Human health, explained from the cell up.

Required for rhodopsin in rod cells (night vision). Regulates immune cell production. Controls skin and mucosal barrier integrity through epithelial cell differentiation.

Retinoic-acid signalling helps regulate gene expression during nervous-system development and cell differentiation. Severe deficiency can affect vision and broader development; extra vitamin A does not improve cognition when intake is already adequate.

Liver and egg yolk provide preformed vitamin A. Carrots, squash, sweet potato and dark leafy greens provide carotenoids that the body can convert to vitamin A. High-dose preformed vitamin A can be toxic, especially in pregnancy.

Vitamin D supports calcium and phosphorus homeostasis and normal bone mineralisation. Its active form binds a nuclear receptor and regulates gene expression in many tissues. Deficiency can impair bone health.

Vitamin-D receptors are present in the nervous system and vitamin D participates in neurodevelopmental and cellular signalling. Low vitamin-D status is associated with several neurological and psychiatric conditions, but association does not prove that supplementation treats them.

Skin can make vitamin D when exposed to enough UVB; the amount varies with time of day, skin tone, clothing, season and location. Food sources include fatty fish, egg yolk and fortified foods. D2 and D3 can both raise vitamin-D status, though D3 often raises it more efficiently.

Vitamin E is a fat-soluble antioxidant that helps protect polyunsaturated fats in cell membranes from oxidative damage. Vitamin C can help regenerate oxidised vitamin E in antioxidant chemistry.

The brain is particularly vulnerable to oxidative stress due to high fat content and oxygen demand. Vitamin E protects neuronal membranes and myelin sheaths. Deficiency causes peripheral neuropathy.

Nuts, seeds, vegetable oils and leafy greens are common sources. High-dose vitamin E supplements can increase bleeding risk in some people and are not a substitute for food sources.

Vitamin K is required to activate several proteins involved in normal blood clotting and bone metabolism. Vitamin-K-dependent Matrix Gla Protein is also involved in regulating vascular calcification; whether routine K2 supplementation prevents cardiovascular disease remains uncertain.

Vitamin K participates in sphingolipid and other nervous-system biology, but its role in human cognition is still an active research area. It is much better established for clotting than for cognitive outcomes.

K1 is abundant in leafy greens such as kangkong and malunggay. Some menaquinones (K2 forms) occur in fermented and animal foods. People taking warfarin or similar anticoagulants should keep vitamin-K intake consistent and discuss changes with their clinician.

Humans cannot complete the final step of vitamin-C synthesis because the ancestral GULO gene became nonfunctional in the haplorhine-primate lineage roughly 60 million years ago. A vitamin-C-rich diet may have made that loss tolerable, but scientists do not know why the original loss became fixed — and there is no evidence that the Chicxulub asteroid directly caused it.

Vitamin C is required for collagen synthesis and contributes to normal immune-cell function and antioxidant defence. Deficiency clearly impairs tissue integrity and immunity; taking very high doses does not “supercharge” immunity in a linear way.

The brain maintains relatively high vitamin-C concentrations. Vitamin C acts as an antioxidant and is also a cofactor for dopamine β-hydroxylase, the enzyme that helps convert dopamine to norepinephrine.

Guava, papaya, citrus, bell pepper and broccoli are strong sources. Vitamin C is sensitive to heat and prolonged storage, but cooked foods can still contribute. Body stores are limited, so regular dietary intake matters.

Thiamine pyrophosphate is a cofactor for enzymes including pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. The brain is especially vulnerable to severe deficiency because of its high energy demand. Wernicke encephalopathy is a medical emergency associated with severe thiamine deficiency.

Pork, whole grains, legumes, nuts and fortified foods provide thiamine. Heavy alcohol use raises thiamine-deficiency risk through poor intake, impaired absorption and altered storage/metabolism.

Riboflavin forms FMN and FAD, coenzymes central to energy and redox metabolism. Riboflavin-dependent enzymes also participate in vitamin B6 activation and one-carbon metabolism. Bright-yellow urine after a riboflavin-containing supplement is common because excess riboflavin is excreted.

Liver, eggs, dairy (or fortified plant milk), leafy greens, mushrooms.

NAD and NADP are central electron carriers and enzyme cofactors. They participate in energy metabolism, redox reactions and DNA-repair pathways. These roles make niacin essential, but they do not mean that pushing NAD levels above normal automatically improves longevity or brain function.

Severe niacin deficiency causes pellagra, classically associated with dermatitis, diarrhoea and dementia. In people who are already sufficient, extra niacin is not established as a cognitive enhancer.

Meat, fish, peanuts, wholegrains, mushrooms. Can also be converted (inefficiently) from tryptophan — roughly 60mg tryptophan per 1mg niacin.

Pantothenic acid is part of coenzyme A (CoA), which carries acyl groups through carbohydrate, fat and amino-acid metabolism. CoA is therefore central to the Krebs cycle, fatty-acid metabolism and many biosynthetic reactions.

CoA contributes acetyl groups used in many pathways, including acetylcholine synthesis and steroid-hormone synthesis. Pantothenic-acid deficiency is rare in people eating varied diets.

Widely distributed — liver, eggs, avocado, legumes, wholegrains. Deficiency is uncommon in varied diets.

Vitamin B6, mainly as pyridoxal-5′-phosphate (PLP), is a cofactor in more than 100 enzyme reactions. It participates in amino-acid metabolism and the synthesis of neurotransmitters including serotonin, dopamine and GABA. Deficiency can cause neurological symptoms, but common symptoms such as anxiety or poor sleep are not specific for B6 deficiency.

Supplements may contain pyridoxine or PLP/P5P. PLP is the active coenzyme form, but there is no universal rule that P5P is superior for everyone. High supplemental B6 can itself cause peripheral neuropathy, so dose matters.

Poultry, fish, potatoes, chickpeas, bananas and fortified foods provide B6. Neuropathy has been reported with excessive supplemental intake; children should never receive high-dose B6 without medical supervision.

Biotin is a cofactor for carboxylase enzymes involved in fatty-acid synthesis, amino-acid metabolism and gluconeogenesis. Severe deficiency can cause neurological and skin symptoms. Raw egg white contains avidin, which binds biotin; normal cooked-egg intake is not a concern.

Eggs, liver, salmon, nuts and seeds provide biotin. Gut microbes can make biotin, but the extent to which colonic production contributes to human requirements is uncertain.

Folate carries one-carbon units used for DNA synthesis and for remethylating homocysteine to methionine. Methionine can then form SAM, a major methyl donor used across many reactions. Vitamin B12 is directly required for methionine synthase, and B6 participates elsewhere in one-carbon and amino-acid metabolism.

Food folate, folic acid, 5-MTHF and folinic acid are related but not interchangeable in every clinical situation. For general nutrition and pregnancy prevention of neural-tube defects, folic acid has the strongest public-health evidence. Folinic acid has been studied clinically in some children with autism and language impairment, including FRAA-positive subgroups; that is a medical treatment question, not a reason to self-dose folate.

Dark leafy greens, legumes, liver and citrus provide folate. Heat and cooking can reduce some folate, but cooked vegetables remain useful sources. For anyone who could become pregnant, public-health guidance specifically recommends folic acid in addition to food folate.

B12 is structurally complex, built around a cobalt-containing corrin ring. Only certain bacteria and archaea can synthesise it from scratch; animals obtain and accumulate B12 through food chains and microbial sources.

B12 is required for normal blood formation, DNA synthesis and nervous-system function. Deficiency can cause numbness, balance problems, cognitive or psychiatric symptoms and spinal-cord injury; neurological damage can occur even without obvious anaemia.

Common supplement forms include cyanocobalamin, methylcobalamin, hydroxycobalamin and adenosylcobalamin. NIH notes that research has not shown one supplemental form to be universally better than the others. Unfortified plant foods are not reliable B12 sources, so strict vegan diets require a dependable fortified-food or supplement source.