The optimal Vitamin B6 thread. How much is too much? What is the ideal vitamer? Why is it so good at countering glycation?

And NAD (it seems to have some level) - at 12 mg/day [which s many times the RDA but not a megadose]

A form of it is also used by the Buck Institute anti-glycation supplement that’s combined with piperine…

B6 is one of the B vitamins you don’t want to megadose too much of…

@Olafurpall did a PDF on this, it would be nice if he could share some of it


@Olafurpall did a PDF on this, it would be nice if he could share some of it

Here is that article I wrote on vitamin B6: Pyridoxamine prevents complications of aging and diabetes

1 Like

Note that although it’s long since I wrote the above article, I still think pyridoxamine is the ideal B6 vitamer to take. I think so because it’s a more effective anti-glycative agent than the other vitamers, and it’s also safer with respect to the risk of neurotoxicity. Vitamin B6 can cause neurotoxicity, and pyridoxine, the most common for of B6 in supplements, is the form most likely to cause neurotoxicity. The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function - PubMed

Regarding toxicity. Vitamin B6 can cause neurotoxicity and while this is normally seen at ultra high doses like a gram or more daily, the dose that causes toxicity is highly individual. Although most people will likely tolerate a few hundred milligrams daily chronically there are reports of toxicity at doses as low as 50 mg daily of pyridoxine. Pyridoxine overdose in premenstrual syndrome - PubMed

A warning to everyone:

DO NOT TAKE VITAMIN B6 IN ANY AMOUNT. Apart from what you already get in food.

I learned this the hard way.

Megavitamin-B6 syndrome is a devastating sequela of vitamin B6 supplementation. Almost unknown or acknowledged in medical circles. It can happen from as little as a single mega dose (such as 100mg) or very low doses (like in energy drinks or multivitamins) over prolonged periods.

The polyneuropathy it causes can be debilitating. You might’ve heard that you can’t get toxicity from water-soluble vitamins like vitamin B (I was also taught this at medical school), Well apparently this doesn’t apply to B6. It can accumulate. The longer you take and the higher the dose is, The quicker you’ll get the toxicity. And it can take many years for the body to excrete the excess, With little to no method or drug to accelerate this. Some people are more susceptible to toxicity, And there is no possible way to find out who is.

I was lucky enough to develop the polyneuropathy symptoms immediately after a single 100mg dose, Meaning i immediately stopped taking any further B6. Yet even with that it took 6 months to recover from the polyneurapthy symptoms from this one single dose (brain fog, Parsethesia, Dizziness, Palpitations, Vertigo, Tinnitus…etc). Unfortunately for many people, especially those who take lower doses, It’ll take much longer to get the symptoms, And by the time they realize they suffer from B6 toxicity, It would’ve accumulated and caused neurological damage to the point some still haven’t fully recovered after a decade of near total b6 abstinence. You can find on Facebook and on internet forums dedicated B6 toxicity threads, Filled with horror stories.

The fact it’s added on in many supplements, Even energy drinks makes me horrified. It’s a public health disaster as far as I’m concerned. There is absolutely no current or theoretical medical benefit to justify taking any B6 supplementation.

1 Like

The unusual issue here is that large quantities of the inactive form inhibit the active form. Large can be a chronic 100mg. Hence i sould suggst p5p is best

1 Like

Your experience is an extremely rare one. It does not mean that it is generally risky to take fairly high doses of B6. And again, it does not apply much to pyridoxamine intake.

I think you’re making a far fetched assumption based partially on you personal experience. You will find B-100 complex vitamins in almost all vitamin/supplement stores. These are taken by millions of people and they contain 100 mg of pyridoxine per pill. Yet we don’t see polyneuropathy being common in people. 100 mg daily is even considered relatively safe by regulatory agencies that normally are overprotective when it comes to safety and assume that everyone must be protected from any potential danger, even if it means a great reduction in their freedom to take care of themselves.


Yes, the inactive form inhibits the active form. To elaborate, pyridoxine competes with pyridoxal-5-phosphate dependent enzymes resulting in reduced enzymatic activity, so the symptoms of too much pyridoxine are the same as that of vitamin B6 deficiency. But no, P5P (pyridoxal-5-phosphate) is not the best form to take. It’s a bit of a waste to take P5P because it will be dephosphorylized in the digestive tract to pyridoxal before being absorbed so you might as well just take pyridoxal. Although pyridoxal is less toxic than pyridoxine, pyridoxamine is even less toxic.

1 Like

The digestion is an interesting point. Do you have a reference for this?

As a matter of interest for other readers of this thread I found symptoms of B6 deficiency occurred after a few weeks chronic supplementation with 100mg of Pyridoxine. Hence I switched to P5P and have not had issues since.

I would normally assume some P5P would make it through without being dephosphorylized.

The only provider I could find:

That is also 200mg. I would assume the molecular weight of the various vitaminers does not vary that much.

Yes. I have references. The intestines contain an enzyme called intestinal alkaline phosphatase that removes phosphate groups from many molecules before they are absorbed. This is the case for the B6 vitamins. Here is a quote from one reference on that:

“Before it can enter cells, PLP is dephosphorylated by ALPL (OMIM 171760).”

The explanation for you not getting the symptoms of deficiency with P5P that you got with pyridozine is not that P5P makes it through without being dephosphhorylized, because it most likely doesn’t. A more likely explanation is that the P5P is dephosphorylized to pyridoxal before absorption and the fact that pyridoxal is less toxic than pyridoxine. Unlike pyridoxine, pyridoxal does not compete with P5P for the B6 dependent enzymes so it doesn’t result in much problems.

The paper you reference does not seem to substantiate precisely what you say, but in the end it does not really matter that much as P5P does not cause the problem that Pyridoxine does. If it gets dephosphorylised and then rephosphorylised then so be it. will not ship Pyridoxamine (or any other product) to USA. The FDA has banned the sale of Pyridoxamine in USA as a supplement : Some company applied to the FDA in 2008 for its use as a drug (FDA Seeks to Ban Pyridoxamine - page 1 - Life Extension) and subsequently went bankrupt but the FDA still says they are bound by US law to block its sale as a supplement to protect the company (now bankrupt) studying its use as a drug! has a US branch and hence, presumably, must remain FDA compliant. Not surprisingly, does NOT sell Pyridoxamine at all, even though most other products available at are sold.

Life Extension (see above link) claims P5P is the best substitute for Pyridoxamine and may even exceed its performance if taken at 2x the dosage (for example, replace 50mg of Pyridoxamine with 100mg of P5P)

Pyridoxamine - an overview | ScienceDirect Topics).

It (pyridoxamine) inhibits AGE formation at three different levels by blocking oxidative degradation of the Amadori products, scavenging of toxic carbonyl products of glucose and lipid degradation, and trapping of reactive oxygen species.

Pyridoxamine inhibited copper-catalyzed LDL oxidation and decreased high glucose-induced superoxide generation and lipid peroxidation in human red blood cells. Furthermore, pyridoxamine inhibited AGE formation and hyperlipedemia and protected against wall thickening of the aorta and renal arterioles in nondiabetic obese rats.

Benfothiamine may also be of value.

Benfotiamine, a thiamine monophosphate derivative, significantly inhibited the development of incipient diabetic nephropathy, neuropathy, and retinopathy in animal models. Benfotiamine was reported to prevent macro- and microvascular endothelial dysfunction and oxidative stress generation following a meal rich in AGEs in type 2 diabetic patients.

1 Like