After a long interaction on Twitter that went something along the lines of “My basal is fairly stable and hasn’t changed in a year” versus Everydayupsanddowns “The only constant is change”, we started to speculate that ongoing endogenous insulin production, even in very small amounts, might actually make a difference to the ability to manage your diabetes.
Then along came a spider, well, no, not a Spider, more a Diabetologist, by the name of Pratik Choudhary. You may have heard of him. He dropped the not so subtle bomb that there’s a lot of documentary evidence that retained beta cells reduces the brittleness of diabetes. Damn it. If only we’d bothered Googling.
So, Google I did. And he’s right, being the kind of person who should be in these matters. There’s a ton of documentary evidence going back many years. Sadly much of it is behind a paywall, (two docs here and here) but it all points to the same thing. That those who have even a small level of endogenous insulin production tend to have more stable blood glucose levels. I guess it makes sense really. Somehow, I think this is something I should have known already…
What’s more interesting is the recent news from Exeter University relating to the amount of beta cells that one might retain. It basically says that if you were diagnosed as a child, you are more likely to have lost more beta cells than if you were diagnosed as a teenager, as the condition is less aggressive the older you become (I’m paraphrasing a little here). Now extrapolating this a little further (and this is proper hypothesis), in theory, it suggests that Type 1 is a continuum and as you get older, your autoimmune response becomes more muted, so the symptoms take longer to appear.
This little hypothesis also ties in nicely with the facts that we know around LADA. It adds fuel to the idea that the sooner you identify type 1 and are able to stop the beta cells producing insulin in any large degree, the sooner you can reduce the attack by the rogue T-Cells. Whether that’s through testing kids for ICAs or GAD antibodies through giving those who present with T2 an antibody test to ensure that, yes, they really are T2, you can potentially improve the outcome of T1 by intervening early.
But wait, there’s more to this discussion. It comes back to protective measures within the body. Some T1s have a large number of severe hypos, requiring hospitalisation and regular ambulance intervention. Some have very few. I, for example, have had two in 27 years. That’s not very many by all accounts. But why? Well it seems as though it could be linked to something I wrote about here.
If you are still producing even small amounts of insulin, then, the signalling between the alpha cells (which produce Glucagon) and the beta cells doesn’t seem to disappear, like it does in those who have lost all insulin production. As a result, even after long term T1D, your body will still react appropriately to low blood glucose levels by causing your liver to pump out glucose. This is even more of a reason to get it diagnosed and treated early. Then there’s the other corollary of this. It may also help you retain your hypo awareness signs even while others lose theirs. although this is truly a hypothesis and not researched anywhere.
So there’s a body of evidence out there that says that:
- Many T1s still have beta cells, and in some cases rather a lot
- Retained beta cells make blood glucose levels more stable
- Retained beta cells make severe hypos less likely
- Retained beta cells could mean retaining hypo awareness
- If a cure can be found to stop the autoimmune attacks and if the beta cells can be made to reproduce and be re-enabled, T1 would be cured.
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