieve precision using CGM data and algorithms in controlling diabetes. Not to mention CGM data isn't that accurate/rapid enough also. All in all, it's just not efficient, calling these systems 'artificial pancreas' is more of a marketing gimmick than reality, thus why a proper cure is needed.

There was a recent "breakthrough" involving the same, except with patient's own stem cells, & not just in mice.

https://stemcellres.biomedcentral.com/articles/10.1186/s1328...

That would mitigate the cancer risk, since immunosuppression would not be required?

> patient's own stem cells

> immunosuppression would not be required

I don't think that's how Type I Diabetes works. People get Type I Diabetes because their immune system attacked their own insulin producing cells in the first place. It's an autoimmune disease. So if you replenish those cells, they'll just get attacked again.

Possibly, it is defo important to keep tabs on how these patients fare after a few years. before we rush to ship this

From above link:

>A 25-year-old woman with type 1 diabetes became the first person to successfully receive a transplant of insulin-producing cells derived from her own reprogrammed stem cells

There were these studies where t1d patients immune system was "restarted" and they became insulin free. https://pubmed.ncbi.nlm.nih.gov/17426276/

If you take rapamycin or a rapalog as an anti-rejection drug, your risk of cancer is lower - not higher - because it's not actually an immune suppressant so much as a drug that prevents hyperimmunity. [1] Other immune suppressants work differently but it's not a blanket true statement that taking anti-rejection drugs will increase your risk of cancer. Depends what you take.

You can read the section in [1] titled "Cancer prevention in humans."

> Starting from 2004, numerous studies demonstrated that rapamycin and everolimus reduced the incidence of various cancers in organ transplant patients.

[edit] In fact in addition to its use as an anti-rejection medication, rapamycin is used as chemotherapy to treat certain forms of cancer.

[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC10103596/

Cancer develops resistance to rapamycin. Cancer always finds a way

My point is cancer is worse than DI. At least you can manage DI

Do you have any evidence that cancer develops resistance to rapamycin? I’d love to read a study.

I apologize for not posting any reference. The topic is well known in oncology

https://pubmed.ncbi.nlm.nih.gov/21389767/

Disclaimer: The newer the article, the less reliable it is. There were well disguised garbage articles in the 2000's, but there are too many now.

Thanks I'm going to give it a read!

Off hand my first thoughts are (a) well it would make sense that the non-rapamycin-sensitive cancer cells would naturally be selected for - but that doesn't mean that your rates of cancer would be higher - and (b) how do you square this with the measured lower cancer rates in transplant patients on rapamycin?

My take, admittedly more research needed on my part, is that the cancer risk of anti rejection drugs is because the immune system would normally nuke some of these from orbit. However rapamycin works differently and doesn’t suppress the immune system so even with resistance developing the cancer risk would still be somewhere between lower and neutral.