When I first began to obtain the background I needed to understand the oxalate issues I found in autism 18 years ago (2005), I attended professional oxalate conferences. I was very surprised to discover they were only attended by kidney doctors and kidney researchers. To them, finding oxalate elevated in autism was an anomaly. In fact, finding oxalate elevated apart from kidney stone disease or genetic hyperoxaluria was in their minds, impossible.
Why did I start studying it? Beginning about thirty years ago, my academic work was all about sulfate and discovering its role in neurodevelopment. Years later, sulfate was found to exchange for oxalate on a special set of transporters called the SLC26A family of transporters.
I had already thoroughly explored the role of sulfate in autism, but this new science meant that now I needed to study oxalate to find out how oxalate could disrupt sulfate and other things important in autism. To accomplish that, I studied the oxalate literature for four months with a special focus on the genetic hyperoxalurias where it was known that oxalate traveled to the whole body.
I attended 7 professional oxalate conferences. To my surprise, the scientists there seemed to have formed an unspoken pact to ignore issues that were not centered around kidney stone disease. They were uninterested in how oxalate affected the general biochemistry wherever it went. I had already spent a decade recognizing complex issues in autism, so I knew that oxalate, by affecting sulfate, could alter neurodevelopment as well as hormone and neurotransmitter regulation, and it was a clear mitochondrial toxin. This new information required a reinterpretation of autism findings.
Before that, I had been studying sulfate's role, but now, oxalate could be a major disruptor. Formate was also a substrate of those transporters. Anyone can find literature about how formate and oxalate have been influencing each other, but I found nothing practically useful.
Chris, this is why I am particularly delighted to find your interest in this field and I like the way you are looking at it in the way it should have been studied a long time ago.
The oxalate field for so many years had blinders on...something that Sally Norton and I had both found and explored independently. Sally has been more into thinking about issues with diet, but I became more concerned about reaching academia and helping them study the oxalate the body makes under stress.
It was impossible to do a study in the US on oxalate in autism because the labs in the US that were skilled in measuring oxalate told me they would not test anyone unless they had kidney disease. That is why I recruited a highly qualified group of scientists to look at oxalate levels in autism, and we got astonishing results. That paper is ranked now in the top 4% of scientific studies and it has had 42 citations. That attention is really great, but it is still not motivating other scientists to look past the kidneys and find other types of diseases related to oxalate.
Chris, the commendable sort of thinking that you are doing is exactly what is needed to move oxalate research forward and into new territory. I eagerly invite you to further explore this fruitful area that has been in sore need of your skill set. I hope that you can generate experimental evidence.
In 2005, with a bunch of grateful autism parents, we formed the TryingLowOxalates network and it has has already helped more than 70,000 people discover the relevance of oxalate to their own health. This is the way we picked up an enormous amount of personal experience about reducing oxalate, but we have not seen nearly the amount of change we want to see in academia.
We're trying to change that. Our group performed the most successful fundraising of anybody this past year for the Oxalosis and Hyperoxaluria Foundation for Giving Tuesday, and that is because our vision is to support the sort of thinking you are doing to move the study of oxalate into a new era, where multidisciplinary and cross-disciplinary work rules the roost instead of being barred from the roost.
Kudos on your deep thinking! I would be delighted to see people like you get funded so that we can together solve the many human diseases related to oxalate.
Best wishes,
Susan Owens
Head of the Autism Oxalate Project at the Autism Research Institute
Founder of the Trying Low Oxalates network since 2005
May 5, 2023·edited May 5, 2023Liked by Chris Masterjohn, PhD
Hopefully you are right about biotin helping to degrade oxalate. But even if biotin does not help to degrade oxalate itself, biotin very likely mitigates the toxic effects of oxalate on gluconeogenesis and fatty acid synthesis from lactate, as described in the articles you briefly referenced by Bannister, looking at the interplay of biotin and oxalate in isolated hepatocytes. I imagine this explains the exercise intolerance reported by those with oxalate issues. Too much build-up of lactate. Personally, I had to stop weightlifting because it started to make me feel nauseous and greatly disrupted my sleep. (I can, however, tolerate small amounts of "alactic" training.) Eating too much meat causes the same problem for me, likely because of the added need for biotin, as you have detailed in other posts. I just started some biotin supplementation (I'm starting at 75 mcg/day and will increase to 150 mcg/day), and will report back.
Dead Sea salt baths saved me when I unexpectedly began dumping. It has been some years, I have triggered major oxalate (or something! formate? It burned on the way out, urine, skin, eyes, lips etc). Once I tried eating a couple leaves of raw swiss chard out of my garden after it had frosted. Immediate burning dumping misery, tender points fibromyalgia style, barely able to walk. Floating in a dead sea salt bath (high magnesium chloride, potassium chloride, some sulfate) for an hour or more at a time, literally melted a ton of it away in a few days through my skin. It felt like something granular was coming out of my knee joints and dissolving. I later triggered another dumping episode experimenting with high dose thiamine. Another with diatomaceous earth. I do more careful experimentation now with slower changes. Now my OAT is normal for oxalate and its precursors; I have some other oddball things that may have to do with high need for riboflavin though. I don't do things like raw kale but I am generally okay with COOKED high oxalate foods these days in reasonable quantities.
As a prolific calcium oxalate kidney stone producer, I have, over the years attempted to find
some dietary modifications (beyond dietary oxalate restriction) that would decrease my oxalate burden. Two of the most promising possibilities I found:
1) Oxalobacter formigenes, an obligate anaerobic probiotic
which utilizes oxalic acid as its sole source of energy. Oxalate degradation by O. formigenes involves three unique proteins, an oxalate:formate membrane transporter, oxalylCoA decarboxylase, and formyl-CoA transferase. There have been several studies confirming significant degradation of intestinal oxalates. Unfortunately, there doesn't seem to be a commercially reliable source of Oxalobacter available. Oxalo Therapeutics has been developing products that treat primary hyperoxaluria and prevent recurrent kidney stones, but nothing, as of yet, seems available. There is one product, available from India and listed on ebay that purports to contain Oxalobacter Formigenes & Other Probiotics for Calcium Oxalate Stones Reduction. Manufactured by Standford Labs, distributed by La Renon ( India). Needless to say, I am dubious!
2) Oxalate decarboxylase: a company called Nephure came out with a powder that one could sprinkle on food several years ago. Unfortunately, I believe the company stopped production. Here is a double blind that was done in 2020 looking at this product: https://pubmed.ncbi.nlm.nih.gov/35372879/
So, there you have it, two low toxicity products that seem quite efficacious for oxalate reduction that are not commercially available. I guess, for now, back to a low oxalate diet!
This is very, very interesting...thanks Chris. I had severe 'oxalate dumping' symptoms a couple of years back.. still traces now. I was 7 times the upper limit on the organic acids test, and lactate was also very high with raised arabinose, high quinolinic, high hva/vma and a bunch of other stuff out. I work with an excellent nutritionist who suggested oat testing for improving health, thyroid and autoimmunity. Following this test, I started a low oxalate keto diet but struggled to get urine ketones up at first.. but it was this that kicked off the symptoms.. blood pressure drops, tachycardia and horrible anxiety followed by cloudy urine and surprisingly a sense of relief that always came along 10 minutes before the bathroom visit.. every 10 days/2 weeks for months, with all sorts of symptoms in between. I couldn't work or drive in that period. It was as if every time blood levels got below a certain threshold then it would restart! I couldn't believe it at first but a lot of testing and research comvinced me that the dumping was a distinct possibility. Repeated oat testing showed decreasing oxalates after some time of this. Often I felt cold, like feverish, with very dry lips and dizzy, histamine type symptoms. I see that biotin may help stabilise mast cells through cyclic gmp? I had seen evidence that oxalate can directly stimulate degranulation. I took b1, b6, magnesium, citrate, calcium with meals and herbs like phylanthus niruri, dandelion, schisandra to help protect kidneys together with a bunch of other stuff finding a few things that helped symptomatically, which included anything that could increase my blood pressure. I still have occasional symptoms..it would be interesting to.see if biotin made things better/worse!
This is great. Please do more research on oxalates. After reading this and the other biotin posts I am going to cautiously experiment with some biotin.
I feel like there must be a way to get back to being able to handle the Oxalates. I happily downed tons of peanut butter and chocolate all the way into my late twenties with no I’ll effect.
Now I can’t even tolerate 50 mg a day and it drives me nuts because even so many healthy things are off limits.
What do you think about the role of magnesium and manganese in pyruvate carboxylase function?
Pyruvate carboxylase seems to be a manganese-containing enzyme. But when manganese is lacking, magnesium can substitute, retaining pyruvate carboxylase's textbook enzyme function. (Scrutton et al., 1972.)
However, "oxalate inhibition" requires 7 times more oxalate to achieve the same effect (in chicken livers) in the Mg version of the enzyme, compared with the Mn version of the enzyme. (Scrutton et al., 1972, Table V.) Maybe the manganese in the enzyme is needed to metabolize oxalate efficiently?
Paradoxically, the manganese content in pyruvate carboxylase may indicate magnesium status.
Magnesium deficiency in rat diet resulted in less manganese in organs and less liver pyruvate carboxylase activity. Magnesium seemed to direct manganese (and also calcium) to the right places. (Kimura et al., 1996.)
Magnesium is so much more abundant than manganese, that we might expect magnesium still could fill in gaps in the enzyme for missing manganese, even in the case of magnesium deficiency. So when we lack magnesium in diet, we might find (paradoxically) more magnesium and less manganese in pyruvate carboxylase? Therefore, in magnesium deficiency, we might find as much as 7x less metabolism of oxalate by pyruvate carboxylase?
In addition to its role promoting manganese delivery to pyruvate carboxylase, magnesium acts as a cofactor in Mg-ATP, as you mentioned.
So poor reaction to oxalate could relate to magnesium deficiency causing low liver manganese, low Mg-ATP, and low pyruvate carboxylase activity?
Could apparent need for more biotin indicate an underlying need for more dietary magnesium to make manganese and pyruvate carboxylase work better?
As you speak with enzymologists about investigating pyruvate carboxylase in the first breakdown step of oxalate (as you mentioned in response to Susan Owens), maybe suggest investigating the roles of magnesium and manganese nutritional status, in addition to biotin?
References:
[1] Kimura, M., Ujihara, M., & Yokoi, K. (1996). Tissue manganese levels and liver pyruvate carboxylase activity in magnesium-deficient rats. Biological Trace Element Research, 52, 171-179. https://doi.org/10.1007/BF02789459
[2] Scrutton, M. C., Griminger, P., & Wallace, J. C. (1972). Pyruvate carboxylase: Bound metal content of the vertebrate liver enzyme as a function of diet and species. Journal of Biological Chemistry, 247(10), 3305-3313. https://doi.org/10.1016/S0021-9258(19)45246-0
I tried supplementing with Biotin after Susan Owens recommended I do so because supplementing with B1 (Benfotianime) would bring on oxalate dumping / clearance for me as well. Both Biotin and B1 do this for me separately. However, the intervals and intensity were a bit different. B Complex will do the same, obviously. Ramping up on these by cutting pills or using 1 drop, etc., however, makes the dumping far less intense and less frequent, and that's my tack right now to ramp up on B1 to solve some of the problems Elliot Overton says B1 supplementation can help with when you've been carnivore for a long time but still don't feel great. So it'd be interesting to know why both B1 and Biotin have similar effects.
I paid for the Vitamins and Minerals book at least 2 years ago. Guess I didn't realize you hadn't written it yet. When do you expect it to print? It's been a long time!!
Ah, thank you so much for this article, Chris!! You have given me the explanation I was seeking. 😁
I have been on a low-vitamin A diet (dairy-free and egg-free, but not vegan--I eat beef and chicken) since 2018, but this year in February I decided to start incorporating a greater number of eggs back into my diet in order to increase my choline intake to between 800 mg and 1200 mg (prior to this, I had been somewhat above the female RDA for choline, but more in the 500 mg to 600 mg range). Turns out, they make me feel horrible, but I wasn't entirely satisfied with blaming retinol for this reaction, as my egg intake never took me beyond the RDA for vitamin A.
Just three to four eggs daily (whites always eaten cooked, yolks sometimes raw) produced unusual symptoms: a red bumpy rash on my leg, what felt like a mild bladder infection not bad enough to go to the doctor about, constipation (normally my digestion is great--I eat a legume-heavy diet), insomnia, and achy hands.
I do not get joint pain normally, at all. So I figured perhaps this weird reaction had something to do with oxalate, but wasn't entirely sure why eggs would trigger dumping so strongly.
I backed off on the eggs to give my gut a rest (it helped), then just this month I tried consuming eight eggs daily for three consecutive days. Chronometer tells me that amount provides nearly 300% of the RDA for biotin?! (I didn't know this when I decided to try it lol.) While doing this, my brain fog was worse than it has been all year, constipation was bad, my back ached (kidney area), my shins hurt, my toes and fingers hurt, everything hurt (kinda like the aches we get during a flu), the rash expanded, and an area on my finger where I had gotten a tendon stitched in the past felt like it had been smashed and was throbbing...
I was at my wit's end wondering why, but now, thanks to you, I feel I must blame all of this on biotin for triggering an oxalate dump! Yours is the best explanation of the dramatic symptoms I've found so far.
It'd be pretty cool if your idea here helps people manage the oxalate dumping process, instead of it feeling super random and overwhelming.
Thanks again SO MUCH, Chris!! 😁🌻☀
P.S. It might be good to include this fact: My oxalate intake has been between 50 mg and 150 mg daily for the past 6 months.
P.P.S. ETA: I should also note I found going full-vegan (particularly focusing on a ridiculous amount of raw fruit) without any added saturated fat from coconut oil (hemp and sunflower seeds seem fine) after ceasing egg consumption resolves the constipation issue within 24 hours for me so far, whilst consuming a meat and saturated-fat heavy diet seemed to prolong it. Will keep testing to confirm this holds true in my case, but this is my initial observation.
I've been troubled with a high pitch ringing in my ears for a few years. My doctor believes I am losing my hearing. My hearing is not perfect (I'm 77 yrs old), but I discovered that I can control the ringing by what I eat. Kale, chard, sweet potato, peanuts and other things make the ringing worse. If I don't eat anything high in Oxalate, it diminishes a great deal but doesn't go away. My brother had a kidney stone, my sister had cystitis, and my mother was put on a low oxalate diet. Until recently, I had been on a vegan diet with occasional small amounts of fish. I'm wondering if increasing my animal protein is going to make this problem worse. If I take biotin, will it make my body dump more and maybe give me a kidney stone, or will it detoxify the crystals? Although nobody seems to know if pomegranate (fresh) is high in oxalate, I got a big uptick in ringing when I ate a few tablespoons. It has apparently been used forever for kidney improvement - I'm wondering if it made me dump oxalate. Some people believe that if you take calcium, it will bind to oxalate and resolve the issues. Since the studies showing that supplemental calcium could cause heart attacks, I'm not anxious to do this. I haven't been eating dairy and am not anxious to go back to it and now dark green leafy containing calcium are not a good idea. .Appreciate your studies on this so much. Thank you.
This is interesting to me. This past week I tried to implement the potato hack - I ate only yellow peeled boiled organic potatoes and broke into a crazy itchy rash on my legs. Could it be oxylate?
If I take biotin will this stop? Or is this saying biotin will make this worse? The only other time I get a rash like this is when I have coconut oil.
Hi, Chris,
When I first began to obtain the background I needed to understand the oxalate issues I found in autism 18 years ago (2005), I attended professional oxalate conferences. I was very surprised to discover they were only attended by kidney doctors and kidney researchers. To them, finding oxalate elevated in autism was an anomaly. In fact, finding oxalate elevated apart from kidney stone disease or genetic hyperoxaluria was in their minds, impossible.
Why did I start studying it? Beginning about thirty years ago, my academic work was all about sulfate and discovering its role in neurodevelopment. Years later, sulfate was found to exchange for oxalate on a special set of transporters called the SLC26A family of transporters.
I had already thoroughly explored the role of sulfate in autism, but this new science meant that now I needed to study oxalate to find out how oxalate could disrupt sulfate and other things important in autism. To accomplish that, I studied the oxalate literature for four months with a special focus on the genetic hyperoxalurias where it was known that oxalate traveled to the whole body.
I attended 7 professional oxalate conferences. To my surprise, the scientists there seemed to have formed an unspoken pact to ignore issues that were not centered around kidney stone disease. They were uninterested in how oxalate affected the general biochemistry wherever it went. I had already spent a decade recognizing complex issues in autism, so I knew that oxalate, by affecting sulfate, could alter neurodevelopment as well as hormone and neurotransmitter regulation, and it was a clear mitochondrial toxin. This new information required a reinterpretation of autism findings.
Before that, I had been studying sulfate's role, but now, oxalate could be a major disruptor. Formate was also a substrate of those transporters. Anyone can find literature about how formate and oxalate have been influencing each other, but I found nothing practically useful.
Chris, this is why I am particularly delighted to find your interest in this field and I like the way you are looking at it in the way it should have been studied a long time ago.
The oxalate field for so many years had blinders on...something that Sally Norton and I had both found and explored independently. Sally has been more into thinking about issues with diet, but I became more concerned about reaching academia and helping them study the oxalate the body makes under stress.
It was impossible to do a study in the US on oxalate in autism because the labs in the US that were skilled in measuring oxalate told me they would not test anyone unless they had kidney disease. That is why I recruited a highly qualified group of scientists to look at oxalate levels in autism, and we got astonishing results. That paper is ranked now in the top 4% of scientific studies and it has had 42 citations. That attention is really great, but it is still not motivating other scientists to look past the kidneys and find other types of diseases related to oxalate.
Chris, the commendable sort of thinking that you are doing is exactly what is needed to move oxalate research forward and into new territory. I eagerly invite you to further explore this fruitful area that has been in sore need of your skill set. I hope that you can generate experimental evidence.
In 2005, with a bunch of grateful autism parents, we formed the TryingLowOxalates network and it has has already helped more than 70,000 people discover the relevance of oxalate to their own health. This is the way we picked up an enormous amount of personal experience about reducing oxalate, but we have not seen nearly the amount of change we want to see in academia.
We're trying to change that. Our group performed the most successful fundraising of anybody this past year for the Oxalosis and Hyperoxaluria Foundation for Giving Tuesday, and that is because our vision is to support the sort of thinking you are doing to move the study of oxalate into a new era, where multidisciplinary and cross-disciplinary work rules the roost instead of being barred from the roost.
Kudos on your deep thinking! I would be delighted to see people like you get funded so that we can together solve the many human diseases related to oxalate.
Best wishes,
Susan Owens
Head of the Autism Oxalate Project at the Autism Research Institute
Founder of the Trying Low Oxalates network since 2005
You are so amazing! I am so glad I fumbled my way into your orbit...
Hopefully you are right about biotin helping to degrade oxalate. But even if biotin does not help to degrade oxalate itself, biotin very likely mitigates the toxic effects of oxalate on gluconeogenesis and fatty acid synthesis from lactate, as described in the articles you briefly referenced by Bannister, looking at the interplay of biotin and oxalate in isolated hepatocytes. I imagine this explains the exercise intolerance reported by those with oxalate issues. Too much build-up of lactate. Personally, I had to stop weightlifting because it started to make me feel nauseous and greatly disrupted my sleep. (I can, however, tolerate small amounts of "alactic" training.) Eating too much meat causes the same problem for me, likely because of the added need for biotin, as you have detailed in other posts. I just started some biotin supplementation (I'm starting at 75 mcg/day and will increase to 150 mcg/day), and will report back.
Dead Sea salt baths saved me when I unexpectedly began dumping. It has been some years, I have triggered major oxalate (or something! formate? It burned on the way out, urine, skin, eyes, lips etc). Once I tried eating a couple leaves of raw swiss chard out of my garden after it had frosted. Immediate burning dumping misery, tender points fibromyalgia style, barely able to walk. Floating in a dead sea salt bath (high magnesium chloride, potassium chloride, some sulfate) for an hour or more at a time, literally melted a ton of it away in a few days through my skin. It felt like something granular was coming out of my knee joints and dissolving. I later triggered another dumping episode experimenting with high dose thiamine. Another with diatomaceous earth. I do more careful experimentation now with slower changes. Now my OAT is normal for oxalate and its precursors; I have some other oddball things that may have to do with high need for riboflavin though. I don't do things like raw kale but I am generally okay with COOKED high oxalate foods these days in reasonable quantities.
Hi Chris,
As a prolific calcium oxalate kidney stone producer, I have, over the years attempted to find
some dietary modifications (beyond dietary oxalate restriction) that would decrease my oxalate burden. Two of the most promising possibilities I found:
1) Oxalobacter formigenes, an obligate anaerobic probiotic
which utilizes oxalic acid as its sole source of energy. Oxalate degradation by O. formigenes involves three unique proteins, an oxalate:formate membrane transporter, oxalylCoA decarboxylase, and formyl-CoA transferase. There have been several studies confirming significant degradation of intestinal oxalates. Unfortunately, there doesn't seem to be a commercially reliable source of Oxalobacter available. Oxalo Therapeutics has been developing products that treat primary hyperoxaluria and prevent recurrent kidney stones, but nothing, as of yet, seems available. There is one product, available from India and listed on ebay that purports to contain Oxalobacter Formigenes & Other Probiotics for Calcium Oxalate Stones Reduction. Manufactured by Standford Labs, distributed by La Renon ( India). Needless to say, I am dubious!
2) Oxalate decarboxylase: a company called Nephure came out with a powder that one could sprinkle on food several years ago. Unfortunately, I believe the company stopped production. Here is a double blind that was done in 2020 looking at this product: https://pubmed.ncbi.nlm.nih.gov/35372879/
So, there you have it, two low toxicity products that seem quite efficacious for oxalate reduction that are not commercially available. I guess, for now, back to a low oxalate diet!
This is very, very interesting...thanks Chris. I had severe 'oxalate dumping' symptoms a couple of years back.. still traces now. I was 7 times the upper limit on the organic acids test, and lactate was also very high with raised arabinose, high quinolinic, high hva/vma and a bunch of other stuff out. I work with an excellent nutritionist who suggested oat testing for improving health, thyroid and autoimmunity. Following this test, I started a low oxalate keto diet but struggled to get urine ketones up at first.. but it was this that kicked off the symptoms.. blood pressure drops, tachycardia and horrible anxiety followed by cloudy urine and surprisingly a sense of relief that always came along 10 minutes before the bathroom visit.. every 10 days/2 weeks for months, with all sorts of symptoms in between. I couldn't work or drive in that period. It was as if every time blood levels got below a certain threshold then it would restart! I couldn't believe it at first but a lot of testing and research comvinced me that the dumping was a distinct possibility. Repeated oat testing showed decreasing oxalates after some time of this. Often I felt cold, like feverish, with very dry lips and dizzy, histamine type symptoms. I see that biotin may help stabilise mast cells through cyclic gmp? I had seen evidence that oxalate can directly stimulate degranulation. I took b1, b6, magnesium, citrate, calcium with meals and herbs like phylanthus niruri, dandelion, schisandra to help protect kidneys together with a bunch of other stuff finding a few things that helped symptomatically, which included anything that could increase my blood pressure. I still have occasional symptoms..it would be interesting to.see if biotin made things better/worse!
Thank you have shared to twitter and facebook.
This is great. Please do more research on oxalates. After reading this and the other biotin posts I am going to cautiously experiment with some biotin.
I feel like there must be a way to get back to being able to handle the Oxalates. I happily downed tons of peanut butter and chocolate all the way into my late twenties with no I’ll effect.
Now I can’t even tolerate 50 mg a day and it drives me nuts because even so many healthy things are off limits.
Thanks. I had an oxylate kidney stone once.
Thanks for this fascinating hypothesis, Chris!
What do you think about the role of magnesium and manganese in pyruvate carboxylase function?
Pyruvate carboxylase seems to be a manganese-containing enzyme. But when manganese is lacking, magnesium can substitute, retaining pyruvate carboxylase's textbook enzyme function. (Scrutton et al., 1972.)
However, "oxalate inhibition" requires 7 times more oxalate to achieve the same effect (in chicken livers) in the Mg version of the enzyme, compared with the Mn version of the enzyme. (Scrutton et al., 1972, Table V.) Maybe the manganese in the enzyme is needed to metabolize oxalate efficiently?
Paradoxically, the manganese content in pyruvate carboxylase may indicate magnesium status.
Magnesium deficiency in rat diet resulted in less manganese in organs and less liver pyruvate carboxylase activity. Magnesium seemed to direct manganese (and also calcium) to the right places. (Kimura et al., 1996.)
Magnesium is so much more abundant than manganese, that we might expect magnesium still could fill in gaps in the enzyme for missing manganese, even in the case of magnesium deficiency. So when we lack magnesium in diet, we might find (paradoxically) more magnesium and less manganese in pyruvate carboxylase? Therefore, in magnesium deficiency, we might find as much as 7x less metabolism of oxalate by pyruvate carboxylase?
In addition to its role promoting manganese delivery to pyruvate carboxylase, magnesium acts as a cofactor in Mg-ATP, as you mentioned.
So poor reaction to oxalate could relate to magnesium deficiency causing low liver manganese, low Mg-ATP, and low pyruvate carboxylase activity?
Could apparent need for more biotin indicate an underlying need for more dietary magnesium to make manganese and pyruvate carboxylase work better?
As you speak with enzymologists about investigating pyruvate carboxylase in the first breakdown step of oxalate (as you mentioned in response to Susan Owens), maybe suggest investigating the roles of magnesium and manganese nutritional status, in addition to biotin?
References:
[1] Kimura, M., Ujihara, M., & Yokoi, K. (1996). Tissue manganese levels and liver pyruvate carboxylase activity in magnesium-deficient rats. Biological Trace Element Research, 52, 171-179. https://doi.org/10.1007/BF02789459
[2] Scrutton, M. C., Griminger, P., & Wallace, J. C. (1972). Pyruvate carboxylase: Bound metal content of the vertebrate liver enzyme as a function of diet and species. Journal of Biological Chemistry, 247(10), 3305-3313. https://doi.org/10.1016/S0021-9258(19)45246-0
I tried supplementing with Biotin after Susan Owens recommended I do so because supplementing with B1 (Benfotianime) would bring on oxalate dumping / clearance for me as well. Both Biotin and B1 do this for me separately. However, the intervals and intensity were a bit different. B Complex will do the same, obviously. Ramping up on these by cutting pills or using 1 drop, etc., however, makes the dumping far less intense and less frequent, and that's my tack right now to ramp up on B1 to solve some of the problems Elliot Overton says B1 supplementation can help with when you've been carnivore for a long time but still don't feel great. So it'd be interesting to know why both B1 and Biotin have similar effects.
I paid for the Vitamins and Minerals book at least 2 years ago. Guess I didn't realize you hadn't written it yet. When do you expect it to print? It's been a long time!!
Ah, thank you so much for this article, Chris!! You have given me the explanation I was seeking. 😁
I have been on a low-vitamin A diet (dairy-free and egg-free, but not vegan--I eat beef and chicken) since 2018, but this year in February I decided to start incorporating a greater number of eggs back into my diet in order to increase my choline intake to between 800 mg and 1200 mg (prior to this, I had been somewhat above the female RDA for choline, but more in the 500 mg to 600 mg range). Turns out, they make me feel horrible, but I wasn't entirely satisfied with blaming retinol for this reaction, as my egg intake never took me beyond the RDA for vitamin A.
Just three to four eggs daily (whites always eaten cooked, yolks sometimes raw) produced unusual symptoms: a red bumpy rash on my leg, what felt like a mild bladder infection not bad enough to go to the doctor about, constipation (normally my digestion is great--I eat a legume-heavy diet), insomnia, and achy hands.
I do not get joint pain normally, at all. So I figured perhaps this weird reaction had something to do with oxalate, but wasn't entirely sure why eggs would trigger dumping so strongly.
I backed off on the eggs to give my gut a rest (it helped), then just this month I tried consuming eight eggs daily for three consecutive days. Chronometer tells me that amount provides nearly 300% of the RDA for biotin?! (I didn't know this when I decided to try it lol.) While doing this, my brain fog was worse than it has been all year, constipation was bad, my back ached (kidney area), my shins hurt, my toes and fingers hurt, everything hurt (kinda like the aches we get during a flu), the rash expanded, and an area on my finger where I had gotten a tendon stitched in the past felt like it had been smashed and was throbbing...
I was at my wit's end wondering why, but now, thanks to you, I feel I must blame all of this on biotin for triggering an oxalate dump! Yours is the best explanation of the dramatic symptoms I've found so far.
It'd be pretty cool if your idea here helps people manage the oxalate dumping process, instead of it feeling super random and overwhelming.
Thanks again SO MUCH, Chris!! 😁🌻☀
P.S. It might be good to include this fact: My oxalate intake has been between 50 mg and 150 mg daily for the past 6 months.
P.P.S. ETA: I should also note I found going full-vegan (particularly focusing on a ridiculous amount of raw fruit) without any added saturated fat from coconut oil (hemp and sunflower seeds seem fine) after ceasing egg consumption resolves the constipation issue within 24 hours for me so far, whilst consuming a meat and saturated-fat heavy diet seemed to prolong it. Will keep testing to confirm this holds true in my case, but this is my initial observation.
I've been troubled with a high pitch ringing in my ears for a few years. My doctor believes I am losing my hearing. My hearing is not perfect (I'm 77 yrs old), but I discovered that I can control the ringing by what I eat. Kale, chard, sweet potato, peanuts and other things make the ringing worse. If I don't eat anything high in Oxalate, it diminishes a great deal but doesn't go away. My brother had a kidney stone, my sister had cystitis, and my mother was put on a low oxalate diet. Until recently, I had been on a vegan diet with occasional small amounts of fish. I'm wondering if increasing my animal protein is going to make this problem worse. If I take biotin, will it make my body dump more and maybe give me a kidney stone, or will it detoxify the crystals? Although nobody seems to know if pomegranate (fresh) is high in oxalate, I got a big uptick in ringing when I ate a few tablespoons. It has apparently been used forever for kidney improvement - I'm wondering if it made me dump oxalate. Some people believe that if you take calcium, it will bind to oxalate and resolve the issues. Since the studies showing that supplemental calcium could cause heart attacks, I'm not anxious to do this. I haven't been eating dairy and am not anxious to go back to it and now dark green leafy containing calcium are not a good idea. .Appreciate your studies on this so much. Thank you.
This is interesting to me. This past week I tried to implement the potato hack - I ate only yellow peeled boiled organic potatoes and broke into a crazy itchy rash on my legs. Could it be oxylate?
If I take biotin will this stop? Or is this saying biotin will make this worse? The only other time I get a rash like this is when I have coconut oil.
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