B Vitamins

B vitamins is a category, not a single nutrient, and the clinical questions are largely about two of them: B12 and folate. Both are central to red blood cell production, neurological function, and the methylation cycle. Both have well-documented deficiency syndromes. Both have meaningful population-level supplementation needs in vegetarians, vegans, older adults, people on metformin or proton pump inhibitors, and pregnancy. The library entries on this page report what the NHS, NICE, BSH, and the Royal College of Obstetricians and Gynaecologists currently recommend, what the diagnostic ambiguity around serum B12 actually means in practice, and what the methylfolate vs folic acid debate does and does not say about clinical outcomes.

What this page covers

The B vitamin entries focus on the questions that actually come up: which form of B12 (cyanocobalamin vs methylcobalamin vs hydroxocobalamin vs adenosylcobalamin), why serum B12 misses functional deficiency and what active B12 / homocysteine / methylmalonic acid add, the folic acid vs methylfolate debate, the MTHFR polymorphism question, B6 toxicity at sustained high dose, and the relevance of homocysteine reduction in cardiovascular and cognitive contexts.

Where the guidance currently sits

The NHS recommends 400 micrograms of folic acid daily before conception and through the first 12 weeks of pregnancy to reduce neural tube defect risk, with 5 mg daily for women with a history of NTD-affected pregnancy or with diabetes or coeliac disease. The BSH recommends investigating B12 deficiency with both serum B12 and a clinical assessment, with active B12, MMA, or homocysteine used as second-line tests when serum B12 is borderline. NICE recommends lifelong B12 replacement (intramuscular hydroxocobalamin or high-dose oral) for confirmed pernicious anaemia. SACN recommended UK-wide folic acid fortification of non-wholemeal flour, which the UK government adopted in 2024.

Where the evidence and the marketing disagree

The methylfolate vs folic acid debate is louder online than the trial evidence supports. For most people without an MTHFR variant, both forms raise red blood cell folate equivalently, and folic acid has the advantage of decades of trial evidence including the NTD prevention data. Methylfolate is genuinely useful for individuals with documented homozygous MTHFR C677T variants who are not converting folic acid efficiently, and the library entry on MTHFR sets out what the genotype data does and does not predict for clinical outcomes. Homocysteine-lowering through B12, B6, and folate has not consistently translated to cardiovascular event reduction in large trials, despite epidemiological associations. The library entries say so.

B6 deserves a specific note: chronic intake above 100 mg daily has been associated with peripheral sensory neuropathy in case reports and small series. The TGA in Australia has formal labelling requirements for products above 50 mg. UK products typically stay well below this threshold for that reason.