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Vitamin B6

Nutrient Name: Vitamin B6.
Synonyms: Adermine hydrochloride, pyridoxal (PL), pyridoxine (PN), pyridoxamine (PM), and their phosphate derivatives: pyridoxal 5′-phosphate (PLP or P5P), pyridoxine 5′-phosphate (PNP), pyridoxamine, pyridoxamine 5′-phospate (PNP), pyridoxine hydrochloride.
Related Substance: Pyritinol.

Summary Table
nutrient description

Chemistry and Forms

Vitamin B6is a water-soluble vitamin that was first isolated in the 1930s by Paul Gyorgy. Catalyzed by pyridoxal kinase, an adenosine triphosphate (ATP)–dependent enzyme, pyridoxal, pyridoxamine, and pyridoxine are converted to pyridoxal 5′-phosphate, the active coenzyme form, which plays the most significant role in human metabolism. Thus, “vitamin B6” is a generic term used to collectively describe the six related compounds that exhibit the biological activity of pyridoxine: pyridoxal (PL), pyridoxine (PN), pyridoxamine (PM), and their phosphate derivatives: pyridoxal 5′-phosphate (PLP or P5P), pyridoxine 5′-phosphate (PNP), and pyridoxamine 5′-phospate (PNP).

In addition to being water soluble, pyridoxine is stable in heat, especially in acid media, but unstable in alkaline solutions and very unstable to light.

Physiology and Function

Humans cannot synthesize vitamin B6, so dietary intake is necessary. Pyridoxine and its vitamers are absorbed in the upper small intestine by simple diffusion. The more acidic the environment, the greater is the absorption. After being transported to the liver, pyridoxine and pyridoxal (oxidized by pyridoxine oxidase) are phosphorylated by pyridoxal kinase to form pyridoxine 5′-phosphate and pyridoxal 5′-phosphate (PLP, the active coenzyme), which is then exported from the liver bound to albumin. Tissue uptake is through extracellular dephosphorylation, followed by metabolic trapping intracellularly as PLP.

Through a variety of reactions involving transamination, deamination, desulfuration, decarboxylation, side-chain cleavage, and one-carbon metabolism, pyridoxine and approximately 100 PLP-dependent enzymes are involved in amino acid metabolism; glycogen release and blood glucose regulation; hemoglobin synthesis and oxygen transport; synthesis of niacin and a variety of lipids, hormones, and neurotransmitters; cysteine metabolism and homocysteine regulation; and formation of alpha-aminolevulinic acid, sphingolipids, and intrinsic factor.

Vitamin B6plays a central role in the metabolism of amino acids through the transfer of NH2to form keto acids and enable oxidation (i.e., transamination) and the removal of amino groups from certain amino acids (i.e., deamination), both reactions enabling their use as sources for energy. Similarly, transfer of the sulfhydryl group from methionine to serine (i.e., desulfuration or trans-sulfuration) enables the formation of cysteine and regulation of homocysteine. The removal of COOH groups from certain amino acids to yield amines (i.e., decarboxylation) is central to the synthesis of neurotransmitters such as serotonin, norepinephrine, and histamine from tryptophan, tyrosine, and histidine, respectively, and the conversion of phosphatidylserine to phosphatidylethanolamine in phospholipid synthesis. Relatedly, PLP is a coenzyme in the synthesis of niacin from tryptophan, thereby supplementing niacin intake from the diet. Dopamine and gamma-aminobutyric acid (GABA) are likewise dependent on B6coenzymes, as is the formation of sphingolipids involved in the development of the myelin sheath surrounding nerve cells. Notably, PLP can be highly concentrated in the brain even when blood levels are low, and dementia may be associated with reduced transport. Pyridoxal 5′-phosphate–dependent enzymes catalyze these and many other essential metabolic transformations.

Equally important is the role of B6, as well as folic acid, B12, and B2, as the source of coenzymes which participate in one-carbon metabolism. Thus, the freely reversible interconversion of serine and glycine is catalyzed by serine hydroxymethyltransferase (SHMT), a reaction that is both folate dependent and PLP dependent. This mobilization of folate-linked single-carbon functional groups enables the biosynthesis of purines and 2′-deoxythymidine 5′-monophosphate and the remethylation of homocysteine to methionine.

A significant portion of the PLP in the human body is bound to glycogen phosphorylase in muscle tissue and in the liver. PLP functions as a coenzyme in the phosphorolytic cleavage of glycogen as glucose-1-phosphate; it also serves as a coenzyme in gluconeogenesis, where amino acids are used to produce glucose. Vitamin B6nutriture may have a beneficial effect on glucose tolerance by activating apokynureninase or kynureninase that has been inactivated by undergoing transamination, particularly under the influence of elevated estrogen levels.

Pyridoxal 5′-phosphate functions as a coenzyme in the formation of alpha-aminolevulinic acid, which is a precursor of heme. Heme is a component of hemoglobin and thus is critical to the formation of erythrocytes and function of transport oxygen. Both pyridoxal and PLP are able to bind to the hemoglobin molecule.

Vitamin B6plays a role in modulating the activities of several major hormones. PLP can bind to steroid hormone receptors and decrease the effects of estrogen, testosterone, and other steroid receptors through competitive inhibition. Notably, exogenous estrogens (i.e., oral contraceptives) may deplete vitamin B6levels, possibly through inhibition of kynureninase by estrogen metabolites and induction of tryptophan oxidase, causing increased oxidative metabolism of tryptophan.

nutrient in clinical practic
Known or Potential Therapeutic Uses

The role of vitamin B6in conventional medicine is controversial but evolving. Other than prevention and treatment of vitamin B6deficiency, standard practice primarily limits the application of B6to intravenous administration for pyridoxine-dependent seizures in infants and adjunctive treatment of acute toxicity from cycloserine, hydralazine, or isoniazid overdose. Furthermore, warnings of potential adverse effects from supplemental use of pyridoxine appear abundantly within conventional medical literature and press releases. Nevertheless, for decades practitioners of nutritional therapeutics have reported significant efficacy in the treatment of individuals with premenstrual syndrome, estrogen overload, adverse effects of oral contraceptives, nausea and vomiting in pregnancy, depression, carpal tunnel syndrome, and asthma. Enhancement of cognitive function and immune system activity, as well as prevention of kidney stones, have also been proposed by numerous researchers and clinicians. The role of B6, independently or in conjunction with folate, riboflavin, and vitamin B12, in regulating hyperhomocysteinemia and reducing the risk of and improving outcomes in vascular disease and heart attacks remains inconclusive. Well-designed, long-term clinical trials investigating both primary and secondary prevention and integrative therapeutics are warranted.

Low circulating vitamin B6is associated with elevation of the inflammation marker C-reactive protein independently of plasma homocysteine levels. Furthermore, inflammation appears to induce a tissue-specific depletion of vitamin B6as vitamin B6coenzymes are used to meet the higher demands of certain tissues during inflammation and the circulating concentration of PLP declines.

Historical/Ethnomedicine Precedent

Vitamn B6has not been used historically as an isolated nutrient.

Possible Uses

Acne, age-related cognitive decline, alcohol withdrawal support, Alzheimer's disease, amenorrhea, anemia (if deficient, and for genetic vitamin B6–responsive anemia), aphthous ulcers, asthma, atherosclerosis, attention deficit disorder, autism, bulimia, burns, carpal tunnel syndrome, celiac disease, childhood intelligence (for deficiency), colorectal cancer (risk reduction), coronary artery disease (risk reduction), dementia, depression, diabetic neuropathy, fibrocystic breast disease, gestational diabetes, human immunodeficiency virus (HIV) support, hyperhomocysteinemia, hypoglycemia, immune response enhancement (critically ill patients), infant seizures (inborn error in B6metabolism), iron-resistant anemia, low back pain, monosodium glutamate (MSG) sensitivity or poisoning, myocardial infarction, nausea and vomiting of pregnancy, nephrolithiasis, Osgood-Schlatter disease, Parkinson's disease, photosensitivity, presurgery and postsurgery support, preeclampsia, pregnancy and postpartum support, premenstrual syndrome, retinopathy, rheumatoid arthritis, schizophrenia, seborrheic dermatitis, sickle cell anemia, sideroblastic anemia, stroke prevention, tardive dyskinesia, toxemia of pregnancy, vertigo.

Deficiency Symptoms

Vitamin B6deficiency can manifest as impaired immunity, irritability, depression, confusion, skin lesions, inflammation of the tongue, sores or ulcers of the mouth, and ulcers of the skin at the corners of the mouth. Inflammation appears to induce a tissue-specific depletion of vitamin B6. Adults given deoxypyridoxine, a B6antagonist, developed depression, nausea, vomiting, mucous membrane lesions, seborrheic dermatitis, peripheral neuritis, and a range of neurological effects, including ataxia, hyperacusis, hyperirritability, altered mobility and alertness, abnormal head movements, and convulsions.

Although frank deficiencies are considered rare, marginal vitamin B6status may be relatively common. 1 Deficiencies of vitamin B6are usually related to an overall deficiency of all the B vitamins. The risk of B6deficiency or insufficiency is greatest in alcoholics, women using oral contraceptives, individuals suffering from depression, and patients with chronic fatigue syndrome and kidney failure. However, several surveys have found that daily intake of B6is less than the recommended dietary allowance (RDA) for a significant proportion of the population. In the United States, 90% of women and 71% of men reportedly have diets deficient in B6, with dietary intake of vitamin B6averaging approximately 1.5 mg and 2 mg daily for women and men, respectively. 2 In industrialized societies, children and the elderly experience B6deficiency more than any other B vitamin, with men and women over 60 years of age consuming an average of approximately 1.2 mg/day and 1.0 mg/day, respectively. 3,4The milling of grain, which removes 40% to 90 % of naturally occurring B6, and exposure to medications and environmental pollutants that act as B6antagonists constitute the greatest causes of vitamin B6deficiency or increased metabolic requirement; food fortification may mitigate some of these losses. Other factors associated with increased risk of deficiency or insufficiency and increased metabolic need include life stages characterized by rapid growth, such as pregnancy and lactation, childhood, and adolescence; increased dietary protein intake; high alcohol and coffee intake; institutionalization; tobacco smoking; chronic digestive and malabsorption disorders, including irritable bowel syndrome, diarrhea, liver disease; and chronic diseases, including asthma, diabetes, heart disease, and rheumatoid arthritis. Some individuals on a very restricted vegetarian diet may be at increased risk of insufficient B6intake.

Dietary Sources

Calf liver, turkey, tuna, spinach, banana, lentils, and potatoes are among the dietary sources relatively rich in vitamin B6. Other foods containing B6include organ meats, pork, poultry, milk, egg yolks, fish, corn, legumes, seeds, grains, wheat, wheat germ, wheat bran, brewer's yeast, green leafy vegetables, green beans, avocados, cantaloupe, cabbage, green peppers, carrots, soybeans, blackstrap molasses, walnuts, peanuts, and pecans.

Vitamin B6in food sources appears as pyridoxine, pyridoxal, and pyridoxamine. Not all forms of dietary B6are equally bioavailable. In a mixed diet, approximately 75% of vitamin B6present is bioavailable. Pyridoxine glucoside, found in certain plant foods, exhibits only 50% the bioavailability as vitamin B6from other food sources or supplements. Furthermore, cooking and food processing can destroy a significant portion of vitamin B6originally present in foods. Freezing of vegetables decreases B6content by 20%, canning by 54%, and processing of grains by 40% to 90%.

The dietary requirement for vitamin B6is proportional to the level of protein consumption, ranging from 1.4 to 2.0 mg daily for a normal adult. The requirement for vitamin B6during pregnancy and lactation increases approximately by 0.6 mg daily.

Nutrient Preparations Available

Pyridoxine hydrochloride and pyridoxal 5′-phosphate (PLP) are the more commonly available forms, with pyridoxal and pyridoxamine also being available as supplements. Pyridoxine hydrochloride is the form most widely used in conventional medicine and typical supplements and has the advantage of efficient transport through cell membranes and the ability to cross the blood-brain barrier. However, many practitioners experienced in nutritional therapeutics frequently administer PLP because it is the activated form and is particularly important in patients with conditions characterized by impaired conversion of pyridoxine hydrochloride to PLP, such as liver disease and zinc or magnesium deficiency. Some sources maintain that PLP is better absorbed, but these claims are contentious.

Dosage Forms Available

Capsules, liquids, liposomal sprays, lozenges, softgels, tablets, effervescent tablets, and enteric-coated tablets. Vitamin B6is usually contained in multivitamins or B-complex formulations, including chewable tablets and liquid drops for children.

Supplemental B6is best taken between or with meals, preferably with doses divided throughout the day. Individuals who experience alterations in sleep patterns with B6may benefit from emphasizing morning intake.

Dosage Range

Adult

Dietary:

  • Men and women: 1.3 to 1.7 mg/day, increasing with age
  • Pregnant women: 1.9 mg/day
  • Lactating women: 2.0 mg/day
  • Note:   Vitamin B6requirements rise with increased dietary protein intake. Before 1998 the U.S. RDA for vitamin B6was expressed in terms of protein intake. However, when the Food and Nutrition Board (FNB) of the Institute of Medicine revised the RDA for vitamin B6in 1998, they factored in protein intake but established fixed RDA levels.

Supplemental/Maintenance: 10 to 40 mg/day.

Optimal daily intake: Women: 50 mg/day; men: 35 mg/day.

Pharmacological/Therapeutic: 50 to 200 mg/day, occasionally as high as 500 mg daily; typically safe at levels of 200 to 300 mg daily; even so, individuals using more than 100 to 200 mg daily for more than 2 months should be supervised by a nutritionally trained health care professional.

Toxic: According to the U.S. Institute of Medicine, conservative practice recommends that adults not consume more than 100 mg of pyridoxine daily, the tolerable upper intake level (UL) for adults. 5 However, no studies have produced evidence of sensory nerve damage, as confirmed by objective neurological examination, at intakes of pyridoxine below 200 mg/day. Intakes up to 200 mg/day are usually safe in adults. Regardless, a daily dose of 500 mg should never be exceeded, even under physician supervision. Most cases of toxicity, particularly sensory neuropathy, have developed in individuals who have ingested doses of pyridoxine in excess of 1000 mg/day for extended periods. 6

Pregnant and lactating women should avoid daily doses of vitamin B6greater than 100 mg daily. Vitamin B6crosses the placenta. However, available evidence suggests safe use during pregnancy.

Pediatric (<18 Years)

Dietary:

  • Infants, birth to 6 months: 0.1 mg/(AI, adequate intake)
  • Infants, 7 to 12 months: 0.3 mg/day (AI)
  • Children, 1 to 3 years: 0.5 mg/day (RDA)
  • Children 4 to 8 years: 0.6 mg/day (RDA)
  • Children 9 to 13 years: 1.0 mg/day (RDA)
  • Adolescents, 14 to 18 years: 1.2 mg/day for females; 1.3 mg/day for males (RDA)

Supplemental/Maintenance

Vitamin B6is usually not recommended for children under 12 years of age.

Pharmacological/Therapeutic

Viatmin B6is usually not recommended for children under 12 years of age, except intravenous administration for pyridoxine-dependent seizures in infants.

Toxic: Tolerable upper intake level (UL) for vitamin B6:

  • Infants, birth to 12 months: Not possible to establish.
  • Children, 1 to 3 years: 30 mg/day
  • Children, 4 to 8 years: 40 mg/day
  • Children, 9 to 13 years: 60 mg/day
  • Adolescents, 14 to 18 years: 80 mg/day

Laboratory Values

At present, there is no generally accepted test for assessing vitamin B6status.

Plasma pyridoxal 5′-phosphate (P5P, PLP; active form of B6): Levels less than 30 nmol/L indicate deficiency.

Plasma total vitamin B6: Levels less than 40 nmol/L indicate deficiency.

Urinary 4-pyridoxic acid: Levels less than 3.0 μmol/day indicate deficiency; 4-pyridoxic acid is the major urinary metabolite of B6.

Erythrocyte glutamic-pyruvic (alanine) transaminase index (EGPT): A ratio greater than 1.25 (or 1.5) indicates deficiency, depending on the amount of PLP added and the method of testing.

Enzymatic assays run before and after addition of PLP can be used to generate an activity coefficient ratio for this PLP-dependent enzyme. This represents the functional availability of erythrocyte vitamin B6in its coenzyme form. The value increases with vitamin B6deficiency.

Erythrocyte glutamic-oxaloacetic (aspartate) transaminase index (EGOT): This dual enzymic assay is effective to detect and measure human deficiencies of both PLP and activity of this PLP-dependent enzyme.

Serum glutamic-oxaloacetic transaminase (SGOT) reactivation: Although primarily used to diagnose and monitor the course of liver disease, decreased levels in this standard measure of aspartate transaminase (AST) can indicate pyridoxine deficiency.

Serum B6: Radioimmunoassay (RIA) of serum pyridoxal phosphate can be used to detect both vitamin B6deficiency and vitamin B6toxicity.

  • Reference range: 18 to 175 nmol/L.

Tryptophan load test (tryptophan challenge): Urinary xanth- urenic acid excretion greater than 65 μmol/L indicates deficiency.

Tryptophan catabolism is PLP dependent. Thus, an oral tryptophan dose (50 mg/kg for children and up to 2 g/kg for adults) is administered and xanthurenic acid measured to provide a functional assessment of vitamin B6status.

safety profile

Overview

Although water soluble and efficiently excreted, vitamin B6occupies the unenviable position of being the only B vitamin for which toxicity is a reasonable concern. Although typical dosage levels in most available supplements are unlikely to produce adverse effects in most healthy individuals, concern surrounds this nutrient, as codified by regulatory agencies worldwide.

Sensory neuropathy is the primary adverse effect caused by chronic pyridoxine overdose. Other effects reported, but without established frequency, include nausea, headache, seizures (after very large intravenous doses), insomnia, suppressed lactation, increased AST levels, decreased serum folic acid levels, and miscellaneous allergic reactions.

Nutrient Adverse Effects

Peripheral neuropathy characterized by loss of reflexes and paresthesias and pain in the extremities constitutes the primary toxic effect associated with vitamin B6administration. Such adverse effects are almost exclusively associated with high-dose intake, in excess of 1000 mg daily, for an extended period. However, several case reports describe individuals exhibiting sensory neuropathies at dosage levels of less than 500 mg daily over several months.

Parry and Bredesen 7 described sensory neuropathy in 16 patients associated with pyridoxine abuse, defining “low-dose pyridoxine” intake as “0.2 to 5g”/day. They noted that “duration of consumption before symptoms was inversely proportional to the daily intake.” Furthermore, they observed that for “all patients with adequate follow-up, improvement followed discontinuation of pyridoxine.” 7

Subsequently, Dalton and Dalton 8 published a paper from a controlled trial describing a “newly recognised neurotoxic syndrome due to pyridoxine (B6) overdose.” They reported an elevated serum B6level in 172 women, “of whom 60% had neurological symptoms, which disappeared when B6was withdrawn and reappeared in 4 cases when B6was restarted.” They observed that the “mean dose of B6in the 103 women with neurological symptoms was 117±92 mgs, compared with 116.2±66 mgs in the control group” and noted “a significant difference (P less than 0.01) in the average duration of ingestion of B6in the neurotoxic group of 2.9±1.9 years compared with 1.6±2.1 years in controls.” Finally, the documented symptoms included “paraesthesia, hyperaesthesia, bone pains, muscle weakness, numbness and fasciculation, most marked on the extremities and predominantly bilateral unless there was a history of previous trauma to the limb.” 8

Very high doses of B6have also been reported to produce exacerbation of acne, breast tenderness, or increased milk production (when administered while lactating). However, in reviewing all available data, the FNB concluded: “The data fail to demonstrate a causal association between pyridoxine intake and other endpoints (e.g., dermatological lesions and vitamin B6dependency in newborns).” 5 Large doses may theoretically result in increased urinary excretion of other B vitamins, leading to imbalances.

The adverse effects observed have been attributed to intake levels that exceed the liver's capacity to convert pyridoxine to PLP. Consequently, administration of PLP may be advantageous (compared with pyridoxine) when high doses are required for therapeutic efficacy, although this concept has not been evaluated in clinical trials, and monitoring for neurotoxicity would still be prudent.

Adverse Effects Among Specific Populations

Pregnancy and Nursing

Pregnant and lactating women should avoid daily doses of vitamin B6greater than 100 mg. Confirmed reports of teratogenicity are lacking.

Infants and Children

Vitamin B6is generally not indicated for children under 12 years of age.

Contraindications

Major contraindication is hypersensitivity to vitamin B6or any component of a B6-containing preparation. A yeast-free form is advisable for individuals who are sensitive to yeast.

Precautions and Warnings

A variety of drugs can interact with vitamin B6, and in some cases, B6may significantly reduce the therapeutic activity of the medication.

interactions review

Strategic Considerations

Vitamin B6represents a substance that, as a dietary constituent, is widely recommended as beneficial for its physiological function and preventive effects but, as a nutritional supplement or therapeutic agent, is obscured by controversy, prejudice, and partial information. The continuing controversy over the causal role or coincident occurrence and consequent clinical significance of hyperhomocysteinemia in cerebrovascular and cardiovascular disease, and the value of folate, B6, B12, and B2in reducing such risks, has kept this key nutrient in the medical news for several years. However, its broader uses by health care professionals remain largely ignored by conventional practitioners and academic researchers.

Coadministration of vitamin B6may counter the pyridoxine-depleting effects of medications such as chemotherapy, methotrexate, theophylline, furosemide and related loop diuretics, isoniazid, cycloserine and other antitubercular agents, and thiosemicarbazide, but especially in individuals and patient populations with high incidences of compromised nutritional status, dysfunctional pharmacogenomic variations, preexisting insufficiency or deficiency, and exacerbating comedication. In most typical situations, coadministration of B6usually mitigates adverse effects, with or without marked deficiency, and without impairing drug efficacy.

High-dose oral contraceptives, gentamicin, neomycin, and other aminoglycoside antibiotics can both interfere with the physiological functions of B6and deplete available levels. Nevertheless, it appears that administration of pyridoxal 5′-phosphate (PLP, the activated form of vitamin B6) may not prevent gentamicin-induced nephrotoxicity, even though it may reduce severity of symptoms. Likewise, with haloperidol and related neuroleptic agents, concomitant B6can prevent or reduce adverse effects, including drug-induced extrapyramidal symptoms, even in the absence of deficiency signs, but may not enhance therapeutic outcomes.

The situation of antiparkinsonian medications is more complicated because high levels of pyridoxine intake can accelerate peripheral metabolism of levodopa to dopamine, reducing the availability of dopa for central nervous system (CNS) conversion to dopamine, and impair the therapeutic activity of levodopa. The clinical significance of this effect is usually absent or minimal given the predominant use of low-dose B6and the standard practice of combining levodopa with a dopa-decarboxylase inhibitor (DDI), such as carbidopa or benserazide, to reduce excessive peripheral metabolism of levodopa and increase amounts available to the CNS. However, because levodopa acts as a vitamin B6antagonist, it can increase the metabolic requirements for pyridoxine. Consequently, coadministration of low-dose vitamin B6, in the presence of a DDI, can prevent or reverse nutrient depletion and adverse sequelae.

In the case of anticonvulsant medications and related barbiturates, amiodarone, erythropoietin and other erythropoiesis-stimulating agents, or tricyclic antidepressants, the coadministration of B6may prevent or mitigate adverse effects and, in some cases, may potentially enhance clinical outcomes. Here the conventional use of vitamin B6with antitubercular medications, particularly isoniazid, represents a widely accepted example of integrative principles in action through the dual activity of reducing adverse drug-induced effects and enhancing clinical outcomes.

Although vitamin B6is considered an effective preventive or treatment for nausea and vomiting of pregnancy in some women, the combination of doxylamine and pyridoxine may enhance these benefits and is widely used in Canada.

In regard to pharmacokinetic interactions, substances such as tetracycline antibiotics, hydralazine, and penicillamine can bind with vitamin B6to form an inactive complex, which is usually excreted in the urine. These interactions tend to decrease drug availability, deplete pyridoxine, and impair B6-related functions, athough not always to a clinically significant degree.

Somewhat similarly, phenelzine can react with PLP to form a metabolically inactive hydrazone compound and thereby reduce vitamin B6levels. Conversely, B6coadministration may reverse drug-induced effects such as neuropathy.

The broad, diverse, and profound implications of the adverse effects of antibiotics, in general, on symbiotic intestinal microflora are only beginning to receive the attention of researchers. The secondary adverse effects of such changes on B-vitamin status and inflammatory processes will undoubtedly become the subject of deeper investigation.

The primary adverse effects and risks of vitamin B6relate to its classic and well-described overdose symptoms, particularly neuropathies. Although frequently emphasized in the medical literature as a cause for concern, and subsequently restricted as an over-the-counter nutritional supplement in the United Kingdom, the occurrence of such adverse effects is minimal given the large number of self-prescribed users of vitamin B6.

nutrient-drug interactions
Amiodarone
Anticonvulsant Medications and Related Barbiturates
Chemotherapy
Doxylamine
Erythropoiesis-Stimulating Agents
Furosemide and Related Loop Diuretics
Gentamicin and Related Aminoglycoside Antibiotics
Haloperidol and Other Neuroleptic Agents
Hydralazine
Isoniazid, Rifampin, and Related Antitubercular Agents
Levodopa, Carbidopa, Benserazide, and Related Antiparkinsonian Medications
Methotrexate
Neomycin
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Penicillamine
Phenelzine and Related Monoamine Oxidase (MAO) Inhibitors
Tetracycline Antibiotics
Theophylline/Aminophylline
Tricyclic Antidepressants (TCAs)
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Amphetamines, Mixed
Beta-Adrenoreceptor Antagonists and Calcium Channel Blockers
Corticosteroids, Oral
Diclofenac, Ketorolac, and Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Erythromycin and Related Macrolide Antibiotics (Oral)
Fenofibrate, Bezafibrate, and Related Fibrates
Hormone Replacement Therapy (HRT): Estrogen-Containing and Synthetic Estrogen and Progesterone Analog Medications
Hydroxychloroquine
Ketorolac
Nitrofurantoin
Risperidone
Selegiline
Selective Serotonin Reuptake Inhibitor and Serotonin-Norepinephrine Reuptake Inhibitor (SSRI and SSRI/SNRI) Antidepressants

Citalopram (Celexa), duloxetine (Cymbalta), escitalopram (S-citalopram; Lexapro), fluoxetine (Prozac, Sarafem), fluvoxamine (Faurin, Luvox), paroxetine (Aropax, Deroxat, Paxil, Seroxat), sertraline (Zoloft), venlafaxine (Effexor).

The conversion of tryptophan to serotonin (5-hydroxytryptamine) is catalyzed by a PLP-dependent enzyme. Dopamine, norepinephrine, and GABA are other neurotransmitters synthesized using PLP-dependent enzymes.

Vitamin B 6 deficiency may be more common in individuals diagnosed with depression than in the general population. In a small study, Russ et al. 220 found that four of seven patients suffering from depression had subnormal plasma concentrations of PLP, the active form of vitamin B 6 . Likewise, Stewart et al. 221 observed that among a group of 101 depressed outpatients, 21% of those assessed had low plasma levels of pyridoxine.

Several animal and human studies have reported an interaction between pyridoxine intake and tryptophan or histidine affecting brain serotonin and histamine metabolism. Using a rat model and applying different levels of pyridoxine, Lee et al. 232 observed that “when dietary tryptophan was fed at the requirement level, excess pyridoxine caused essentially no changes in hypothalamic serotonin and 5HIAA … [but that with] elevated tryptophan intake, excess pyridoxine significantly increased serotonin and 5HIAA (+32%, +20%) in the hypothalamus.” They interpreted these findings to “indicate a clear interaction between substrate and coenzyme precursor which influences brain metabolism of histamine and serotonin.” Ten years later (1998), Schaeffer et al. 233 fed seven female rats (vs. one control) “10, 100, 175 or 250x the National Research Council recommended level of pyridoxine HCl (7 mg/kg) for 10 wk and measured serum amino acids, amino acids and neurotransmitters in brain regions and the binding properties of serotonin receptors in the cerebral cortex using a ketanserin binding assay.” They found that “excess dietary pyridoxine affected brain and serum concentrations of some amino acids and binding properties of cortical serotonin receptors in a biphasic pattern over the range of concentrations fed in this study.” Bhagavan and Brin 193 studied serotonin and pyridoxal phosphate (PLP) levels in the blood of 11 hyperactive children and 11 controls and noted significantly lower levels of serotonin in the hyperactive patients compared with controls. They found no differences in PLP content of blood between the two groups. However, when four children who had displayed low serotonin levels were administered oral doses of pyridoxine, these investigators observed an appreciable increase in the serotonin content and a very large increase in the PLP content of blood in the hyperactive patients. These preliminary and indirect research findings suggest that pyridoxine intake, especially relative to tryptophan intake, can alter serotonin levels. However, the clinical significance of these data to vitamin B 6 supplementation in human patients being treated with serotonin reuptake inhibitors has yet to be thoroughly and systematically researched.

Physicians treating individuals diagnosed with depression or other conditions using serotonin reuptake inhibitors are advised to assess vitamin B 6 status and consider coadministration of vitamin B 6 , or possibly a B-complex formulation. However, close supervision, regular monitoring, and dose titration are warranted given the theoretical potential for excessive serotonin buildup with suppression of reuptake. Patients stabilized on antidepressants should be advised to avoid sudden changes in dose levels of pyridoxine or other B vitamins, including abrupt termination of supplementation. Further research through well-designed and adequately powered clinical trials is recommended to determine the safety and efficacy of such concomitant therapy and, on confirmation, clinical guidelines for synergistic support. Research into the concomitant application of vitamin B 6 and an SSRI for the management of premenstrual syndrome also deserves consideration.

Health care providers are advised to educate patients as to the therapeutic benefits of a balanced healthy diet, supportive social engagement, regular exercise, and exposure to sunlight and fresh air and strongly encourage building these synergistic lifestyle practices.

Sulfamethoxazole, Trimethoprim-Sulfamethoxazole, and Related Sulfonamides Antibiotics
nutrient-nutrient interactions
Coenzyme Q10
Folic Acid (Folate)
Iron
Magnesium
Vitamin B 2 (Riboflavin)
Vitamin B 12
Zinc
herb-nutrient interactions
Ginger
Citations and Reference Literature
  • 1.Azuma J, Kishi T, Williams RH, Folkers K. Apparent deficiency of vitamin B6 in typical individuals who commonly serve as normal controls. Res Commun Chem Pathol Pharmacol 1976;14:343-366.View Abstract
  • 2.Kant AK, Block G. Dietary vitamin B-6 intake and food sources in the US population: NHANES II, 1976-1980. Am J Clin Nutr 1990;52:707-716.
  • 3.Albertson AM, Tobelmann RC, Engstrom A, Asp EH. Nutrient intakes of 2- to 10-year-old American children: 10-year trends. J Am Diet Assoc 1992;92:1492-1496.View Abstract
  • 4.Van der Wielen RP, de Groot LC, van Staveren WA. Dietary intake of water soluble vitamins in elderly people living in a Western society (1980-1993). Nutr Res 1994;14:605-638.
  • 5.Food and Nutrition Board, Institute of Medicine. Vitamin B-6. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B-6, Vitamin B-12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press; 1998:150-195.
  • 6.Bender DA. Non-nutritional uses of vitamin B6. Br J Nutr 1999;81:7-20.View Abstract
  • 7.Parry GJ, Bredesen DE. Sensory neuropathy with low-dose pyridoxine. Neurology 1985;35:1466-1468.View Abstract
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