Vitamin B6 (vitamin B6) is an organic nutrient of the vitamin B complex that appears in three natural, related, water-soluble forms: the alcohol pyridoxine (or pyridoxol), the aldehyde pryidoxal, and the amine pryridoxamine. All of these forms are converted in the human body into a single biologically active form, pyridoxal 5-phosphate. An essential nutrient for humans, vitamin B6 is common in meat, fish, liver, wholegrain cereal, and beans.
Vitamin B6 is essential in the metabolism of proteins, fats, and carbohydrates and is a cofactor in many reactions of amino acid metabolism, including transamination, deamination, and decarboxylation. It also is necessary for the enzymatic reaction governing the release of glucose from glycogen. Vitamin B6 is necessary to make some of the neurotransmitters and hormones necessary for good health in humans, as well as in the formation of hemoglobin and antibodies.
Vitamin B6 deficiency in humans is rare because it is readily acquired in foods. In addition, pyridoxine is relatively stable and thus can be used in vitamin supplements or in fortifying food. Thus, the discovery and understanding of this essential compound has allowed supplementation for those cases where deficiency might normally occur, such as a vegan diet, poor absorption in the gastrointestinal tract (such as with alcoholism), genetic disorders, or certain drugs that inactivate the vitamin.
Overview and structure
Vitamins, such as vitamin B6, are organic nutrients that are obtained through the diet and are essential in small amounts for normal metabolic reactions in humans. Vitamin B6 is part of the vitamin B complex, a group of eight, chemically distinct, water-soluble vitamins that were once considered a single vitamin (like vitamin C), but now are seen as a complex of vitamins that have loosely similar properties and generally are found in the same foods.
A pyridine derivative, vitamin B6 can refer to any of three chemically related and water-soluble forms: pyridoxine (PN), pyridoxol (PL), and pyridoxamine (PM). Pyridoxine is an alcohol and also has been known as pyridoxol and adermin, while pyridoxal is an aldehyde, and pyridoxamine is an amine. All three forms of vitamin B6 are heterocyclic organic compounds. They are based on a pyridine ring, with hydroxyl, methyl, and hydroxymethyl substituents. Pyridoxine differs from pyridoxamine by the substituent at the "4" position. The molar mass of pyridoxine (PN) is 168.19 grams. PN is the form that is given as vitamin B6 supplement.
Four additional forms of this vitamin are known as well: Pyridoxine 5'-phosphate (PNP); pyridoxal 5'-phosphate (PLP), which is metabolically active form; pyridoxamine 5'-phosphate (PMP); and 4-pyridoxic acid (PA), which the catabolite that is excreted in the urine.
All forms except PA can be interconverted. In the human body, pyridoxine, pyridoxol, and pyridoxamine are converted into the same biologically active form, pyridoxal 5'-phosphate (PLP, pyridoxal-phosphate, pyridoxal-5-phosphate, P5P), PLP is a prosthetic group of some enzymes. This activated compound plays a vital role as the cofactor of a large number of essential enzymes in the human body.
Enzymes dependent on PLP focus a wide variety of chemical reactions mainly involving amino acids. The reactions carried out by the PLP-dependent enzymes that act on amino acids include transfer of the amino group, decarboxylation, racemization, and beta- or gamma-elimination or replacement. Such versatility arises from the ability of PLP to covalently bind the substrate, and then to act as an electrophilic catalyst, thereby stabilizing different types of carbanionic reaction intermediates. Overall, the Enzyme Commission (EC) has catalogued more than 140 PLP-dependent activities, corresponding to ~4 percent of all classified activities.
Vitamin B6 was discovered in the 1930s during nutrition studies on rats. The vitamin was named pyridoxine to indicate its structural homology to pyridine. Later, it was shown that vitamin B6 could exist in two other, slightly different, chemical forms, termed pyridoxal and pyridoxamine.
Sources, absorption, and excretion
Vitamin B6 is widely distributed in foods in both its free and bound forms. Good sources include meats, whole grain products, dairy, vegetables, and nuts. Grains that contain B vitamins are often lost in the processing (Turner and Frey 2005). Among the best plant sources of vitamin B6 are bananas, potatoes, mangos, and avocados (Turner and Frey 2005). Apples and fruits are poor sources (Brody 2004).
Cooking, storage, and processing losses of vitamin B6 vary and in some foods may be more than 50 percent (McCormick 2006), depending on the form of vitamin present in the food. Plant foods lose the least during processing as they contain mostly pyridoxine, which is far more stable than the pyridoxal or pyridoxamine found in animal foods. For example, milk can lose 30-70 percent of its vitamin B6 content when dried (Combs 2008). Ideally, fresh foods are used, as much of this vitamin is destroyed by freezing (Turner and Frey 2005).
Vitamin B6 is absorbed in the jejunum and ileum via passive diffusion. With the capacity for absorption being so great, animals are able to absorb quantities much greater than what is needed for physiological demands. The absorption of pyridoxal phosphate and pyridoxamine phosphate involves their phosphorylation catalyzed by a membrane-bound alkaline phosphatase. Those products and non-phosphorylated vitamins in the digestive tract are absorbed by diffusion, which is driven by trapping of the vitamin as 5'-phosphates through the action of phosphorylation (by a pyridoxal kinase) in the jejunal mucosa. The trapped pyridoxine and pyridoxamine are oxidized to pyridoxal phosphate in the tissue (Combs 2008).
The products of vitamin B6 metabolism are excreted in the urine; the major product of which is 4-pyridoxic acid. It has been estimated that 40-60 percent of ingested vitamin B6 is oxidized to 4-pyridoxic acid. Several studies have shown that 4-pyridoxic acid is undetectable in the urine of vitamin B6 deficient subjects, making it a useful clinical marker to assess the vitamin B6 status of an individual (Combs 2008). Other products of vitamin B6metabolism that are excreted in the urine when high doses of the vitamin have been given include pyridoxal, pyridoxamine, and pyridoxine and their phosphates.
Dietary reference intakes
According to Turner and Frey (2004), the Recommended Daily Allowances are as follows:
|Life Stage Group||RDA|
15 and older
19 and older
The following is the listing of the Recommended Dietary Allowances (RDA), Adequate Intake (with asterisk), and Tolerable Upper Intake Level (ULs) according to the Institute of Medicine (IOM 2001). The Upper Intake Level refers to the maximum level likely to pose no threat of adverse effects.
|Life Stage Group||RDA/AI*||UL|
50- >70 yrs
50- >70 yrs
Vitamin B6, in the form of pyridoxal phosphate, is involved in many aspects of macronutrient metabolism, neurotransmitter synthesis, histamine synthesis, hemoglobin synthesis and function, and gene expression. The primary role of vitamin B6, again performed by the active form pyridoxal phosphate, is to act as a coenzyme to many other enzymes in the body that are involved predominantly in metabolism. Pyridoxal phosphate generally serves as a coenzyme for many reactions and can help facilitate decarboxylation, transamination, racemization, elimination, replacement, and beta-group interconversion reactions (Combs 2008).
Vitamin B6 is involved in the following metabolic processes:
- Amino acid, glucose, and lipid metabolism
- Neurotransmitter synthesis
- Histamine synthesis
- Hemoglobin synthesis and function
- Gene expression
Amino acid metabolism
Pyridoxal phosphate is involved in almost all amino acid metabolism, from synthesis to breakdown.
- Transamination. Transaminase enzymes needed to break down amino acids are dependent on the presence of pyridoxal phosphate. The proper activity of these enzymes are crucial for the process of moving amine groups from one amino acid to another.
- Transsulfuration. Pyridoxal phosphate is a coenzyme needed for the proper function of the enzymes cystathionine synthase and cystathionase. These enzymes work to transform methionine into cysteine.
- Selenoamino acid metabolism. Selenomethionine is the primary dietary form of selenium. Pyridoxal phosphate is needed as a cofactor for the enzymes that allow selenium to be used from the dietary form. Pyridoxal phosphate also plays a cofactor role in releasing selenium from selenohomocysteine to produce hydrogen selenide. This hydrogen selenide can then be used to incorporate selenium into selenoproteins (Combs 2008).
- Conversion of tryptophan to niacin. Vitamin B6 is also required for the conversion of tryptophan to niacin and low vitamin B6 status will impair this conversion (Combs 2008).
PLP is also used to create physiologically active amines by decarboxylation of amino acids. Some notable examples of this include: histadine to histamine, tryptophan to serotonin, glutamate to GABA (gamma-aminobutyric acid), and dihydroxyphenylalanine to dopamine.
Vitamin B6 also plays a role in gluconeogenesis. Pyridoxal phosphate can catalyze transamination reactions that are essential for providing amino acids as a substrate for gluconeogenesis. Also, vitamin B6 is a required coenzyme of glycogen phosphorylase (Combs 2008), the enzyme that is necessary for glycogenolysis to occur.
Vitamin B6 is an essential component of enzymes that facilitate the biosynthesis of sphingolipids (Combs 2008). Particularly, the synthesis of ceramide requires PLP. In this reaction, serine is decarboxylated and combined with palmitoyl-CoA to form sphinganine, which is combined with a fatty acyl CoA to form dihydroceramide. Dihydroceramide is then further desaturated to form ceramide. In addition, the breakdown of sphingolipids is also dependent on vitamin B6 since S1P Lyase, the enzyme responsible for breaking down sphingosine-1-phosphate, is also PLP dependent.
Neurotransmitter, histamine, and hemoglobin synthesis
- Neurotransmitters. Pyridoxal phosphate-dependent enzymes play a role in the biosynthesis of four important neurotranmsitters: serotonin, epinephrine, norepinephrine, and gamma-aminobutyric acid (Combs 2008).
- Histamine. Pyridoxal phosphate is involved in the metabolism of histamine (Combs 2008).
- Heme synthesis and hemoglobin action. Pyridoxal phosphate aids in the synthesis of heme and can also bind to two sites on hemoglobin to enhance the oxygen binding of hemoglobin (Combs 2008).
Pyridoxal phosphate has been implicated in increasing or decreasing the expression of certain genes. Increased intracellular levels of the vitamin will lead to a decrease in the transcription of glucocorticoid hormones. Also, vitamin B6 deficiency will lead to the increased expression of albumin mRNA. Also, pyridoxal phosphate will influence gene expression of glycoprotein IIb by interacting with various transcription factors. The result is inhibition of platelet aggregation (Combs 2008).
Since many foods contain vitamin B6, severe vitamin B6 deficiency is rare (Brody 2004), although mild deficiencies are common, in spite of the low daily requirements (Turner and Frey 2005). A deficiency only of vitamin B6 is relatively uncommon and often occurs in association with other vitamins of the B complex. The elderly and alcoholics have an increased risk of vitamin B6 deficiency, as well as other micronutrient deficiencies (Bowman and Russell 2006). Since good sources are meats, fish, dairy, and eggs, one of the risk groups for deficiency are vegans, and a balanced vitamin B supplement is encouraged to prevent deficiency (Turner and Frey 2005). Those taking birth control pills also are a risk to have abnormally low levels (Turner and Frey 2005), as well as the taking of certain drugs (hydrolazine, penicillamine) or cases of particular genetic disorders (Brody 2004).
The classic clinical syndrome for B6 deficiency is a seborrheic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy (James et al. 2006).
While severe vitamin B6 deficiency results in dermatologic and neurologic changes, less severe cases present with metabolic lesions associated with insufficient activities of the coenzyme pyridoxal phosphate. The most prominent of the lesions is due to impaired tryptophan-niacin conversion. This can be detected based on urinary excretion of xanthurenic acid after an oral tryptophan load. Vitamin B6 deficiency can also result from impaired transsulfuration of methionine to cysteine. The pyridoxal phosphate-dependent transaminases and glycogen phosphorylase provide the vitamin with its role in gluconeogenesis, so deprivation of vitamin B6 results in impaired glucose tolerance (Combs 2008).
The Institute of Medicine (IOM 2001) notes that "No adverse effects associated with Vitamin B6 from food have been reported. This does not mean that there is no potential for adverse effects resulting from high intakes. Because data on the adverse effects of Vitamin B6 are limited, caution may be warranted. Sensory neuropathy has occurred from high intakes of supplemental forms."
Supplements that result in an overdose of pyridoxine can cause a temporary deadening of certain nerves such as the proprioceptory nerves, causing a feeling of disembodiment common with the loss of proprioception. This condition is reversible when supplementation is stopped (NIH 2008).
Because adverse effects have only been documented from vitamin B6 supplements and never from food sources, this article only discusses the safety of the supplemental form of vitamin B6 (pyridoxine). Although vitamin B6 is a water-soluble vitamin and is excreted in the urine, very high doses of pyridoxine over long periods of time may result in painful neurological symptoms known as sensory neuropathy. Symptoms include pain and numbness of the extremities, and in severe cases difficulty walking. Sensory neuropathy typically develops at doses of pyridoxine in excess of 1,000 milligrams (mg) per day. However, there have been a few case reports of individuals who developed sensory neuropathies at doses of less than 500 mg daily over a period of months. None of the studies, in which an objective neurological examination was performed, found evidence of sensory nerve damage at intakes of pyridoxine below 200 mg/day. In order to prevent sensory neuropathy in virtually all individuals, the Food and Nutrition Board of the Institute of Medicine set the tolerable upper intake level (UL) for pyridoxine at 100 mg/day for adults. Because placebo-controlled studies have generally failed to show therapeutic benefits of high doses of pyridoxine, there is little reason to exceed the UL of 100 mg/day. Studies have shown, however, that in the case of individuals diagnosed with autism, high doses of vitamin B6 given with magnesium may be beneficial (Pfeiffer et al. 1998).
Preventive roles and therapeutic uses
Vitamin B6 is considered to have therapeutic uses in terms of having a calming effect on the nervous system and possibly alleviating insomnia by increasing serotonin levels in the brain. There also is evidence that vitamin B6 reduces nausea for some women who experience morning sickness, and does not have harmful impacts on the fetus. It also is used to decrease the risk of heart disease through lowering of homocysteine levels (Turner and Frey 2004).
At least one preliminary study has found that this vitamin may increase dream vividness or the ability to recall dreams. It is thought that this effect may be due to the role this vitamin plays in the conversion of tryptophan to serotonin (Ebben et al. 2002).
Nutritional supplementation with high dose vitamin B6 and magnesium is claimed to alleviate the symptoms of autism and is one of the most popular complementary and alternative medicine choices for autism. Three small randomized controlled trials have studied this therapy; the smallest one (with 8 individuals) found improved verbal IQ in the treatment group and the other two (with 10 and 15 individuals, respectively) found no significant difference. The short-term side effects seem to be mild, but there may be significant long-term side effects of peripheral neuropathy (Angley et al. 2007). Some studies suggest that the B6-magnesium combination can also help attention deficit disorder, citing improvements in hyperactivity, hyperemotivity/aggressiveness, and improved school attention (Mousain-Bosc et al. 2006).
ReferencesISBN links support NWE through referral fees
- Angley, M., S. Semple, C. Hewton, F. Paterson, and R. McKinnon. 2007. Children and autism. Part 2: Management with complimentary medicines and dietary interventions. Aust Fam Physician 36(10): 827–30. PMID 17925903. Retrieved December 11, 2008.
- Bender, D. A., and A. E. Bender. 2005. A Dictionary of Food and Nutrition. New York: Oxford University Press. ISBN 0198609612.
- Bowman, B. A., and R. M. Russell. Present Knowledge in Nutrition, 9th Edition. Washington, DC: International Life Sciences Institute. ISBN 9781578811984.
- Brody, T. 2004. Vitamin B6 deficiency. Pages 3513-3515 in J. L. Longe, The Gale Encyclopedia of Medicine, volume 5. Detroit: Gale Grou/Thomson Learning. ISBN 0787654949.
- Combs, G. F. 2008. The Vitamins: Fundamental Aspects in Nutrition and Health. San Diego: Elsevier. ISBN 9780121834937.
- Ebben, M., A. Lequerica, and A. Spielman. 2002. Effects of pyridoxine on dreaming: A preliminary study. Perceptual & Motor Skills 94(1): 135-140.
- Institute of Medicine (IOM) of the National Academies, Food and Nutrition Board. 2001. Daily Reference Intakes: Vitamins. National Academy of Sciences. Retrieved December 11, 2008.
- James, W. D., T. G. Berger, D. M. Elston, and R. B. Odom. 2006. Andrews' Diseases of the Skin: Clinical Dermatology, 10th edition. Philadelphia: Saunders Elsevier. ISBN 0721629210.
- McCormick, D. B. 2006. Vitamin B6 In B. A. Bowman, and R. M. Russell, (eds.), Present Knowledge in Nutrition, 9th edition, vol. 2. Washington, D.C.: International Life Sciences Institute. ISBN 9781578811984.
- Mousain-Bosc, M., M. Roche, A. Polge, D. Pradal-Prat, J. Rapin, and J. P. Bali. 2006. Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6. I. Attention deficit hyperactivity disorders. Magnes Res. 19(1): 46-52. PMID: 16846100.
- National Institutes of Health (NIH), Office of Dietary Supplements. 2008. Dietary Supplement Fact Sheet: Vitamin B6. National Institutes of Health. Retrieved December 11, 2008.
- Pfeiffer, S. I., J. Norton, L. Nelson, and S. Shott. 1995. Efficacy of vitamin B6 and magnesium in the treatment of autism: A methodology review and summary of outcomes. J Autism Dev Disord. 25(5):481-93. Comment in J Autism Dev Disord. 28(1998, issue 6): 580-1. Retrieved December 11, 2008.
- Rowland, B., and R. J. Frey. 2005. Vitamin B6. In J. L. Longe, The Gale Encyclopedia of Alternative Medicine. Farmington Hills, Mich: Thomson/Gale. ISBN 0787693960.
All links retrieved May 9, 2020.
- The B6 database A database of B6-dependent enzymes at University of Parma
- Vitamin B6 Information Sheet from the Linus Pauling Institute at Oregon State University
|All B vitamins | All D vitamins|
|Retinol (A) | Thiamine (B1) | Riboflavin (B2) | Niacin (B3) | Pantothenic acid (B5) | Pyridoxine (B6) | Biotin (B7) | Folic acid (B9) | Cyanocobalamin (B12) | Ascorbic acid (C) | Ergocalciferol (D2) | Cholecalciferol (D3) | Tocopherol (E) | Naphthoquinone (K)|
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