In 2019 I had Megavitamin-B6 syndrome. I'm curious about the most common situation where people get it (chronic supplementation vs. acute overdose), and I have a hypothesis about how that may come about. Ideally, I'd like to see if it pans out in a model, and if it does maybe see if I can get some attention from interested biologists. But my background is in CS, not biology and I feel like I'd have a lot to learn. So anyone who would collaborate or just get me pointed in the right direction would be helpful.
In short it seems the chronic supplementation does factor in, but it also seems that plenty of people supplement for a very long time (more than 2 years) and never have an issue, sometimes at or above NOAEL or the even the LOAEL (100mg/day and 200mg/day in the US).
From many of the people I've talked to (and my own experience) it seems like something happens where someone takes a consistent dose of supplemental b6 for a year or more (at a reasonably high dose, say, 25mg/day or more) then at some point they take something else with b6 (or maybe are taking a poorly calibrated supplement that has more b6 than advertised) and then they start to develop toxicity, even if it the total dose is still below the "NOAEL."
So, my guess is that metabolic pathways adjust to receiving some daily dose of b6 and then become inflexible somehow (like a homeostatic thing) and can't ramp up the bandwidth/rate to process it in to 4-pyridoxic acid, the form where it's excreted.
Soo... I kind of want to see if that's plausible in a realistic model.