Guest guest Posted June 8, 2012 Report Share Posted June 8, 2012 , Thank You So Much For This Post!!!! This is an issue I've determined I need to look closer at...my dad's doctor just put him on a low oxalate, with this post I've decided I need to dig deeper. 1) May I have your permission to send him a copy of this great info? 2) We've recently found our family to have an issues with MTHFR gene mutation. To me it seams like many issues between oxalates & MTHFR coorelate. Do you have any insight, research or info on a possible coorelation between the 2? I'd highly appreciate your thoughts & I Thank You In Advance!!!! Rita ps...I did not trim as I want to keep the info together for future reference w/my spreadsheet. > > > > Noel, > > > > I'm not but I do wish to comment. Our son used to have approximately 4 second delay in his response to a verbal request (based upon daily data collection in our intensive therapy program).In the past year and a half that has gone away. Sometimes he takes a bit longer to process the verbal input before he acts- particularly when it's late, and he's tired. > > > > Our behaviorist descibed what was happening as an auditory professing issue. We did not pursue actual testing, although this can be done ( it's a little too similar to the EEG and I hope to not have tob relive that one!) When we first had his hearing checked at Duke Childrens Hospital, they had the technology in house to test the brain's response to sound. I'll bet they still do. > > Hope this helps! > > > > > > > > Sent from my iPhone > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 8, 2012 Report Share Posted June 8, 2012 Rita, Certainly you can share that with your dad's doctor. I wish more people grasped why the whole folic acid cycle interacting with remethylation becomes irrelevant when someone is in oxidative stress. Have you ever heard about that? Dick Deth talked about this years ago at a DAN! conference, and what he said is that the body turns OFF both cycles working together at methionine synthase WHEN the cell is in oxidative stress. That happens on purpose because it is so critical that the body get rid of the oxidative stress by routing homocysteine to glutathione...a one way trip away from remethylation, with no return ticket. Why does that switch exist? Glutathione is what can turn the oxidative stress off, but you have to have the glutathione in these very same places (within a compartment of cells) for it to be able to turn off the oxidative stress. So, your body tries to make it. A huge unforeseen problem is that oxalate all by itself creates HUGE oxidative stress. Once it has gotten into the inner working of cells, you can throw all the folinic acid in the world at this problem, but it won't do any good if the body has turned off this " maintenance " system until the oxidative stress is resolved. The existence of this switch is why a much greater emphasis needs to be placed on recognizing oxidative stress. In this situation, it becomes a problem to be giving high doses of vitamin C. Why? Because once vitamin C is oxidized, it converts in large amounts to oxalate, which is a powerful PRO oxidant. The treatment will in time lead to greater oxidative stress. That will mean that many enzymes (including methionine synthase) will stop working as more oxalate is around to raise the oxidative stress level and deplete glutathione. This is why supplements chosen to help the folic acid cycle or remethylation work better will not in this situation be effective. Why not effective? Because the reason the enzyme isn't working is not LACK of substrate (as in deficiency) but it is because the cell is in so much oxidative stress that the needed cofactors won't be able to bind properly where they are needed. This whole issue needs a lot more study, but this change can be observed on the OAT. You usually can't see it until the correction for creatinine that the labs do for spot urine tests has been removed. Why would that be? When the body gets low in B6 activity (which seems to happen in oxidative stress) then the kidney tubule cells will start extracting creatinine from blood and will start secreting it to urine in high amounts. When people decided to use creatinine to correct for urine concentration decades ago, doctors thought creatinine was never secreted. Years later, as scientists studied it, they found out that many different situations lead to higher secretion of creatinine to urine, not only oxalate issues and B6 deficiency, but also stuff like sickle cell anemia and some antibiotics. Even though the scientists have known this stuff for years and years, that information never reached the right people to get them to change medical practice in getting rid of using creatinine to " correct " urine concentration. So whenever creatinine secretion is increased to urine, all the analytes on whatever test go artificially low when they are ratioed to creatinine. This is why your doctor may look at the test and think things are better if the only thing he watches is whether a value has moved over or under a reference range. Things won't go over reference ranges when creatinine is high because the ratio to creatinine has shifted all the numbers low. (A big denominator makes the numerator smaller.) In healthy children, pyroglutamate, which is the key marker of oxidative stress on OATs, never goes over 11, but you may have noticed that Great Plains has its reference range set at 62 for children. That is almost six times what you see in healthy children. The ironic thing is that the Great Plains range is lower than most other labs...the ones who probably get their reference population from people who have some sort of illness...people who ordered their test trying to figure out how to get better. When someone is in oxidative stress because of oxalate, their urine concentration of everything may look low on the test.... as much as three times lower than it really is. I've even seen it be five times lower in some adults. You can see you would have to be eighteen times normal in this situation to be flagged as high in pyroglutamate on the Great Plains test and many more times normal at labs that don't flag it until you are over 100. See how we can end up with misleading information? It is very unfortunate that the labs have their reference ranges for pyroglutamate set this high since it is such an important marker for recognizing a situation when the body has had to go into a huge shift. Lest you think ill of the labs serving the autism community, even Labcorp and Quest have ranges way too high. What sets the range is how sick the people are who are in a reference population. Doctors (and others) assume the reference population is people who are healthy with no genetic ties to autism, but does any lab use thoroughly healthy controls with no links to autism? Not really. I've asked a lot of them, and inevitably the reference population is some subset of patients that order the test. This is like setting your norms for a healthy weight by the average weights you get from people weighing in at Weight Watchers. When I noticed this problem many years ago, I looked at the people in a database of OAT tests from children with autism (237 tests) that I had collected over about ten years. I saw that only two of those 237 tests would be flagged by the current pyroglutamate range at Great Plains. Actually, I also saw that NONE of the children would have been flagged for pyroglutamate being high at all the other labs. This database only included children diagnosed with a condition that is highly associated in the medical literature with oxidative stress. What can you conclude except that our labs are telling people things are OK, when, really, they are not? Just today, for example, I got an OAT on a teenager who started to have tics that very well may have been caused by his oxalate being so high that it tangled with his magnesium chemistry. (I got tics for about a week last year when I accidentally ate plantain not realizing it was extremely high in oxalate. I was fine for half a day, and then the tics began and lasted the better part of a week. I know how out of control these tics can make you feel.) So, today, after adjusting the OAT in this teenager for the change in urine concentration that was reflected on his test (calculated from his data), his creatinine had shifted to three times higher than normal in proportion to everything else on the test. After I made the adjustment to get rid of the creatinine effect,and to correct the urine concentration a different way, then his pyroglutamate ended up being 70 something. Now his oxalate was over 300 and his marker for endogenous oxalate (glycolic acid) was about 250. These shifts that couldn't be seen before (because of the creatinine) could certainly explain the dramatic changes his mother has seen in him lately. In my database that now has 540 OATs, I can see the metabolism starting to fall apart in people when their adjusted glycolic acid goes over forty, and it becomes seriously disrupted over 75 (after the urine adjustment). But really, what had happened to him? The young man's doctor, not knowing about or noticing the shift in creatinine, didn't think this young man was in oxidative stress since his pyroglutamate wasn't flagged as high. The doctor did notice that ascorbic acid was low on the test and circled it. (Ascorbic acid will immediately oxidize when it is introduced to an oxidative environment. When this happens, it converts into dehydroascorbic acid which doesn't show up on the OAT, so it makes the test (incorrectly) seem low in ascorbic acid.) The young man's doctor, not realizing this issue, and assuming he was deficient in vitamin C, gave this teenager orders to take 20 grams of vitamin C, which he did. After that, the boy totally crashed and they thought maybe he was having a reaction to a pharmaceutical drug he was on, so they started to take him off the drug. This whole story might have gone completely differently had his doctor been knowledgeable about oxalate and how it may artificially lower the analytes on tests ratioed to creatinine. I wish he knew to bring down oxidative stress by OTHER antioxidants. He probably didn't know you should avoid vitamin C at levels over 200 mgs/day when someone is this high in oxidative stress. Since the doctor didn't recognize the problem, he treated with a treatment whose ill effects may unfortunately last weeks. This is why, Rita, getting back to what you said, you you may not succeed in getting MTHFR to work better (and a whole host of other enzymes) when their active sites are being compromised from doing their jobs because of oxidative stres. Deep inside your cells, the chemistry is struggling when this happens, and the wrong sorts of molecules are sticking to and gumming up the works in a lot of enzymes. The sad thing about this is that scientists have determined that urinary ascorbic acid is a very poor indicator of overall body vitamin C status. I wish the doctors knew this! So if you have an OAT that has just about no vitamin C on it, the low number may not mean you are deficient, but it may mean you are in oxidative stress. I just looked in my larger (autism + others) database at which levels of vitamin C were matched by which levels of pyroglutamate. There are a LOT of extremely high ascorbic acids. 27% are over the Great Plains reference range of 200 (after adjustment) and 18% over 500. If I look only at those with ascorbic acid over 500, the association of ascorbic acid to pyroglutamate, which again, is the marker of oxidative stress, looks completely random. There is no evidence of these high levels of ascorbic acid improving pyroglutamate in the least. In fact the trendline for pyroglutamate is a completely straight line when I sort ascorbic acid from highest to lowest in those with the high levels over 500. Take home message: the biggest deal for improving folic acid and remethylation is lowering oxidative stress and you can tell you've succeeded if you've lowered pyroglutamate into levels you see in healthy children, which is below 11. > > , > Thank You So Much For This Post!!!! > This is an issue I've determined I need to look closer at...my dad's doctor just put him on a low oxalate, with this post I've decided I need to dig deeper. > 1) May I have your permission to send him a copy of this great info? > 2) We've recently found our family to have an issues with MTHFR gene mutation. To me it seams like many issues between oxalates & MTHFR coorelate. Do you have any insight, research or info on a possible coorelation between the 2? > I'd highly appreciate your thoughts & I Thank You In Advance!!!! > Rita > > ps...I did not trim as I want to keep the info together for future reference w/my spreadsheet. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2012 Report Share Posted June 9, 2012 Wow, that was a fantastic post, . Â I 100% agree that some of the biggest gains we've seen is in increasing our antioxidant support (outside of Vit C). Â I did (foolishly) try Vit C again when we were on a chelation round at 300 mg...let me just say I wrecked havoc that I've only started correcting again -- this was one mean beast! Â No matter how I try to problem solve and try to think our way around the Vit C problem (we have chronically low Vit C, for other people reading this who might not know) and no matter what I do, Vit C is a no-go for us, even small doses like 100 mg -- it's taken me abt 3 weeks after I gave Maia 300 mg of Vit C when she was on round 3 weeks ago to start to regain control of the situation again -- those 300 mg/day for only 3 days undid abt 8 months worth of work we did with addressing oxidative stress and increasing glutathione....all kinds of ASD symptoms came back with an angry vengeance. Â I find I keep saying this in hindsight -- was right... Â Rita, Certainly you can share that with your dad's doctor. I wish more people grasped why the whole folic acid cycle interacting with remethylation becomes irrelevant when someone is in oxidative stress. Have you ever heard about that? Dick Deth talked about this years ago at a DAN! conference, and what he said is that the body turns OFF both cycles working together at methionine synthase WHEN the cell is in oxidative stress. That happens on purpose because it is so critical that the body get rid of the oxidative stress by routing homocysteine to glutathione...a one way trip away from remethylation, with no return ticket. Why does that switch exist? Glutathione is what can turn the oxidative stress off, but you have to have the glutathione in these very same places (within a compartment of cells) for it to be able to turn off the oxidative stress. So, your body tries to make it. A huge unforeseen problem is that oxalate all by itself creates HUGE oxidative stress. Once it has gotten into the inner working of cells, you can throw all the folinic acid in the world at this problem, but it won't do any good if the body has turned off this " maintenance " system until the oxidative stress is resolved. The existence of this switch is why a much greater emphasis needs to be placed on recognizing oxidative stress. In this situation, it becomes a problem to be giving high doses of vitamin C. Why? Because once vitamin C is oxidized, it converts in large amounts to oxalate, which is a powerful PRO oxidant. The treatment will in time lead to greater oxidative stress. That will mean that many enzymes (including methionine synthase) will stop working as more oxalate is around to raise the oxidative stress level and deplete glutathione. This is why supplements chosen to help the folic acid cycle or remethylation work better will not in this situation be effective. Why not effective? Because the reason the enzyme isn't working is not LACK of substrate (as in deficiency) but it is because the cell is in so much oxidative stress that the needed cofactors won't be able to bind properly where they are needed. This whole issue needs a lot more study, but this change can be observed on the OAT. You usually can't see it until the correction for creatinine that the labs do for spot urine tests has been removed. Why would that be? When the body gets low in B6 activity (which seems to happen in oxidative stress) then the kidney tubule cells will start extracting creatinine from blood and will start secreting it to urine in high amounts. When people decided to use creatinine to correct for urine concentration decades ago, doctors thought creatinine was never secreted. Years later, as scientists studied it, they found out that many different situations lead to higher secretion of creatinine to urine, not only oxalate issues and B6 deficiency, but also stuff like sickle cell anemia and some antibiotics. Even though the scientists have known this stuff for years and years, that information never reached the right people to get them to change medical practice in getting rid of using creatinine to " correct " urine concentration. So whenever creatinine secretion is increased to urine, all the analytes on whatever test go artificially low when they are ratioed to creatinine. This is why your doctor may look at the test and think things are better if the only thing he watches is whether a value has moved over or under a reference range. Things won't go over reference ranges when creatinine is high because the ratio to creatinine has shifted all the numbers low. (A big denominator makes the numerator smaller.) In healthy children, pyroglutamate, which is the key marker of oxidative stress on OATs, never goes over 11, but you may have noticed that Great Plains has its reference range set at 62 for children. That is almost six times what you see in healthy children. The ironic thing is that the Great Plains range is lower than most other labs...the ones who probably get their reference population from people who have some sort of illness...people who ordered their test trying to figure out how to get better. When someone is in oxidative stress because of oxalate, their urine concentration of everything may look low on the test.... as much as three times lower than it really is. I've even seen it be five times lower in some adults. You can see you would have to be eighteen times normal in this situation to be flagged as high in pyroglutamate on the Great Plains test and many more times normal at labs that don't flag it until you are over 100. See how we can end up with misleading information? It is very unfortunate that the labs have their reference ranges for pyroglutamate set this high since it is such an important marker for recognizing a situation when the body has had to go into a huge shift. Lest you think ill of the labs serving the autism community, even Labcorp and Quest have ranges way too high. What sets the range is how sick the people are who are in a reference population. Doctors (and others) assume the reference population is people who are healthy with no genetic ties to autism, but does any lab use thoroughly healthy controls with no links to autism? Not really. I've asked a lot of them, and inevitably the reference population is some subset of patients that order the test. This is like setting your norms for a healthy weight by the average weights you get from people weighing in at Weight Watchers. When I noticed this problem many years ago, I looked at the people in a database of OAT tests from children with autism (237 tests) that I had collected over about ten years. I saw that only two of those 237 tests would be flagged by the current pyroglutamate range at Great Plains. Actually, I also saw that NONE of the children would have been flagged for pyroglutamate being high at all the other labs. This database only included children diagnosed with a condition that is highly associated in the medical literature with oxidative stress. What can you conclude except that our labs are telling people things are OK, when, really, they are not? Just today, for example, I got an OAT on a teenager who started to have tics that very well may have been caused by his oxalate being so high that it tangled with his magnesium chemistry. (I got tics for about a week last year when I accidentally ate plantain not realizing it was extremely high in oxalate. I was fine for half a day, and then the tics began and lasted the better part of a week. I know how out of control these tics can make you feel.) So, today, after adjusting the OAT in this teenager for the change in urine concentration that was reflected on his test (calculated from his data), his creatinine had shifted to three times higher than normal in proportion to everything else on the test. After I made the adjustment to get rid of the creatinine effect,and to correct the urine concentration a different way, then his pyroglutamate ended up being 70 something. Now his oxalate was over 300 and his marker for endogenous oxalate (glycolic acid) was about 250. These shifts that couldn't be seen before (because of the creatinine) could certainly explain the dramatic changes his mother has seen in him lately. In my database that now has 540 OATs, I can see the metabolism starting to fall apart in people when their adjusted glycolic acid goes over forty, and it becomes seriously disrupted over 75 (after the urine adjustment). But really, what had happened to him? The young man's doctor, not knowing about or noticing the shift in creatinine, didn't think this young man was in oxidative stress since his pyroglutamate wasn't flagged as high. The doctor did notice that ascorbic acid was low on the test and circled it. (Ascorbic acid will immediately oxidize when it is introduced to an oxidative environment. When this happens, it converts into dehydroascorbic acid which doesn't show up on the OAT, so it makes the test (incorrectly) seem low in ascorbic acid.) The young man's doctor, not realizing this issue, and assuming he was deficient in vitamin C, gave this teenager orders to take 20 grams of vitamin C, which he did. After that, the boy totally crashed and they thought maybe he was having a reaction to a pharmaceutical drug he was on, so they started to take him off the drug. This whole story might have gone completely differently had his doctor been knowledgeable about oxalate and how it may artificially lower the analytes on tests ratioed to creatinine. I wish he knew to bring down oxidative stress by OTHER antioxidants. He probably didn't know you should avoid vitamin C at levels over 200 mgs/day when someone is this high in oxidative stress. Since the doctor didn't recognize the problem, he treated with a treatment whose ill effects may unfortunately last weeks. This is why, Rita, getting back to what you said, you you may not succeed in getting MTHFR to work better (and a whole host of other enzymes) when their active sites are being compromised from doing their jobs because of oxidative stres. Deep inside your cells, the chemistry is struggling when this happens, and the wrong sorts of molecules are sticking to and gumming up the works in a lot of enzymes. The sad thing about this is that scientists have determined that urinary ascorbic acid is a very poor indicator of overall body vitamin C status. I wish the doctors knew this! So if you have an OAT that has just about no vitamin C on it, the low number may not mean you are deficient, but it may mean you are in oxidative stress. I just looked in my larger (autism + others) database at which levels of vitamin C were matched by which levels of pyroglutamate. There are a LOT of extremely high ascorbic acids. 27% are over the Great Plains reference range of 200 (after adjustment) and 18% over 500. If I look only at those with ascorbic acid over 500, the association of ascorbic acid to pyroglutamate, which again, is the marker of oxidative stress, looks completely random. There is no evidence of these high levels of ascorbic acid improving pyroglutamate in the least. In fact the trendline for pyroglutamate is a completely straight line when I sort ascorbic acid from highest to lowest in those with the high levels over 500. Take home message: the biggest deal for improving folic acid and remethylation is lowering oxidative stress and you can tell you've succeeded if you've lowered pyroglutamate into levels you see in healthy children, which is below 11. > > , > Thank You So Much For This Post!!!! > This is an issue I've determined I need to look closer at...my dad's doctor just put him on a low oxalate, with this post I've decided I need to dig deeper. > 1) May I have your permission to send him a copy of this great info? > 2) We've recently found our family to have an issues with MTHFR gene mutation. To me it seams like many issues between oxalates & MTHFR coorelate. Do you have any insight, research or info on a possible coorelation between the 2? > I'd highly appreciate your thoughts & I Thank You In Advance!!!! > Rita > > ps...I did not trim as I want to keep the info together for future reference w/my spreadsheet. > Quote Link to comment Share on other sites More sharing options...
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