Residual insulin secretion in individuals with type 1

[Amity Island]

Contrary to the presumption that type 1 diabetes leads to an absolute insulin deficiency, many individuals with type 1 diabetes have circulating C-peptide years after the diagnosis. We studied factors affecting random serum C-peptide concentration in individuals with type 1 diabetes and the association with diabetic complications.

https://www.thelancet.com/journals/landia/article/PIIS2213-8587(23)00123-7/fulltext

 

[Robin]

This has been observed in previous studies. My consultant is certainly happy with the concept that I need so little basal that I'm probably producing some residual insulin, but not enough to ramp up production when I eat. (I was diagnosed aged 50)

 

[Amity Island]

This has been observed in previous studies. My consultant is certainly happy with the concept that I need so little basal that I'm probably producing some residual insulin, but not enough to ramp up production when I eat. (I was diagnosed aged 50)

Robin,

Does this mean that type 1 diabetes (with some residual insulin) can be controlled by diet (low carb) and exercise alone?

Thanks

 

[Robin]

Robin,

Does this mean that type 1 diabetes (with some residual insulin) can be controlled by diet (low carb) and exercise alone?

Thanks

No. 'Residual', I think, means ' little bit, but not enough to be useful'. When I was diagnosed, I'd actually been on a low carb diet as a method of weight loss, and I then found that I’d increased the amount I was eating, inadvertently, because I was still losing weight, even eating masses of cheese, nuts, etc. Apparently that was the only thing that kept me out of hospital with DKA. Trying to exercise was a joke, any exertion (carrying a couple of bags of shopping home up a gradual incline) felt like wading through treacle.
So even with a very low carb diet, my first HbA1c was 16.0% on the old scale (don’t know what that equates to on the new scale, most of the charts don’t go up that high).

 

[everydayupsanddowns]

Robin,

Does this mean that type 1 diabetes (with some residual insulin) can be controlled by diet (low carb) and exercise alone?

Thanks

The Joslin Centre (Boston) has studied their medallists and found both cPeptide and GAD antibodies - suggesting a cycle of beta cell recovery and ongoing destruction in some cases of T1 even after many decades.

I believe research is ongoing to see whether the autoimmune attack can be halted, and/or the beta cells protected in some way.

 

[Amity Island]

The Joslin Centre (Boston) has studied their medallists and found both cPeptide and GAD antibodies - suggesting a cycle of beta cell recovery and ongoing destruction in some cases of T1 even after many decades.

I believe research is ongoing to see whether the autoimmune attack can be halted, and/or the beta cells protected in some way.

For many years it was believed type 1 was the failure of the beta cells but we now know it's a constant attack on them. They always have the potential to produce insulin, if we can only prevent the attack. Sounds simple in theory.

Incidentally, type 1 in mice is artificially created by giving them streptozotocin.

Streptozotocin (STZ) is a naturally occurring chemical derived from Streptomyces achromogenes that is particularly toxic to the insulin-producing beta cells of the pancreas in mammals

 

[rebrascora]

I do wonder why they haven't considered using immunosuppressant drugs like Methotrexate on newly diagnosed Type 1s. It is a widely used drug for other conditions so reasonable well known. My partner is prescribed it for his severe eczema and my sister was prescribed it for PMR, so it is used for other autoimmune conditions.... makes you wonder why not try it on Type 1s, particularly in the early stages. It does involve regular blood tests to check liver function I believe, so maybe it is the potential threat to the liver which has prevented it's use in diabetes since our liver is part of our hypo safety net.

Having said that, it might mean we were permanently trapped in the honeymoon period and I for one would not relish that!
Although if we continue to regenerate and kill off beta cells then are we effectively trapped in the honeymoon period anyway. It might explain some of the frustrating variability of diabetes that we tend to blame on the Diabetes Fairy!

 

[everydayupsanddowns]

I do wonder why they haven't considered using immunosuppressant drugs like Methotrexate on newly diagnosed Type 1s. It is a widely used drug for other conditions so reasonable well known. My partner is prescribed it for his severe eczema and my sister was prescribed it for PMR, so it is used for other autoimmune conditions.... makes you wonder why not try it on Type 1s, particularly in the early stages. It does involve regular blood tests to check liver function I believe, so maybe it is the potential threat to the liver which has prevented it's use in diabetes since our liver is part of our hypo safety net.

Having said that, it might mean we were permanently trapped in the honeymoon period and I for one would not relish that!
Although if we continue to regenerate and kill off beta cells then are we effectively trapped in the honeymoon period anyway. It might explain some of the frustrating variability of diabetes that we tend to blame on the Diabetes Fairy!

I would imagine it’s the risk/reward balance. And that insulin is available, effective, and pretty much side-effect free for most people?

But yes… I guess it would come with its own complexities, depending on how steadily and predictably any beta cells ‘helped out’.

And we’d need to add another few entries onto the 42 factors list!

 

[everydayupsanddowns]

For many years it was believed type 1 was the failure of the beta cells but we now know it's a constant attack on them. They always have the potential to produce insulin, if we can only prevent the attack.

I suspect it may be another of those ’in some cases’ situations? So some T1s will lose all beta cells and have no detectable GAD antibodies in fairly short order, while others will had detectable GAD/cPep for decades.

That’s why GAD isn’t a definitive test for T1. It can help… but it’s not a 100% indication one way or another. T1 is still best diagnosed on clinical factors.

 

[Inka]

The Joslin Centre (Boston) has studied their medallists and found both cPeptide and GAD antibodies - suggesting a cycle of beta cell recovery and ongoing destruction in some cases of T1 even after many decades.

I believe research is ongoing to see whether the autoimmune attack can be halted, and/or the beta cells protected in some way.

And that’s so exciting - the idea that we might be able to re-grow our own beta cells. I hope, if we stopped the immune attack, we’d be able to regrow enough that we could control our blood sugar properly and not need exogenous insulin. What a cure that would be! As long as the means of stopping the immune attack was safe and tolerable and didn’t inadvertently put us at risk.

I always wondered if the immune system could be trained to tolerate the beta cells, rather like they do with some intolerances. There was an interesting if technical study here of Tregs:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8275894/

.

 

[Amity Island]

And that’s so exciting - the idea that we might be able to re-grow our own beta cells. I hope, if we stopped the immune attack, we’d be able to regrow enough that we could control our blood sugar properly and not need exogenous insulin. What a cure that would be! As long as the means of stopping the immune attack was safe and tolerable and didn’t inadvertently put us at risk.

I always wondered if the immune system could be trained to tolerate the beta cells, rather like they do with some intolerances. There was an interesting if technical study here of Tregs:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8275894/

.

Another article suggests the reason the beta cells are attacked is because they are seen as a foreign body, not part of the natural body. Really strange.