Pyridoxine deficiency and toxicity

Jasvinder Chawla MD MBA (Dr. Chawla of Loyola University Medical Center and Chief of Neurology at Hines VA Hospital has no relevant financial relationships to disclose.)
Zachary N London MD, editor. (Dr. London of the University of Michigan has no relevant financial relationships to disclose.)
Originally released October 29, 2010; last updated April 10, 2018; expires April 10, 2021

This article includes discussion of pyridoxine deficiency and toxicity, B6 deficiency, and B6 toxicity. 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, as well as 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 healthy immune system functions, to protect the heart from cholesterol deposits, and to prevent kidney stone formation.

In combination with folic acid and vitamin B12, vitamin B6 lowers the levels of homocysteine, an amino acid linked to heart disease and stroke, and possibly to other diseases such as osteoporosis and Alzheimer disease. Diclofenac plus B vitamins including pyridoxine have been shown to produce better analgesic effect than diclofenac alone. Nearly 1 out of 2 Americans takes vitamins and dietary supplements, and at least 8 out of 10 Americans consider vitamins and supplements safe. This perception may lead to an increased incidence of vitamin toxicity. Vitamin B6 biosynthesis is required for survival of Mycobacterium tuberculosis in vivo and, thus, might represent a candidate pathway for the development of new antitubercular agents.

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.

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 red blood cells, the immune system, central nervous system function, 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 body's genetic material.


• 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 dermatitis, neuropathy, confusion, and insomnia.


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

Historical note and terminology

There are 6 forms of vitamin B6: pyridoxal (PL), pyridoxine (PN), pyridoxamine (PM), and their phosphate derivatives, including pyridoxal 5'-phosphate (PLP), pyridoxine 5'-phosphate (PNP), and pyridoxamine 5'-phospate (PMP). Pyridoxal 5'-phosphate is the active coenzyme form and has the most importance in human metabolism. In the body, pyridoxine is found primarily in the liver and muscles. Pyridoxine is utilized by the liver to synthesize pyridoxal 5'-phosphate. Pyridoxal 5'-phosphate functions as transamination and decarboxylation coenzymes, which are involved in amino acid and protein metabolism. Pyridoxal 5'-phosphate is also involved as a coenzyme in the synthesis of heme, niacin, and serotonin.

Vitamin B6 deficiency is rare because most foods contain the vitamin. Physiologic availability depends on dietary supply, intact absorption, and conversion of pyridoxamine and pyridoxine into the only active cofactor, pyridoxal 5'-phosphate, in liver (Plecko and Stockler 2009). Pyridoxine supplementation has been marketed for use by bodybuilders and for the treatment of premenstrual syndrome, carpal tunnel syndrome, schizophrenia, childhood autism, and attention deficit hyperactivity disorder, with variable results. Diclectin delayed-release formulation of doxylamine succinate and pyridoxine hydrochloride is effective and well-tolerated in treating nausea and vomiting of pregnancy (Koren et al 2010).

The relationship between pyridoxine overdose levels and histological damage has been well characterized (Windebank et al 1985). Pyridoxine given in large doses is thought to selectively destroy the large-diameter peripheral sensory nerve fibers, leaving motor fibers intact. Pyridoxine overdose has been used in the scientific community as a new paradigm of pure sensory neuropathy loss. Diverse models have been used on a variety of animals, such as rats (Poindron and Piguet 2008), dogs (Chung et al 2008), guinea pigs (Xu et al 1989) and cats (Stapley et al 2002). Additional models of acute auditory neuropathy have been studied after massive administrations of pyridoxine (Hong et al 2009). By the use of these models, a variety of side effects previously listed can be easily isolated and studied, allowing specific treatments that can be precisely targeted to these conditions.

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