I’m at the beginning of research about b6, so my knowledge is limited. As regards b12, I have been diagnosed with PA for about 6 or 7 years I think now. I self inject hydroxocobalamin every week (initially every 2 days). Info on here about that has been so incredibly valuable, thank you.
I discovered by chance last week that I have a genetic thing called Morton’s toe, not the same as Morton’s neuroma. It’s a longer second toe and toe joint. Causes plantar fasciitis amongst other stuff, that’s how I came across it. Morton’s toe also means b6 can’t be converted into its useable form, called p5p or PLP.
People can have a high b6 level when tested because it’s sitting there unconverted and unused.
Symptoms of P5P deficiency apparently include some similar to b12 deficiency, also diabetes (which I have), and many of the dreadful menstrual problems I had when I was younger.
Age 51 I’m still learning so much about how my body works! I just thought it might be useful to share in case others have this too.
I’ve spent 1.5 months on keto and yesterday came off insulin, I’m so happy about this. With any luck the P5P supplements will allow some reintroduction of carbs... I’ll be cautious, but I miss baked potatoes, pasta, cake...
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earthnymph
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Yup, helvella mentioned a couple of weeks back that taking B6 supplements in the form of pyridoxal-5-phosphate is a much better idea than taking it as pyridoxine.
The other day, a supplement company responded to a Thyroid UK member about their vitamin formulation. If you are interested, the relevant posts are linked below.
They seem unimpressed by the paper I referred to suggesting that it is not relevant in the context of a living human being but only in an in vitro test.
If you get the chance, I'd be interested to see your opinion of what they said.
So, I couldn’t wait til later and have just read the posts, paper abstract and summary, and response. Bear in mind I’m a little way along the ASD spectrum, my logic may not be the same as many people’s.
Whatever the cellar type, a dosage dependant reaction was that cells were killed off by b6 in its unconverted form. They weren’t killed off by P5P or the other forms.
B6 unconverted undermined the activity of P5P, or prevented it totally, dependent on dosage.
The drug company (with an agenda I’m not sure of) seems to want to dismiss these findings. Maybe they want to say their supplements are valid and sell lots of them?
If someone is unable to convert b6 to P5P, it seems likely to me that they will have b6 sitting in their bloodstream or stored (I’ve no idea about these mechanisms at the moment) just from a normal diet, let alone if they supplement.
If a deficiency of P5P causes symptoms ascribed to a lack of b6 (an understandable conclusion in the absence of detailed tests), then the person may well think supplementing b6 is a good idea. If they can’t convert it and already have b6 floating around, it seems likely they could cause further damage.
So, in my limited and recently gained understanding: not good to supplement b6 (any cell damage is bad unless you’re targeting dodgy ones like cancer). I started supplementing P5P this week, and from this information I feel this is a much safer and far more logical choice.
Thanks very much for the additional insight, I really appreciate it 😊
In their response - they have a fair point in saying that pyridoxine does have a rather large first-pass effect. When absorbed from the gut the pyridoxine will enter the liver before going anywhere else. And the liver does seem pretty efficient at converting it to P5P. So the amunts encountering other cells will be small.
However, I can't find anything about how much pyridoxine the liver can handle. There will be some dose that will swamp first-pass metabolism, releasing more pyridoxine into the general circulation.
What that dose may be is pretty much a guess. But it's a good reason not to take large amounts of pyridoxine.
I'll be finishing off my low dose (just 5 mg pyridoxine) before I switch to P5P, because I reckon all of that will be metabolised before it gets to the main blood supply.
It does seem strange, maybe they are trying to appeal to all markets, or maybe there’s a minimum number of ingredients to use a certain label? I’m pretty cynical about these things, and I’m guessing there’s a financial reason somewhere...
I'm really intrigued by the Morton's toe..(also sometimes called Morton's Foot).
My second toe is longer than by big toe although not really significantly longer.
Do you know how to distinguish Morton's toe from just having a second toe that is a bit longer.
B12 treatment made many of my symptoms disappear but I've always felt there is something else going on...one symptom that has persisted is weak arms...I suspect an issue with mitochondria.
Do you know what a safe dose of PLP (P5P) is?
I've read that high doses of B6 can cause problems.
It’s really the metatarsal joint that’s relevant. My second toe is only a bit longer, but the toe joint is further forward too. I looked in a mirror while I moved my foot joints with my hands to see, as I couldn’t tell from on top of my foot. You can squeeze to feel joint position too.
I’ve also felt there was something more than b12d. It seems the nightmare of periods I had all my life are likely to have been due to this too.
I’ve gone with 40mg daily of p5p. This is hard to find information about, i haven’t found anything yet on p5p specifically. I went on safe doses of b6 in the end.
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