Wow, thanks for the support! To get the first few voice notes, I sent it to family and some colleagues. It was a smoke test to see if anyone would actually record without me literally begging them haha.. and they did! After that, I was confident to start sharing the project more widely and here we are today.
Vitamin C’s relationship with cancer risk appears complex and context-dependent. While maintaining adequate blood levels (≥60.19 μmol/L) is associated with reduced cancer mortality, supplementation may increase postmenopausal breast cancer risk by 32% in women with already high dietary intake. This suggests a U-shaped relationship where both deficiency and excess may be detrimental, emphasizing the importance of personalized approaches to vitamin C intake.
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.
Even though it is water soluble, yes it can accumulate, especially at the higher doses found in supplements. The primary way this happens is via unaware supplementation. Usually people are unaware that their product contains b6 - it's in a lot of products that are not advertised to contain it.
So even though it is water soluble it can still accumulate when taken at these high doses. Most supplements contain pyridoxine, which can acumulate and damage peripheral nerves. Indeed the form of B6 is important, and manufacturers take advantage of the fact that consumers (and medical practitioners) are unaware of the difference. Taking P-5-P may be less risky than pyridoxine hydrochloride, a cheaper option that is included in most supplements.
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