Your write-up was well-constructed. Thanks!

I will add a few things just to raise awareness, if it hasn't been raised already. I apologize if I missed something in my reading.

I'm the kid whose diagnosis was at a time when we didn't have fingerstick glucometers, human synthetic insulin, or any of the myriad of modern medical approaches to ameliorating the effects of living with T1D. Five decades later I can offer some insight having survived that long with reasonably well-managed T1D while making mistakes with diet, exercise, and insulin and learning from those mistakes. I've also worked in medical devices and healthcare so it's not all n=1. I am the lucky diabetic, FWIW.

It's all about executive function in the end. And you can read below how the disease may impact executive function.

A diabetic beneath a certain threshold of blood glucose may seem to be operating in the lizard brain, particularly with respect to what may seem like an addiction when he eats an entire quart of ice cream in a single sitting, alone. To make matters worse, these thresholds, just like ISF and CR are dynamic, day-to-day. One day, the kid's functional with a BG of 60 and may feel and behave terribly with a BG of 80. This is hard to describe to someone who thinks that the whole thing is linear. Quite the converse. There are points where these changes can feel like falling off a cliff. Having had an IV of insulin once, I can tell you that the adrenalin rush is like falling off a cliff - nor far from the insulin shock therapy scene in "A Beautiful Mind".

I owe a debt of gratitude to the researchers who ran the DCCT[5] when I participated in the mid 80s. Most of what I know I learned from the world-class researchers from that team and being treated at some of the best pediatric diabetes clinics in the US.

I lost a brother-in-law to T1D at an age younger than I am now, so I understand the emotional impact of the disease and what it can do to damage us in ways beyond our comprehension. It's a family sensemaking operation, for sure, because much of what you'll hear seems apocryphal but there is a wisdom that accrues from managing a disease like this without losing your mind.

1. Nicolas Bolo's research at Harvard demonstrates that there is a correlated relationship between changes in blood glucose and the brain's default mode network. [1,2]
2. Insulin is synthesized locally in the cerebral cortex. [3]
3. Exercise can raise blood glucose (in addition to lowering it) depending on the pre-exercise feeding and insulin load, the implication being glycogen release, fat burning, and anaerobic activity. [6]

It's early for a child but from my experience, prefer fat burning to carb-loading as most of the research supports. [4]

Also, while I appreciate the hope and forward-looking perspective of many of the companies involved in making solutions to these problems, we should be careful not to give false hope. There is no question that a child diagnosed now will fare better than one diagnosed without the same technology and access to care - that's provable from HbA1c data.

However, there are serious issues, for instance, in what happens when a closed loop system runs into the fact that interstitial subcutaneous fat measure as a proxy to actual blood glucose is imperfect - particularly at the edges of sleep and exercise, where the draw on fat stores (due to Somogyi effect during sleep and or fat-burning during exercise, respectively) can result in poor data veracity from CGMs that is not at a clinical standard, resistant to calibration, and treated by the industry as if its a PR problem that is dealt with best by crisis management, when it's got to be taken as seriously as calibration in a self-driving car, because that's what it is - self-driving diabetes. An insulin pump and a CGM want to be called "autonomy" when they get beyond the endless MVP, but we're not there yet.

How do I know this? Nearly every sensor I've used since September 2021 has failed catastrophically and been replaced under warranty. I'm wearing two competing brands this very moment just to cross-calibrate beyond my fingersticks.

So when I say failed catastrophically, there are myriad problems there, but the big ones are reporting a high BG when BG is actually low, or vice versa. The false high when low can result in an insulin overdose, and the false low when high can result in DKA. Imagine either of those situations happening while the patient is running a marathon, and you have a rough idea how these device can produce experiences that start to resemble the reasons we study Therac 25. [9]

So, I'm hopeful for young diabetics that they can enjoy the nearly disease-free days that I have more life-long, perhaps with less round-the-clock hypervigilance and what seems like an unintentional PhD in metabolism, tech, and pharmacology.

Just remember, most of what we are treating here is a side effect of exogenous insulin. Minimize exogenous insulin and you minimize the side effects. Minimize side effects and the patient reports less inflammation, better energy, better performance of both brain and body, etc. Literally everything improves with less insulin, much like we see in the general, non-diabetic population around the development of type II diabetes with insulin resistance.
In that regard, the two researchers to keep an eye on going forward are the Denise Faustman's Lab at MGH [7], and Valter Longo's Lab at UCLA [8].

Hope my ranting, raving, and rambling help someone somewhere. Please forgive me, the sensors are having a rhetorical dialog about blood glucose data veracity and its impact on healthcare. There's still lots of work to be done.

[1] https://diabetesjournals.org/diabetes/article/60/12/3256/144...
[2] https://www.youtube.com/watch?v=UwL_iMLbm1k
[3]https://link.springer.com/article/10.1007/s00125-016-3996-2#....
[4] https://www.levelshealth.com/
[5] https://www.niddk.nih.gov/about-niddk/research-areas/diabete...
[6] https://www.virtahealth.com/
[7] https://www.faustmanlab.org/clinical-trials/
[8] https://www.longolab.org/
[9] https://en.wikipedia.org/wiki/Therac-25