I suspect the muscle spasms I had that responded so dramatically to biotin were caused by low glycogen levels secondary to impaired gluconeogenesis secondary to oxalate toxicity. I suspect the biotin simply knocked off some of the oxalate that had been blocking the biotin-depedent enzymes responsible for gluconeogenesis. But maybe you ar…
I suspect the muscle spasms I had that responded so dramatically to biotin were caused by low glycogen levels secondary to impaired gluconeogenesis secondary to oxalate toxicity. I suspect the biotin simply knocked off some of the oxalate that had been blocking the biotin-depedent enzymes responsible for gluconeogenesis. But maybe you are right that oxalate is not just being displaced but actually degraded. Dang, I hope you are right about that. Would a folic acid supplement work as well as THF in promoting the second step of the degradation pathway?
I haven't measured my blood glucose in a year or so, but it has never been low. Is it possible that the body prioritizes blood sugar at the expense of muscle glycogen synthesis?
I'm basing my theory regarding the muscle spasms on the fact that one day I decided to go low carb, and the spasms suddenly returned, despite being on the same dose of biotin. The spasms quickly resolved the next day when I went back on carbs. Also, before starting biotin, for months I tried increasing and decreasing the amount of sodium, calcium, potassium, and magnesium in my diet and nothing helped in the slightest.
I guess my main question would be, what is the overall quantity of biotin-dependent enzymes in the human body? If one were to suddenly displace all of the oxalate that might be bound to these enzymes, perhaps by taking a megadose of biotin, could that increase free and/or plasma oxalate to a degree that might cause dumping symptoms?
Well, your last questions I basically the great unknown. I’ve never seen a paper showing the oxalate stays stuck to the enzyme in a suicide inhibitor fashion, and my hypothesis is it is just being converted to formate.
In any case, muscle glycogen is depleted with exercise and liver glycogen is depleted with fasting or low carb. Low carb will not deplete muscle glycogen directly but it will prevent it from refilling after exercise.
The blood sugar will certainly take priority, but it is not very plausible that muscle glycogen depletion causes spasms. If this were the case low carb would cause spasms in everyone.
I find it more likely you have an issue with fat or BCAA metabolism.
Another important point is that it is not at all possible for biotin to displace oxalate on the enzymes because biotin does not bind to the oxalate-binding part of the enzyme. I covered here where they bind and the papers I cite have diagrams showing the binding locations.
I suspect the muscle spasms I had that responded so dramatically to biotin were caused by low glycogen levels secondary to impaired gluconeogenesis secondary to oxalate toxicity. I suspect the biotin simply knocked off some of the oxalate that had been blocking the biotin-depedent enzymes responsible for gluconeogenesis. But maybe you are right that oxalate is not just being displaced but actually degraded. Dang, I hope you are right about that. Would a folic acid supplement work as well as THF in promoting the second step of the degradation pathway?
That seems plausible, but the principle is insufficient to explain the four cases where high doses provoked dumping symptoms.
I would think if your gluconeogenesis were impaired your blood sugar would be low.
If you have the nutrients needed for recycling, any form of folate should be adequate.
The drawback of folic acid is it could overwhelm DHFR.
Foilinic acid would be a natural form that is less subject to overwhelming DHFR and is not subject to the methyl trap.
I haven't measured my blood glucose in a year or so, but it has never been low. Is it possible that the body prioritizes blood sugar at the expense of muscle glycogen synthesis?
I'm basing my theory regarding the muscle spasms on the fact that one day I decided to go low carb, and the spasms suddenly returned, despite being on the same dose of biotin. The spasms quickly resolved the next day when I went back on carbs. Also, before starting biotin, for months I tried increasing and decreasing the amount of sodium, calcium, potassium, and magnesium in my diet and nothing helped in the slightest.
I guess my main question would be, what is the overall quantity of biotin-dependent enzymes in the human body? If one were to suddenly displace all of the oxalate that might be bound to these enzymes, perhaps by taking a megadose of biotin, could that increase free and/or plasma oxalate to a degree that might cause dumping symptoms?
Well, your last questions I basically the great unknown. I’ve never seen a paper showing the oxalate stays stuck to the enzyme in a suicide inhibitor fashion, and my hypothesis is it is just being converted to formate.
In any case, muscle glycogen is depleted with exercise and liver glycogen is depleted with fasting or low carb. Low carb will not deplete muscle glycogen directly but it will prevent it from refilling after exercise.
The blood sugar will certainly take priority, but it is not very plausible that muscle glycogen depletion causes spasms. If this were the case low carb would cause spasms in everyone.
I find it more likely you have an issue with fat or BCAA metabolism.
Another important point is that it is not at all possible for biotin to displace oxalate on the enzymes because biotin does not bind to the oxalate-binding part of the enzyme. I covered here where they bind and the papers I cite have diagrams showing the binding locations.
Yes, very important point.