Thank you very much for the article. So, I am one of these anomalies, and I was tired of proving to doctors that cases like mine exist. I estimate my 'autoimmune event' occurred 17 years ago, but even in my childhood, there were signs of low beta-cell activity (fatigue, constantly blue extremities).
Anyway... I frame health and illness within a framework of energy availability and I abolish rigid categories in metabolism. The cell doesn't care whether it is sitting in front of an overfull or a half-empty plate. If nothing arrives, nothing arrives. I would also broaden the scope much, much further, but that is speculation: how do you see this? I believe that for many of the conditions involving extreme chronic fatigue that I won't name here... could it be an insulin-timing problem?
Through stoic serenity and a doctor who was willing to look at physiology rather than ICD codes, I managed to secure basal insulin for myself, and I still run this protocol at my own discretion and according to my own rhythms. This goes hand-in-hand with a "restricted" diet and regular movement several times a day, which poses no problem for me because I have the routine down.
As a 4 year LADA T1d I am very strict with my diet but my insulin resistance is not improving. In fact, it seems to be going in the wrong direction. I am so tired of the anxiety caused by my Dexcom alarms that I’m high or low. Currently, I am taking about 25-30 units of insulin a day- I am not overweight - and walk daily! Any input or advice from anyone is appreciated!
it's not possible for someone to help you with very little info like this. Your total daily insulin looks fine, your weight seems to be fine, and your claim about 'insulin resistance" is abstract.
From my experience, however, people often confuse "insulin resistance" with "absorption variability", which is a huge problem for people who use pumps (because the infusion set over days amplifies the effect).
Insulin "resistance" means that a portion of the insulin you're taking doesn't actually reach the cells, and instead gets circulated out before having any effect. Hence, you have to take MORE insulin to achieve the same result.
What you're more likely experiencing is insulin absorption variability, where the insulin sits in your interstitial tissue for arbitrary amounts of time, and diffuses into your bloodstream at unexpected rates.
Because people are unaware of this, when their sugar is up, they believe the "insulin on board" estimates say they don't have enough to cover the BG level, so they take more insulin to bring it down... only to find that the past injections that the "calculator" thought was long gone suddenly start to take effect.
Hence, unexpected hypos and hypers. the roller coaster.
If I had a dime for every time I warn people not to believe "insulin onboard" estimates, I'd be a gazillionaire.
How do you become a part of these trials? I am a LADA T1d for the past 4 years and would love to take part in trials to end my insulin dependence….any info that is available please share - ty
I think you make some very important points here in your article.
I'd add one thing to the financial analysis: If you are indeed a non-autoimmune T1D, then you can factor into autologous transplantation the fact that you do not need immunosuppressants of any sort and should have a significantly simplified follow up compared to encapsulated or "hypoimmune" β-cell transplantation.
All that, of course, if you fall into the non-autoimmune category…
Now, I still do not think the current T1D research was really designed from the top down instead of from the base up, though. The progression went from "how do β-cells differentiate during organogenesis" to "how to make β-cells from iPSCs", then "how to make β-cells from adult stem cells".
The work on how to prevent the cells from being destroyed by the immune system (in your description, the top of the pyramid), came later (well, it was worked on in parallels on donor-derived islets, but for iPSCs and SCs it did).
I had no idea that 22% of T1D were in the same category as I am. I went to Mayo two years ago to try to find causation and solution with no luck except comment that at the end of the day, they treat someone who does not fall into the main T1D category the same regardless.
Thank you very much for the article. So, I am one of these anomalies, and I was tired of proving to doctors that cases like mine exist. I estimate my 'autoimmune event' occurred 17 years ago, but even in my childhood, there were signs of low beta-cell activity (fatigue, constantly blue extremities).
Anyway... I frame health and illness within a framework of energy availability and I abolish rigid categories in metabolism. The cell doesn't care whether it is sitting in front of an overfull or a half-empty plate. If nothing arrives, nothing arrives. I would also broaden the scope much, much further, but that is speculation: how do you see this? I believe that for many of the conditions involving extreme chronic fatigue that I won't name here... could it be an insulin-timing problem?
Through stoic serenity and a doctor who was willing to look at physiology rather than ICD codes, I managed to secure basal insulin for myself, and I still run this protocol at my own discretion and according to my own rhythms. This goes hand-in-hand with a "restricted" diet and regular movement several times a day, which poses no problem for me because I have the routine down.
As a 4 year LADA T1d I am very strict with my diet but my insulin resistance is not improving. In fact, it seems to be going in the wrong direction. I am so tired of the anxiety caused by my Dexcom alarms that I’m high or low. Currently, I am taking about 25-30 units of insulin a day- I am not overweight - and walk daily! Any input or advice from anyone is appreciated!
it's not possible for someone to help you with very little info like this. Your total daily insulin looks fine, your weight seems to be fine, and your claim about 'insulin resistance" is abstract.
From my experience, however, people often confuse "insulin resistance" with "absorption variability", which is a huge problem for people who use pumps (because the infusion set over days amplifies the effect).
Insulin "resistance" means that a portion of the insulin you're taking doesn't actually reach the cells, and instead gets circulated out before having any effect. Hence, you have to take MORE insulin to achieve the same result.
What you're more likely experiencing is insulin absorption variability, where the insulin sits in your interstitial tissue for arbitrary amounts of time, and diffuses into your bloodstream at unexpected rates.
Because people are unaware of this, when their sugar is up, they believe the "insulin on board" estimates say they don't have enough to cover the BG level, so they take more insulin to bring it down... only to find that the past injections that the "calculator" thought was long gone suddenly start to take effect.
Hence, unexpected hypos and hypers. the roller coaster.
If I had a dime for every time I warn people not to believe "insulin onboard" estimates, I'd be a gazillionaire.
I talk about that and more here:
https://danheller.substack.com/p/the-insulin-absorption-roller-coaster
How do you become a part of these trials? I am a LADA T1d for the past 4 years and would love to take part in trials to end my insulin dependence….any info that is available please share - ty
there aren't any such trials. that's the point of my article.
I think you make some very important points here in your article.
I'd add one thing to the financial analysis: If you are indeed a non-autoimmune T1D, then you can factor into autologous transplantation the fact that you do not need immunosuppressants of any sort and should have a significantly simplified follow up compared to encapsulated or "hypoimmune" β-cell transplantation.
All that, of course, if you fall into the non-autoimmune category…
Now, I still do not think the current T1D research was really designed from the top down instead of from the base up, though. The progression went from "how do β-cells differentiate during organogenesis" to "how to make β-cells from iPSCs", then "how to make β-cells from adult stem cells".
The work on how to prevent the cells from being destroyed by the immune system (in your description, the top of the pyramid), came later (well, it was worked on in parallels on donor-derived islets, but for iPSCs and SCs it did).
Very interesting.
I had no idea that 22% of T1D were in the same category as I am. I went to Mayo two years ago to try to find causation and solution with no luck except comment that at the end of the day, they treat someone who does not fall into the main T1D category the same regardless.
Excellent article.