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Premenstrual Syndrome (PMS)
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Look Up > Supplements > Vitamin B6 (Pyridoxine)
Vitamin B6 (Pyridoxine)
Dietary Sources
Commercial Preparations
Therapeutic Uses
Dosage Ranges and Duration of Administration
Side Effects/Toxicology


Vitamin B6 is a water-soluble vitamin that occurs naturally in three forms: pyridoxine (PN), pyridoxal (PL), and pyridoxamine (PM). The basic structure of vitamin B6 is a pyridine ring with a substituted 4 position. Substitution with a hydroxymethyl group leads to PN; substitution with a formyl group leads to PL; and substitution with an aminomethyl group leads to PM. All three forms can also be phosphorylated at position 5, which results in PLP, PMP, and PNP. PLP and PMP are the active coenzyme forms of the vitamin.

Absorption of vitamin B6 takes place in the jejunum by a passive, nonsaturable process. In the blood, vitamin B6 is transported in the plasma and red blood cells. Ninety percent of circulating vitamin B6 is in the form of PL and PLP. The liver absorbs most of the circulating vitamin B6 and converts it to PLP, which (after hydrolysis of the phosphate group) is then available to other tissues. The phosphorylation and hydrolysis of PL in the liver is just one example of how the metabolism of vitamin B6 from absorption through storage is highly regulated by phosphorylation. The liver is also the conversion site for 40% to 60% of the daily vitamin intake to 4-pyrudixic acid (4-PA), which is excreted in the urine. The major storage depot of vitamin B6 in the body is muscle tissue, which contains 80% to 90% of the total body pool, most of it in the form of PLP bound to glycogen phosphorylase.

The active coenzyme forms of vitamin B6, PLP and PMP, take part in enzymatic reactions that affect several cellular and systemic processes throughout the body. The primary reactions involve aminotransferases, decarboxylations, side chain cleavages, and dehydratases.

Vitamin B6 is involved with the following cellular and systemic processes:

  • Gluconeogenesis—through transamination reactions and as the essential coenzyme of glycogen phosphorylase
  • Niacin formation—during the enzymatic conversion of tryptophan to niacin
  • Lipid metabolism—phospholipid biosynthesis is PLP-dependent
  • Nucleic acid synthesis and immune system processes—serine transhydroxymethylase, a PLP-dependent enzyme is involved in 1-carbon metabolism and therefore DNA synthesis. Normal DNA synthesis is an important process in proper immune function.
  • Hormone modulation—PLP modulates the expression of cytosolic aspartate aminotransferase by preventing the glucocorticoid receptor from binding to the glucocorticoid response element of the aspartate aminotransferase gene.
  • Nervous system processes—PLP is involved in several enzymatic reactions that result in the production of neurotransmitters such as gamma-aminobutyric acid, dopamine, norepinephrine, serotonin, and histamine.

Decreased plasma PLP concentrations have been reported in many disease states. These include renal disease, alcoholism, coronary heart disease, breast cancer, Hodgkin's disease, and diabetes. The finding of decreased plasma PLP in many of these studies must be taken in the context that the other forms of B6 were not measured, leaving open the possibility that vitamin B6 levels are not truly lowered in these conditions.

Dietary Sources

The best sources of vitamin B6 are chicken, fish, kidney, liver, pork, and eggs. The following are also good sources.

  • Yeast
  • Wheat germ
  • Whole grain cereals
  • Legumes
  • Potatoes
  • Bananas
  • Oatmeal

PL and PLP are the predominate forms of vitamin B6 found in animal food products. PM and PN and their phosphorylated forms are the predominant forms found in plant food products. A glucoside form of the vitamin in which a glucose is linked to the 5 position is also found in vegetables, but this form of the vitamin is not efficiently absorbed by the human body.


Pyridoxine is a white, crystalline, odorless compound that is readily soluble in water and alcohol. Food processing and storage can result in considerable loss of active vitamin B6. The range of vitamin B6 losses during freezing are from 36% to 55%.

Commercial Preparations

Pyridoxine hydrochloride is the most commonly found commercial preparation of vitamin B6. It is formulated into tablets in multivitamin form (including chewable children's multivitamins), B-complex form, or by itself in doses ranging from 1 to 150 mg.

Therapeutic Uses
  • Prophylactic use in multivitamin form to prevent the symptoms of vitamin B6 deficiency such as stomatitis, glossitis, cheilosis, irritability, depression, and confusion
  • Counteracts sideroblastic anemia that occurs with the use of the antituberculin drugs isoniazid and pyrazinamide, and the peripheral neuritis that occurs with isoniazid use
  • Treatment of isoniazid overdose
  • Counteracts antivitamin B6 activity of penicillamine, cycloserine, and hydralazine
  • To control pyridoxine-dependent seizures that occur in neonates, infants, and toddlers. These seizures result from an inborn error of metabolism that causes abnormal binding of PLP to glutamic acid decarboxylase and results in a reduction of gamma-aminobutyric acid (GABA) synthesis
  • To control the nausea and vomiting of pregnancy. Doses of 30 to 75 mg per day benefit some women, and doses of up to 40 mg per day have not been proven to be teratogenic. Careful consideration should be taken when prescribing more than the RDA of vitamin B6 because of the risk of neurologic problems with excessive doses
  • Some premenstrual syndromes can be improved by vitamin B6 at a dose of 150 mg per day. Vitamin B6 therapy at these doses must be used with caution because of the risk of neurologic symptoms.
  • Together with folic acid and vitamin B12, vitamin B6 reduces high plasma levels of homocysteine, which is an independent risk factor for cardiovascular disease.

Dosage Ranges and Duration of Administration

As one's protein intake increases, so too does the requirement for vitamin B6. The RDA for vitamin B6 has been established as that needed for two times the RDA of protein intake.

RDA for:

  • Neonates to 6 mos.0.3 mg
  • Infants 6 mos. to 1 year0.6 mg
  • Children: 1 to 3 years1.0 mg
  • 4 to 6 years1.1 mg
  • 7 to 10 years1.4 mg
  • Boys: age 11 to 14 years1.7 mg
  • Men: age 15 years +2.0 mg
  • Girls: age 11 to 14 years1.4 mg
  • Women age 15 to 18 years1.5 mg
  • Women age 19 years +1.6 mg
  • Pregnant women2.2. mg
  • Lactating women2.1 mg

Side Effects/Toxicology

Prolonged ingestion of high doses of vitamin B6 (as little as 200 mg of pyridoxine per day) can result in severe sensory neuropathy and ataxia. Discontinuing the use of vitamin B6 supplements can result in a complete recovery within 6 months.

  • Because of the risk of neurotoxicity from chronic use of large daily doses of vitamin B6, caution must be used when prescribing vitamin B6 therapy for premenstrual syndrome, and the nausea and vomiting of pregnancy.
  • Vitamin B6 enhances the peripheral decarboxylation of levodopa thereby reducing its effectiveness in treating Parkinson's disease.

Cycloserine; Isoniazid

Antituberculosis medications such as cycloserine and isoniazid (INH) reduce the pyridoxine blood levels and may lead to peripheral neuritis (Wada 1998). Supplementation with vitamin B6 during therapy with either of these medications prevents the development of both deficiency and peripheral neuropathy.


In one study, 13 stable patients on chronic hemodialysis received pyridoxine (5 mg/day) in combination with erythropoietin (EPO) (Mydlik et al. 1997). EPO therapy increased hemoglobin synthesis, which decreased erythrocyte pyridoxine status.The pyridoxine concentration in erythrocytes was restored by increasing the dose to 20 mg/day. Supplementation with pyridoxine may be warranted in EPO-treated patients.


Administration of vitamin B6 (50 to 150 mg/day) during treatment with 5-FU has been reported to reverse 5-FU-induced palmar-plantar erythrodysesthesia without any adverse effects or interruption of chemotherapy (Fabian et al. 1990). Palmar-plantar erythrodysesthesia, a skin condition that can make holding objects, driving, or walking painful, may occur in cancer patients undergoing continuous infusions of 5-FU.


In the presence of pyridoxine, the hypotensive effects of hydralazine are diminished (Vidrio 1990).


Vitamin B6 reduces the therapeutic effects of levodopa by increasing the intestinal metabolism of levodopa to dopamine (Awad 1984; Ebadi et al. 1982). The anti-Parkinson effect of levodopa is decreased as a result of the inability of dopamine to cross the blood brain barrier. This antagonistic interaction between pyridoxine and levodopa is more likely to occur at higher pyridoxine doses. It is suggested that pyridoxine supplements not be taken with levodopa.

Monoamine Oxidase Inhibitors (MAOIs)

There have been case reports of MAOIs such as tranylcypromine and phenelzine interfering with vitamin B6 and reducing blood levels of this nutrient (Harrison et al. 1983; Heller and Friedman 1983). MAOI-induced decreases in pyridoxine status have been associated with peripheral neuropathy and carpal tunnel syndrome, both of which respond well to pyridoxine supplementation.


Supplementation with vitamins B1, B2, and B6 (10 mg each) at the start of tricyclic antidepressant therapy improved cognitive functioning and depression ratings in 14 geriatric patients undergoing treatment with nortriptyline (Bell et al. 1992). B vitamins may augment the treatment of depression in elderly patients.

Oral Contraceptives

Oral contraceptives deplete vitamin B6 levels, possibly through induction of tryptophan oxidase (Bermond 1982; Prasad et al. 1976; Slap 1981). Side effects such as depression may be due to altered metabolism of vitamin B6 and other B vitamins (Kane 1976). Please refer to the depletions monograph on oral contraceptives for additional information.


In a study involving 144 rheumatoid arthritis patients treated with penicillamine (125 to 1000 mg/day), 17% developed vitamin B6 deficiency; however, there were no clinical signs of deficiency (Rumsby and Shepherd 1981). Chronic penicillamine therapy may warrant monitoring of pyridoxine status.

Phenobarbital; Phenytoin

A study with 27 epileptic patients aged 15 to 54 who received phenobarbitone (90 mg/day phenobarbital) and diphenylhydantion (300 mg/day phenytoin) regularly for 3 to 32 years noted that serum levels of vitamin B6 and B12 were increased significantly relative to controls (Dastur and Dave 1987). Increased serum vitamin levels may be indicative of hepatic damage from anticonvulsant therapy. However, supplementation with vitamin B6 may decrease the pharmacologic effects of phenytoin (Hines Burnham et al 2000).


In one study, the bioavailability of tetracycline hydrochloride was reduced significantly by concomitant administration of vitamin B complex to healthy subjects (Omray 1981). Patients should be cautioned to take vitamin B complex supplements at different times from tetracycline.


Slow-release theophylline lowered serum vitamin B6 levels by 40% in 16 asthmatic children treated this medication for over a year (Shimizu et al. 1996).


Awad AG. Diet and drug interactions in the treatment of mental illness – a review. Can J Psychiatry. 1984;29:609-613.

Ballal RS, Jacobsen DW, Robinson K. Homocysteine: update on a new risk factor. Cleve Clin J Med. 1997;64:543-549.

Bell IR, Edman JS, Morrow FD, et al. Brief communication: Vitamin B1, B2, and B6 augmentation of tricyclic antidepressant treatment in geriatric depression with cognitive dysfunction. J Am Coll Nutr. 1992;11(2):159-163.

Berger AR, Schaumburg HH, Schroeder C, Apfel S, Reynolds R. Dose response, coasting and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity. Neurology. 1992;42:1367-1370.

Bermond P. Therapy of side effects of oral contraceptive agents with vitamin B6. Acta Vitaminol Enzymol. 1982;4(1-2):45-54.

Brush MG, Bennett T, Hansen K. Pyridoxine in the treatment of premenstrual syndrome: a retrospective survey in 630 patients. Br J Clin Pract. 1998;42:448-452.

Dastur DK, Dave UP. Effect of prolonged anticonvulsant medication in epileptic patients: serum lipids, vitamins B6, B12, and folic acid, proteins, and fine structures of the liver. Epilepsia. 1987;28(2):147-159.

Diegoli MS, da Fonseca AM, Diegoli CA, Pinoltti JA. A double-blind trial of four medications to treat severe premenstrual syndrome. Int J Gynaecol Obstet. 1998;62:63-67.

Ebadi M, Gessert CF, Al Sayegh A. Drug-pyridoxal phosphate interactions. Q Rev Drug Metab Drg Interact. 1982;4(4):289-331.

Ekhard ZE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington, DC: ILSI Press; 1996:191-201.

Fabian CJ, Molina R, Slavik M, Dahlberg S, Giri S, Stephens R. Pyridoxine therapy for palmar-plantar erythrodysesthesia associated with continuous 5-fluorouracil infusion. Invest New Drugs. 1990;8(1):57-63.

Folsom AR, Nieto FJ, McGovern PG, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins: the atherosclerosis risk in communities. Circulation. 1998;98:204-210.

Gospe SM. Current perspectives on pyridoxine-dependent siezures. J Pediatr. 1998;132:919-923.

Hardman JG, Limbird LE, eds. Goodman and Gillman's Pharmacological Basis of Therapeutics. 9th ed. New York: McGraw-Hill; 1996:1326-1333.

Harrison, W, Stewart J, Lovelace R, Quitkin F. Case report of carpal tunnel syndrome associated with tranylcypromine. Am J Psychiatry. 1983;140(9):1229-1230.

Heller CA, Friedman PA. Pyridoxine deficiency and peripheral neuropathy associated with long-term phenelzine therapy. Am J Med. 1983;75(5):887-888.

Hines Burnham, et al, eds. Drug Facts and Comparisons. St. Louis, MO:Facts and Comparisons; 2000:18.

Kane FJ. Evaluation of emotional reactions to oral contraceptive use. Am J Obstet Gynecol. 1976;126(8):968-972.

Keniston RC, Nathan PA, Leklem JE, Lockwood RS. Vitamin B6, vitamin C, and carpal tunnel syndrome. A cross-sectional study of 441 adults. J Occup Environ Med. 1997;39:949-959.

Mahan LK, Arlin MT, eds. Krause's Food, Nutrition, and Diet Therapy. 8th ed. Philadelphia, Pa: WB Saunders Co; 1992:96-97.

Murphy PA. Alternative therapies for nausea and vomiting of pregnancy. Obstet Gynecol. 1998;91:149-155.

Mydlik M, Derzsiova K, Zemberova E. Metabolism of vitamin B6 and its requirement in chronic renal failure. Kidney Int. 1997;52:S56-S59.

National Research Council: Recommended Dietary Allowances. 10th ed. Washington, DC: National Academy Press; 1989;158-165.

O'Connell BJ. The pediatrician and the sexually active adolescent: treatment of common menstrual disorders. Pediatr Clin North Am. 1997;44:1391-1404.

Omray A. Evaluation of pharmacokinetic parameters of tetracylcine hydrochloride upon oral administration with vitamin C and vitamin B complex. Hindustan Antibiot Bull. 1981;23(VI):33-37.

Prasad AS, Lei KY, Moghissi KS, et al. Effect of oral contraceptives on nutrients. III. Vitamins B6, B12, and folic acid. Am J Obstet Gynecol. 1976;125(8):1063-1069.

Recommended Dietary Allowance. American Academy of Sciences. Accessed at on January 8, 1999.

Rumsby PC, Shepherd DM. The effect of penicillamine on vitamin B6 function in man. Biochem Pharmacol. 1981;30(22):3051-3053.

Shimizu T, Maeda S, Arakawa H, et al. Relation between theophylline and circulating vitamin levels in children with asthma. Pharmacol. 1996;53:384-389.

Slap GB. Oral contraceptives and depression: impact, prevalence and cause. J Adolesc Health Care. 1981;2(1):53-64.

Vidrio H. Interaction with pyridoxal as a possible mechanism of hydralazine hypotension. J Cardiovasc Pharmacol. 1990;15(1):150-156.

Wada M. The adverse reactions of anti-tuberculosis drugs and its management [in Japanese]. Nippon Rinsho. 1998;56(12):3091-3095.

Copyright © 2000 Integrative Medicine Communications

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