Remaining insulin production in type 1 prevalent

Interesting article. This gives me more hope that they’re on the right track with research. Previous understandings that type 1 diabetes unequivocally meant an absolute vs a relative insulin deficiency left much less hope for avenues of future treatment…


I went from the science news article back to the actual scientific paper at to better understand what they found in terms of these type 1’s who are still producing insulin.

First some background so the numbers make sense. They used an “ultra-sensitive ELISA” test to look for c-peptide. For this test, they set 1.17 pmol/L as the minimum detection level: anything below was considered “no measurable c-peptide.” To calibrate your understanding of this number, less than 600 pmol/L is considered proof of diabetes, and less than 200 pmol/L is considered severe insulin deficiency. (These are fasting numbers: if you drink glucose, that can stimulate a weak but not completely failed pancreas to desperately produce a bit more insulin and c-peptide.) Now this ultra-sensitive ELISA test had a coefficient of variation of 3.8% intra-assay and 5.5% inter-assay at a measurement of 37 pmol/L. Which basically means the errors are small compared to the levels they are measuring.

Now for the measurements. They had 46 type 1s who had some remaining insulin production: the average amount was 28.6 pmol/L plus or minus 15. That’s about 1/6th or 1/7th of the amount that’s considered a severe insulin deficiency. So it’s quite a meager amount. There were 67 patients who had no measurable insulin production (recall, this means less than 1.17 pmol/L.)

So when the science news article says “almost half of patients produce insulin” it’s actually about 40% of these type 1 patients, and even while fasting so not challenging themselves with a glucose load, on average they were producing about 1/20th of the amount of insulin that would be considered proof of diabetes.

So yes, 40% of the type 1s in that study had some beta cells available for regeneration, but they’d have to multiply their beta cell population by more than 20-fold to get out of the diabetic category. For the other 60%, they are worse off by another factor of 25 (or more.)

I’d say the paper was interesting because it investigates why some 40% didn’t have their beta cells more or less completely wiped out. But in any case, for a cure they would be needing to multiply their beta cell population by large factors, like 100 or 1000. I don’t know whether that’s something that would regenerate all by itself, or whether there would need to be 2 interventions, one to stop the autoimmune attack and a second one to stimulate/facilitate reproduction of beta cells.


Really nice write-up @bkh, quite interesting.

Thanks for digging into the details. I’m not a scientist and don’t understand all the finer points as well as some but to me it’s still encouraging. With zero insulin production, there is little hope of improving the situation. With even a tiny bit it makes me think there’s some possibility. With only one seed one can eventually possibly grow an orchard… with zero seeds one can not…



That makes sense.

Yeah, I’m half waiting for Jen to come in and straighten me out. She’s seen through my blunders and oversights several times so far, and I’m really thankful to accept those corrections so any errors I happen to make don’t stick around as if they were true.


I saw this video a while back (it’s six years old?):

The speaker looked at pancreases from autopsies and found some beta cells in most people with T1 and says evidence suggests we are able to make some new beta cells as adults but they are getting killed off by the immune system. But that lends some hope to a cure if the autoimmune process can be stopped.


Great analysis, @bkh, thank you!

In the quote above, what impresses me is not the quantity of beta cells, but the fact that, however few, some exist and regenerate. I could be wrong, but it seems to me that the fact of having regenerating beta cells at hand, however few, could make a big difference to venues of research.


Hello @Sam, and @bkh, I enjoyed reading the articles.
I have participated two times in the Joslin Medalist Study. There were 1000 participants, and all of them had been T1 for 50+ years. (Some had been T1 for more than 70 years.) In an early report, when there had been 500+ participants, it was found that more than 60% of them were still producing insulin. I do not presently have the numbers indicating the c-peptide results, but it can be found online by researching “Joslin Medalist Study”.
I attended a medalist meeting at the Joslin Diabetes Center in 2011. There were more than 100 medalists at that meeting. Dr King, head of the Medalist Study, announced that many of us possess a “special inner protection” that protects our eyes, kidneys and nervous systems. He says that is why so many of us do not have any serious complications. There was one member in the audience that day who occasionally produces enough insulin that she stops taking insulin for awhile, and then continues her insulin later on. She was to be studied more closely at Joslin, but I do not know the results of her study.

The only diabetes related complication that I have is neuropathy. I have numbness in my feet and legs, and I have some minor problem with balance. I don’t have pain, so I do not need medication. That is my own personal status, however, my c-peptide was found to be “less than 0.1%”. It seems peculiar to me that my c-peptide can be so low, and my diabetes health can be so good. My eyes, kidneys and heart are in great shape despite the lack of insulin production, and my being T1 for 72 years. I am not the only participant with low c-peptide and good diabetes health. It seems that more research is needed to explain that.