Pyridoxine deficiency and toxicity

Douglas J Lanska MD FAAN MS MSPH (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

Originally released October 29, 2010; last updated May 2, 2020; expires May 2, 2023

This article includes discussion of pyridoxine deficiency and toxicity, vitamin B6 deficiency, vitamin B6 toxicity, and pyridoxine-dependent epilepsy. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Pyridoxine, or vitamin B6, deficiency and toxicity can involve changes predominantly in hematologic, dermatologic, cardiovascular, gastrointestinal, and neurologic systems. Pyridoxine 5'-phosphate is an essential cofactor in various transamination, decarboxylation, glycogen hydrolysis, and synthesis pathways involving carbohydrate, sphingolipid, amino acid, heme, and neurotransmitter metabolism. Vitamin B6 is required for the production of serotonin and helps to maintain a healthy immune system, protect the heart from cholesterol deposits, and prevent kidney stone formation.

Neurologic disorders reflecting both pyridoxine deficiency and pyridoxine toxicity have been recognized. Both overdose and deficiency may cause peripheral neuropathy. Pyridoxine deficiency causes injury of motor and sensory axons whereas an overdose of pyridoxine causes a pure sensory neuropathy or neuronopathy with sensory ataxia.

Some drugs, such as isoniazid and enzyme-inducing antiepileptic drugs, interfere with pyridoxine metabolism.

Several hereditary conditions disrupt pyridoxine metabolism, including pyridoxine-dependent epilepsy.

Key points


• Vitamin B6, also called pyridoxine, is 1 of 8 water-soluble B vitamins. Pyridoxine acts as a coenzyme in the breakdown and utilization of carbohydrates, fats, and proteins.


• Pyridoxine is essential in numerous biochemical pathways involving the nervous system, red blood cells, the immune system, protein metabolism, homocysteine metabolism, and the production of energy.


• Pyridoxine is important for maintaining healthy nerve and muscle cells and it aids in the production of DNA and RNA.


• The recommended daily dose of pyridoxine is 2.0 mg/day for adult men and 1.6 mg/day for adult women. Higher amounts may be recommended for certain conditions.


• Common sources of pyridoxine include brewer's yeast, carrots, chicken, eggs, fish, meat, peas, spinach, sunflower seeds, whole grains, bread, liver, cereals, spinach, green beans, and bananas.


• Symptoms of pyridoxine deficiency include neuropathy, confusion, dermatitis, and insomnia.


• Pyridoxine overdose causes a sensory neuronopathy characterized by poor coordination, numbness, and decreased sensation to touch, temperature, and vibration.


• Several hereditary conditions disrupt pyridoxine metabolism, including pyridoxine-dependent epilepsy and pyridoxamine 5'-phosphate oxidase deficiency (PNPOD).

Historical note and terminology

Pyridoxine (vitamin B6) was discovered in 1934 by Hungarian-born American biochemist, nutritionist, and pediatrician Paul György (1893-1976) (Rosenberg 2012). At that time vitamin B6 was recognized as a new component of the vitamin B complex of water-soluble vitamins that cured a nutritional skin disorder of rats called “rat acrodynia.” Young rats kept on a semisynthetic diet with added vitamin B1 (thiamine) and B2 (riboflavin) developed severe skin lesions with edema, erythema, and scaliness affecting their paws, snout, nose, and ears. Using rat acrodynia as a bioassay, György and his colleagues successfully isolated and characterized vitamin B6. Vitamin B6 was subsequently isolated and crystallized by Samuel Lepkovsky (1899-1984) in 1938 (Lepkovsky 1938) and first synthesized (by 2 different research groups) in 1939 (Harris and Folkers 1939; Kuhn et al 1939).

Pyridoxine-dependent epilepsy was first described in 1954 by pediatrician Andrew D Hunt Jr and colleagues at the Children's Hospital of Philadelphia and the Department of Pediatrics at the University of Pennsylvania School of Medicine, Philadelphia (Hunt et al 1954).

Sensory neuronopathy from pyridoxine abuse was first recognized in the 1980s, initially by neurologist Herbert H Schaumburg and colleagues at Albert Einstein College of Medicine in 1983 (Schaumburg et al 1983).

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