Overview of water-soluble vitamin deficiencies

Water-soluble vitamins are absorbed from the gastrointestinal tract directly into the circulation. They are excreted through the kidneys, but excessive intake can saturate excretion and cause adverse effects. Most water-soluble vitamins are not stored in the body, so deficiencies can occur quickly in people with inadequate intake. People who are malnourished or have inadequate energy and protein intake are at high risk of water-soluble vitamin deficiencies.

See Clinical aspects of key water-soluble vitamins for the physiological function of key water-soluble vitamins, and the effects of and risk factors for deficiency. Dietary sources of key water-soluble vitamins are listed in Dietary sources of key vitamins, minerals and trace elements.

The evidence for the optimal dosage of water-soluble vitamin supplementation and outcomes is limited; dosages given in this topic are a guide only.

Note: The evidence for the optimal dosage of water-soluble vitamin supplementation and outcomes is limited; dosages given in this topic are a guide only.

Supplementation of water-soluble vitamins should not continue indefinitely; review after 3 months.

Table 1. Clinical aspects of key water-soluble vitamins
thiamine (vitamin B₁) pyridoxine (vitamin B₆) vitamin B₁₂ folate ascorbic acid (vitamin C)
thiamine (vitamin B₁)
physiological function	metabolism of carbohydrates, fat and branched-chain amino acids
effects of deficiency	severe lactic acidosis beriberi with neurological and cardiac effects Wernicke–Korsakoff syndrome peripheral neuropathy decreased immune function
risk factors for deficiency	hazardous alcohol use liver disease malnutrition bariatric surgery
pyridoxine (vitamin B₆)
physiological function	synthesis of lipids, neurotransmitters, steroid hormones and haemoglobin
effects of deficiency	anaemia peripheral neuropathy rash depression
risk factors for deficiency	older age malnutrition
vitamin B₁₂
physiological function	DNA synthesis closely linked with folate; each depends on the other for activation
effects of deficiency	demyelination of neurones (leading to peripheral neuropathy, spinal cord damage, optic atrophy and dementia) impaired red blood cell formation, megaloblastic anaemia
risk factors for deficiency	autoimmune gastritis (pernicious anaemia) gastrectomy significant small bowel resection, particularly terminal ileal resection bariatric surgery vegan diet intestinal disorders that might affect absorption (eg coeliac disease, inflammatory bowel disease) medications (eg metformin)
folate
physiological function	DNA synthesis purine/pyrimidine and amino acid metabolism
effects of deficiency	increased risk of neural tube defects (spina bifida and anencephaly) if mother is deficient during pregnancy megaloblastic anaemia homocysteine concentration may rise (risk factor for cardiovascular disease)
risk factors for deficiency	decreased intake (eg eating disorder, elderly, disabled or isolated people) conditions resulting in malabsorption hazardous alcohol use smoking increased metabolic need (eg rapid growth, pregnancy, burns, blood loss, damage to the gastrointestinal tract, haematological conditions associated with an increased cell turnover) drugs (eg methotrexate, sulfasalazine)
ascorbic acid (vitamin C)
physiological function	collagen synthesis immune defence antioxidant absorption of iron
effects of deficiency	follicular hyperkeratosis impaired wound healing impaired immune function bleeding gums anaemia muscle degeneration scurvy
risk factors for deficiency	after illness or surgery smoking inadequate intake (particularly of fruit and vegetables)