What impairs vitamin B6 production/utilization?

[Learner1]

That's super interesting, I have super low estradiol too.

Low estradiol and low B6 leads to low serotonin (which I have a lot of symptoms of), so hopefully fixing both these things should help a lot.

Thanks for the reply

B1, B2, B3, B6 as P5P, B12, and D are all worth looking into for tinnitus. Too much B6 as pyridoxine HCl can actually cause tinnitus - P5P does not lead to overdose

 

[Outlaw]

B1, B2, B3, B6 as P5P, B12, and D are all worth looking into for tinnitus. Too much B6 as pyridoxine HCl can actually cause tinnitus - P5P does not lead to overdose

Super interesting thanks.

I assume the excess B6 in my blood is pyridoxine, since it hasn't been "activated"?

So basically it's possible to have at the same time 1) an excess of pyridoxine (non activated) and 2) a functional deficiency of P5P (due to the faulty methylation).

Am I understanding that right?

 

[Learner1]

Yes

 

[Outlaw]

Yes

Just curious, where did you learn that excess pyridoxine can cause tinnitus? I googled it but didnt find anything

 

[Learner1]

Just curious, where did you learn that excess pyridoxine can cause tinnitus? I googled it but didnt find anything

I can't find it when I looked again, but I'm sure it was true.

Both pyridoxine HCl deficiency and overload can cause neuropathy, and I believe tinnitus is a form of neuropathy.

My own experience is that I seemed to have a huge need for B6, which I took as 250mg pyridoxal-5-phosphate and still my tests said I was deficient. My doctor suggested I switch out 100mg of the P5P with pyridoxine HCl, and I got neuropathy within a week.

There are warnings that the upper limit of B6 is 200mg, but I believe it's because the pyridoxine HCl isn't used properly, it needs to convert. I went back to all P5P at 200mg, then over a couple of months, went gradually up to 350mg, which was helpful, and I no longer was deficient on tests. The neuropathy went away after about 3 weeks of the P5P.

I eventually found that I have a bunch of pathways that all want B6, including a oxaluria caused by antibiotics. As I dealt with that, I've been able to reduce my intake to about 150mg a day of P5P.

 

[Outlaw]

I can't find it when I looked again, but I'm sure it was true.

Both pyridoxine HCl deficiency and overload can cause neuropathy, and I believe tinnitus is a form of neuropathy.

My own experience is that I seemed to have a huge need for B6, which I took as 250mg pyridoxal-5-phosphate and still my tests said I was deficient. My doctor suggested I switch out 100mg of the P5P with pyridoxine HCl, and I got neuropathy within a week.

There are warnings that the upper limit of B6 is 200mg, but I believe it's because the pyridoxine HCl isn't used properly, it needs to convert. I went back to all P5P at 200mg, then over a couple of months, went gradually up to 350mg, which was helpful, and I no longer was deficient on tests. The neuropathy went away after about 3 weeks of the P5P.

I eventually found that I have a bunch of pathways that all want B6, including a oxaluria caused by antibiotics. As I dealt with that, I've been able to reduce my intake to about 150mg a day of P5P.

That's interesting thanks.

What you read was about pyridoxine causing neuropathy, or tinnitus specifically?

So raising P5P will lower excess levels of pyridoxine? I though I just had to kickstart my methylation with methylation support to convert the accumulated unconverted B's.

 

[Learner1]

That's interesting thanks.

What you read was about pyridoxine causing neuropathy, or tinnitus specifically?

So raising P5P will lower excess levels of pyridoxine? I though I just had to kickstart my methylation with methylation support to convert the accumulated unconverted B's.

You might find this helpful in explaining The difference in effect between P5P and pyridoxine. I have had no trouble with high dose P5P because it's the form that's used in the body while pyridoxine has to convert, And it's a little dangerous, and my book.

I think you're instincts are correct and trying to increase B6, and I think P5P is the best way to do it. I would also look into the use of R5P, riboflavin-5-phosphate.

 

[Outlaw]

You might find this helpful in explaining The difference in effect between P5P and pyridoxine. I have had no trouble with high dose P5P because it's the form that's used in the body while pyridoxine has to convert, And it's a little dangerous, and my book.

I think you're instincts are correct and trying to increase B6, and I think P5P is the best way to do it. I would also look into the use of R5P, riboflavin-5-phosphate.

Thank you very much.

If you don't mind I have one more question for you. I eat a lot of chicken and brocoli, is it possible this causes my high B6 (~3x the max range), or is it highly improbable that diet alone could explain such a high level?

The way I see it, no way could diet be solely responsible for such a high level, but I'm just looking to confirm!

 

[Learner1]

Thank you very much.

If you don't mind I have one more question for you. I eat a lot of chicken and brocoli, is it possible this causes my high B6 (~3x the max range), or is it highly improbable that diet alone could explain such a high level?

The way I see it, no way could diet be solely responsible for such a high level, but I'm just looking to confirm!

From broccoli and chicken alone, looks like the most you can practically get in a day is about 3mg. If you have fabulous digestion and a low need for B6, which is used in over 100 processes in the body, I suppose it might look high, but I find it hard to believe when my body needs 2-300mg a day above the chicken and broccoli I eat.

 

[Gondwanaland]

Thank you very much.

If you don't mind I have one more question for you. I eat a lot of chicken and brocoli, is it possible this causes my high B6 (~3x the max range), or is it highly improbable that diet alone could explain such a high level?

The way I see it, no way could diet be solely responsible for such a high level, but I'm just looking to confirm!

It happened to me: eating broccoli daily impaired my thyroid function and I believe this on its own would impair B6 activation.

 

[Learner1]

It happened to me: eating broccoli daily impaired my thyroid function and I believe this on its own would impair B6 activation.

There are numerous benefits to eating broccoli, including sulforaphane, and preventing cancer. It is also one of the safest vegetables for those with oxalate problems. Taking B6 as P5P is an easy answer, And I've counted up 15 different things that ME/CFS patients commonly take that impair absorption of T4, levothyroxine, So the answer is just to take more, plus T3, liothyronine if needed. Not to be scared of broccoli, which has other useful nutrients, too

 

[Outlaw]

It happened to me: eating broccoli daily impaired my thyroid function and I believe this on its own would impair B6 activation.

How would brocoli impair B6 activation?

The way I see it, it might raise the quantity of unactivated B6 in my blood, but it doesn't explain why it doesn't convert to P5P, which is a methylation issue

 

[Learner1]

How would brocoli impair B6 activation?

The way I see it, it might raise the quantity of unactivated B6 in my blood, but it doesn't explain why it doesn't convert to P5P, which is a methylation issue

Agreed.

It's preferable just to take P5P ..

 

[Outlaw]

Agreed.

It's preferable just to take P5P ..

Upon further verification, my high B6 levels are not pyridoxine, but rather P5P. So it looks like it's not an activation problem.... its looks like it's just accumulating

It keeps rising since 2 years... now it's at 317 (range 20-90)

 

[JES]

Have you supplemented a lot with B6 or P5P?

My old lab value was 158 nmol/l and I also think they tested the active P5P form. On the other hand, another enzyme marker for B6 activity was mildly low, which suggests B6 (or P5P) is accumulating in the blood for me as well and doesn't get properly utilized.

So the next questions are can this be fixed and does this relate in some way to ME/CFS? I'm not convinced it necessarily relates to my ME/CFS symptoms, but I would for sure like to have those values in better range as it obviously does *something*.

 

[Outlaw]

I spoke to Josh Leisk, who was (is?) active around here, and he says it's due to an immune/biofilm component.

It's absolutely not trivial though.

I have the exact same as you. High serum P5P, yet low functional B6 markers on my OAT.

And I never took B6 in my life

 

[Learner1]

On the other hand, another enzyme marker for B6 activity was mildly low, which suggests B6 (or P5P) is accumulating in the blood for me as well and doesn't get properly utilized.

So the next questions are can this be fixed and does this relate in some way to ME/CFS?

I spoke to Josh Leisk, who was (is?) active around here, and he says it's due to an immune/biofilm component

B6 is used in over 100 different chemical reactions in our bodies. If it's accumulating, one wonders what is not using it. Many times it's because cofactors for reactions are missing - minerals? Amino acids? ?? Or is it really accumulating?

 

[Outlaw]

B6 is used in over 100 different chemical reactions in our bodies. If it's accumulating, one wonders what is not using it. Many times it's because cofactors for reactions are missing - minerals? Amino acids? ?? Or is it really accumulating?

Apparently B2, zinc, mag, B12 and lysine could do it

But I think it might also be methylation issues

Could also be alkaline phosphatase but mine was tested and fine

 

[datadragon]

Supplementation with high concentrations of the pyridoxine form of Vitamin B6 competitively inhibits the active Pyridoxal 5' phosphate (P5P) form which actually leads to decreased vitamin B6 function rather than enhancing it https://www.sciencedirect.com/science/article/abs/pii/S0887233317301959?via=ihub

Vitamin B6 normally needs Zinc, Magnesium, and Vitamin B2 (flavin mononucleotide (FMN); also known as riboflavin-5’-phosphate) in the conversion to active B6 (P5P). Levels may start to appear high even without supplementation due to non conversion. As zinc absorption is lowered and also becomes less available to utilize under inflammation/infection conditions, conversion to active B6 can become impacted during that time which becomes problematic mainly if inflammation becomes Chronically high for awhile.

The active form of Vitamin B6 (P5P) prevents IL-1β production by inhibiting NLRP3 inflammasome activation and suggest its potential for preventing inflammatory diseases driven by the NLRP3 inflammasome. https://pubmed.ncbi.nlm.nih.gov/27733681/

The marginal vitamin B6 deficiency appears to relate to an increased risk of inflammation-related diseases, Recent studies have revealed that vitamin B6 treatment increases cardiac levels of imidazole dipeptides (eg, carnosine, anserine, and homocarnosine), histamine, and -aminobutyric acid (GABA) and suppresses P2X7 receptor-mediated NLRP3 inflammasome. These modulations may implicate possible cardioprotective mechanisms of vitamin B6. These modulations may also be involved in the underlying mechanisms through which vitamin B6 suppresses oxidative stress and inflammation. (the active pyridoxal 5 phosphate (P5P) NOT pyridoxine which lowers active b6) https://link.springer.com/article/10.1007/s00394-021-02665-2

 

[Outlaw]

Supplementation with high concentrations of the pyridoxine form of Vitamin B6 competitively inhibits the active Pyridoxal 5' phosphate (P5P) form which actually leads to decreased vitamin B6 function rather than enhancing it https://www.sciencedirect.com/science/article/abs/pii/S0887233317301959?via=ihub

Vitamin B6 normally needs Zinc, Magnesium, and Vitamin B2 (flavin mononucleotide (FMN); also known as riboflavin-5’-phosphate) in the conversion to active B6 (P5P). Levels may start to appear high even without supplementation due to non conversion. As zinc absorption is lowered and also becomes less available to utilize under inflammation/infection conditions, conversion to active B6 can become impacted during that time which becomes problematic mainly if inflammation becomes Chronically high for awhile.

The active form of Vitamin B6 (P5P) prevents IL-1β production by inhibiting NLRP3 inflammasome activation and suggest its potential for preventing inflammatory diseases driven by the NLRP3 inflammasome. https://pubmed.ncbi.nlm.nih.gov/27733681/

The marginal vitamin B6 deficiency appears to relate to an increased risk of inflammation-related diseases, Recent studies have revealed that vitamin B6 treatment increases cardiac levels of imidazole dipeptides (eg, carnosine, anserine, and homocarnosine), histamine, and -aminobutyric acid (GABA) and suppresses P2X7 receptor-mediated NLRP3 inflammasome. These modulations may implicate possible cardioprotective mechanisms of vitamin B6. These modulations may also be involved in the underlying mechanisms through which vitamin B6 suppresses oxidative stress and inflammation. (the active pyridoxal 5 phosphate (P5P) NOT pyridoxine which lowers active b6) https://link.springer.com/article/10.1007/s00394-021-02665-2

Yeah but I called the lab and my high B6 values are actually p5p, so it's already active

And I never supplemented B6