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Started taking B6 and feeling funny. Help Please. :(

Violeta

Senior Member
Messages
2,895
With this combo I was able to reach 750mg of magnesium but I'm currently running into a manganese defiency because of the B2 healing my liver from its iron overload.

What are your manganese deficiency symptoms? TIA
 
Messages
70
This is an important issue.. I've got a new hypothesis, via some guy on the Longecity Forum
Supposedly he's read up on b6 for countless years, says that old studies say to take b6/p5p in a 1:1 ratio, and that prevents all side-effects

It's a post by @plasticperson in the middle of the page
http://www.longecity.org/forum/topic/74664-p5p-b6-toxicity/

Supposedly there is or was a supplement that provided the two in a 1:1 ratio...
Anyone willing to try?
 

aquariusgirl

Senior Member
Messages
1,732
Like I said earlier I then ran into issues with the B2 causing light orange stool, insomnia, fatigue etc.. Just started on additional manganese to see if that is the solution for that :)

@McGyver .,,I’m guessing that’s copper dumping!
You need a copper binder.
 

aquariusgirl

Senior Member
Messages
1,732
For me, high B6 was a functional deficiency...,supplementing makes me dump oxalates & metals ...,.hence the spaciness the OP talks about.

Need to take binders & mag citrate to bind metals & oxalates.
 

JES

Senior Member
Messages
1,320
For me, high B6 was a functional deficiency...,supplementing makes me dump oxalates & metals ...,.hence the spaciness the OP talks about.

Need to take binders & mag citrate to bind metals & oxalates.

B6 does not cause oxalate dump, at least according to this study. B6 acts on over a hundred of enzymes that control amino acids and serves as cofactor in the making of neurotransmitters such as serotonin and norepinephrine. All of this could be causing the spaciness. I agree that high B6 can mean functional deficiency, my vitamin B6 blood test was out of charts high and I hadn't been supplementing with it before the test.

@GenDylan I agree with the use of P5P, requires one less step of conversion and seems to cause less restlessness symptoms for me. In fact I don't see a reason to take B6 in form of pyridoxine at all when we are talking about the same vitamin, but one is in more active form.
 
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aquariusgirl

Senior Member
Messages
1,732
Hey take it up with Susan Costen Owens. Oxalates expert.
I think a lot of things cause oxalates dumping .....especially ALA.
 
Messages
70
B6 does not cause oxalate dump, at least according to this study. B6 acts on over a hundred of enzymes that control amino acids and serves as cofactor in the making of neurotransmitters such as serotonin and norepinephrine. All of this could be causing the spaciness. I agree that high B6 can mean functional deficiency, my vitamin B6 blood test was out of charts high and I hadn't been supplementing with it before the test.

@GenDylan I agree with the use of P5P, requires one less step of conversion and seems to cause less restlessness symptoms for me. In fact I don't see a reason to take B6 in form of pyridoxine at all when we are talking about the same vitamin, but one is in more active form.

See P5P still gives me the bad neurapathy... I do think I am really b6 deficient, so the guys theory of taking both in equal amounts, makes some sense to me
 

Gondwanaland

Senior Member
Messages
5,092
Please see this thread

There are 2 sides of this coin:

https://www.ncbi.nlm.nih.gov/m/pubmed/28716455/
The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function.
Vrolijk MF, et al. Toxicol In Vitro. 2017.

This one is about innate error, but I suppose one can acquire something like it from metabolic derangement:
https://www.ncbi.nlm.nih.gov/pubmed/21305354
J Inherit Metab Dis. 2011 Apr;34(2):529-38. doi: 10.1007/s10545-011-9279-7. Epub 2011 Feb 9.
Pyridoxal 5'-phosphate in cerebrospinal fluid; factors affecting concentration.
Footitt EJ1, Heales SJ, Mills PB, Allen GF, Oppenheim M, Clayton PT.
Author information

Abstract
Analysis of pyridoxal 5'-phosphate (PLP) concentration in 256 cerebrospinal fluid (CSF) samples from patients with neurological symptoms showed that the variance is greater than indicated by previous studies. The age-related lower reference limit has been revised to detect inborn errors of metabolism that lead to PLP depletion without a high false positive rate: < 30 days, 26 nmol/L; 30 days to 12 months, 14 nmol/L; 1-2 years, 11 nmol/L; > 3 years, 10 nmol/L. Inborn errors leading to PLP concentrations below these values include pyridoxine-dependent epilepsy due to antiquitin deficiency, and molybdenum cofactor deficiency that leads to the accumulation of sulfite, a nucleophile capable of reacting with PLP. Low PLP levels were also seen in a group of children with transiently elevated urinary excretion of sulfite and/or sulfocysteine, suggesting that there may be other situations in which sulfite accumulates and inactivates PLP. There was no evidence that seizures or the anticonvulsant drugs prescribed for patients in this study led to significant lowering of CSF PLP. A small proportion of patients receiving L-dopa therapy were found to have a CSF PLP concentration below the appropriate reference range. This may have implications for monitoring and treatment. A positive correlation was seen between the CSF PLP and 5-methyl-tetrahydrofolate (5-MTHF) and tetrahydrobiopterin (BH(4)) concentrations. All are susceptible to attack by nucleophiles and oxygen-derived free-radicals, and CSF has relatively low concentrations of other molecules that can react with these compounds. Further studies of CSF PLP levels in a wide range of neurological diseases might lead to improved understanding of pathogenesis and possibilities for treatment.
 

alicec

Senior Member
Messages
1,572
Location
Australia
B6 does not cause oxalate dump, at least according to this study.

And I can quote this study showing that B6 does reduce oxalate production in dialysis patients.

Both studies though are fairly irrelevant to the general question since they are looking at a particular group of patients who have uraemia and renal disease. Elevated plasma oxalate is observed in these patients but the cause of this is not clear, or there may be a number of causes.

B6 was tried in these patients as a means of reducing oxalates because it is the mainstay of treatment for primary hyperoxaluria (PH). It doesn't always work for these patients either but for responders, it is very effective.

The reason for this variability in response in the PH patients is the type of defect in the B6 dependent enzyme alanine glyoxalate transaminase (AGXT), which is the cause of the defective oxalate metabolism in these patients. Some mutant enzymes are simply unable to function at all and no amount of B6 can stimulate them, whereas some, including the most common of the genetic defects causing PH, do have some residual activity which can be boosted by B6.

The cause of hyperoxalosis in the kidney dialysis patients is not so clear cut and the variability of cause is presumably responsible for the variability in B6 response.

PH is rare but serves as a good model for the defective metabolism that is behind secondary excessive endogenous oxalate production. The latter is much more common than realised and is the subject of the research of Susan Costen Owens who @aquariusgirl has referred to.

Essentially what she and others have shown is that oxidative stress can induce conformational changes in AGXT (and indeed all transaminase enzymes) which mean they no longer bind B6 efficiently and so exhibit poor function. This leads to a self perpetuating cycle of oxalate accumulation and spreading metabolic derangement.

B6 treatment is very successful in stimulating the sluggish enzyme, just as with PH, and results in reduction of oxalate production.

As oxalate blood levels fall, the body is encouraged to get rid of its tissue oxalate stores, and this process - so called oxalate dumping - can have unpleasant symptoms.

So don't allow a small study of a group of patients with unique problems to blind you to an long history of B6 treatment of PH and a more recent history of secondary hyperoxaluria in various chronic conditions.
 

Freddd

Senior Member
Messages
5,184
Location
Salt Lake City
Currently I can't figure out what has happened to me over the past few months but thanks for your suggestions - I'll rethink things in light of these. Something has become very unbalanced.

I used to happily take 600-800 mg magnesium (as bisglycinate) orally plus a 4-5 ml magnesium chloride topically - had done for years - now I've had to drop all of the oral dose though have continued the topical.

It certainly feels to me that I have slowly depleted something but I can't figure out exactly what. Certainly I'll try more boron - I have some of the 3 mg stuff which I took for a while a long time ago. I've been taking 50 mg riboflavin (or 35 mg riboflavin 5 phosphate) daily for a very long time, the trace mineral prep contains 2.5 mg manganese and 50 mg pyridoxal 5 phosphate has been a minimum dose of B6 for some time (I have added considerably more as pyridoxine at times as a way of dealing with oxalate problems).

I only stopped the B6 completely for a short time - it became clear quickly that this was not a good idea and for now I am back to 50 mg P5P. While I had to reduce the methyl folate and B12 considerably it seems too that this is not a good idea and I am trying to increase very slowly (I once used to tolerate quite high doses).

Have to do more experimenting!

I found that if I took a modest amount of everything, only the nutrient lack that stops cell formation shows its symptoms. The symptoms are caused by the fail points. Sp Methyl Trap caused by low mecbl or any other cobalamin in place of where the MeCbl ought to be, caused methyltrap. Low folate also causes the same symptoms but s little differently. There are at least 8 patterns of paradoxical folate deficiency, and all but methyltrap need methylfolate.

The link below may be helpful.

https://www.quora.com/Has-someone-u..._filter__=all&__nsrc__=1&__snid3__=1808215186
 

renski

Senior Member
Messages
338
Location
Honolulu
High p5p in blood can be a co-factor or another nutrient is depleted, I know when I was on b1, r5p and trace minerals my p5p was high in blood, it’s in range now but something I was taking seemed to be inactivating the b6, although the b6 marker on gpl oat wasn’t showing any changes (was still very deficient on oats)