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The title mentions high doses and long periods, but let’s quantify it more accurately: Cases of toxicity have been reported at doses as low as 21 mg per day, t

The title mentions high doses and long periods, but let’s quantify it more accurately: Cases of toxicity have been reported at doses as low as 21 mg per day, the recommended daily intake is 1.3 to 2 mg. The person in question was diagnosed with issues possibly caused by this after 2 years. Edit: Clarification, the 21 mg figure isn’t from this article but from a related document released by Australian Therapeutic Goods Administration. https://consultations.tga.gov.au/medicines-regulation-division/low-neg-risk-2021-2022/user_uploads/low-negligible-risk-annual-consultation-2021-2022---final-decisions.pdf https://consultations.tga.gov.au/medicines-regulation-divisi... Another news source: https://www.theguardian.com/australia-news/2025/jan/05/simon-never-linked-the-pain-in-his-hands-and-feet-to-multivitamins-but-a-pathology-test-did https://www.theguardian.com/australia-news/2025/jan/05/simon...

SoftTalker 1y ago
I checked the daily multivitamin I take and it has 40mg of B6. Edit: read it again and that's based on 2 tablets per day (I take one) so I guess I get 20mg. Might cut it to every other day though.
- puzzlingcaptcha 1y ago
  Mine is 1.05mg... 40mg seems excessive, even accounting for bioavailability.
- mudkipdev 1y ago
  Mine only has 4.3 mg, that's definitely not right
- rapsey 1y ago
  If it is not p-5-p form of B6 (highly likely) stop taking that multivitamin.
- LightHugger 1y ago
  40mg is far over daily limit of 12mg the eu placed on b6 supplements. and even 12mg is likely too high.
mdavid626 1y ago
> Cases of toxicity have been reported at doses as low as 21 mg per day, the recommended daily intake is 1.3 to 2 mg. The person in question was diagnosed with issues possibly caused by this after 2 years. That's very hard to believe. In my "normal" vitamin B-Complex supplement there is 20mg of B6 in the daily dose. If 21mg per day would cause nerve damage, that we'd know (and it would be an epidemic).
- jefozabuss 1y ago
  I've been taking "Opti-Men" from Optimum Nutrition for like 10 years now and it seems to have 50mg in a (full) serving that I take. Since B6 is water soluble doesn't it mean most of it might just leave our body if not needed? (No storage in fat)
  - richarlidad 1y ago
    This is the mechanism of action: Vitamin B6 is an antioxidant and coenzyme involved in amino acid, carbohydrate and lipid metabolism. Humans cannot directly produce active vitamin B6 (pyrixodal phosphate). However, salvage pathways allow the enzymatic conversion of vitamin B6 vitamers, including pyridoxine, pyridoxal and pyridoxamine by the enzyme pyridoxal kinase, into active vitamin B6. In the body, active vitamin B6 is involved in metabolic reactions including GABA synthesis, monoamine neurotransmitter metabolism, the metabolism of polyunsaturated fatty acids and phospholipids, amino acid metabolism and the conversion of tryptophan to niacin. Vitamin B6 reduces homocysteine levels by acting as a coenzyme for both cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) in the transsulfuration pathway following a postprandial methionine-load (after a meal). In the fasting state, homocysteine is primarily metabolised via the remethylation pathway which does not require vitamin B6. In the transsulfuration pathway, homocysteine is converted to cystathionine by CBS, then to cysteine by CSE. During moderate vitamin B6 deficiency, CSE exhibits much greater loss of activity compared to CBS. However cysteine production is preserved due to an accumulation of cellular and plasma cystathionine in a larger substrate pool which compensates for reduced CSE activity. As CBS is a vitamin B6-dependent enzyme, CBS deficiency (typically genetic causes) can result in elevated fasting and post-methionine load homocysteine due to impaired synthesis of cystathionine from homocysteine. Elevated homocysteine levels increase oxidative stress, may inhibit nitric oxide synthesis, increase vascular endothelial cell damage and accelerate low-density lipoprotein (LDL) deposition in arteries. Vitamin B6 may significantly decrease the rate of formation of kidney stones in patients with type I primary hyperoxaluria, a condition caused by a deficiency of the liver-specific enzyme alanine-glyoxylate:aminotransferase by reducing levels of urinary oxalate. The protective effect of vitamin B6 supplementation for kidney stones appears to only occur in women (-34% risk) and not men.

SoftTalker 1y ago

I checked the daily multivitamin I take and it has 40mg of B6. Edit: read it again and that's based on 2 tablets per day (I take one) so I guess I get 20mg. Might cut it to every other day though.

puzzlingcaptcha 1y ago
Mine is 1.05mg... 40mg seems excessive, even accounting for bioavailability.
mudkipdev 1y ago
Mine only has 4.3 mg, that's definitely not right
rapsey 1y ago
If it is not p-5-p form of B6 (highly likely) stop taking that multivitamin.
LightHugger 1y ago
40mg is far over daily limit of 12mg the eu placed on b6 supplements. and even 12mg is likely too high.

mdavid626 1y ago

> Cases of toxicity have been reported at doses as low as 21 mg per day, the recommended daily intake is 1.3 to 2 mg. The person in question was diagnosed with issues possibly caused by this after 2 years. That's very hard to believe. In my "normal" vitamin B-Complex supplement there is 20mg of B6 in the daily dose. If 21mg per day would cause nerve damage, that we'd know (and it would be an epidemic).

jefozabuss 1y ago
I've been taking "Opti-Men" from Optimum Nutrition for like 10 years now and it seems to have 50mg in a (full) serving that I take. Since B6 is water soluble doesn't it mean most of it might just leave our body if not needed? (No storage in fat)
- richarlidad 1y ago
  This is the mechanism of action: Vitamin B6 is an antioxidant and coenzyme involved in amino acid, carbohydrate and lipid metabolism. Humans cannot directly produce active vitamin B6 (pyrixodal phosphate). However, salvage pathways allow the enzymatic conversion of vitamin B6 vitamers, including pyridoxine, pyridoxal and pyridoxamine by the enzyme pyridoxal kinase, into active vitamin B6. In the body, active vitamin B6 is involved in metabolic reactions including GABA synthesis, monoamine neurotransmitter metabolism, the metabolism of polyunsaturated fatty acids and phospholipids, amino acid metabolism and the conversion of tryptophan to niacin. Vitamin B6 reduces homocysteine levels by acting as a coenzyme for both cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) in the transsulfuration pathway following a postprandial methionine-load (after a meal). In the fasting state, homocysteine is primarily metabolised via the remethylation pathway which does not require vitamin B6. In the transsulfuration pathway, homocysteine is converted to cystathionine by CBS, then to cysteine by CSE. During moderate vitamin B6 deficiency, CSE exhibits much greater loss of activity compared to CBS. However cysteine production is preserved due to an accumulation of cellular and plasma cystathionine in a larger substrate pool which compensates for reduced CSE activity. As CBS is a vitamin B6-dependent enzyme, CBS deficiency (typically genetic causes) can result in elevated fasting and post-methionine load homocysteine due to impaired synthesis of cystathionine from homocysteine. Elevated homocysteine levels increase oxidative stress, may inhibit nitric oxide synthesis, increase vascular endothelial cell damage and accelerate low-density lipoprotein (LDL) deposition in arteries. Vitamin B6 may significantly decrease the rate of formation of kidney stones in patients with type I primary hyperoxaluria, a condition caused by a deficiency of the liver-specific enzyme alanine-glyoxylate:aminotransferase by reducing levels of urinary oxalate. The protective effect of vitamin B6 supplementation for kidney stones appears to only occur in women (-34% risk) and not men.