Vitamin B6 is the term for three related compounds, pyridoxine, pyridoxal and pyridoxamine and their phosphorylated derivatives which are pyridoxine 5'-phosphate, pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate. Vitamin B6 technically refers to all six of these vitamers, although vitamin B6 is used interchangeably with pyridoxine.
Pyridoxine, pyridoxine 5'-phosphate and pyridoxine glucosides are found in plant foods. Glycosylated pyridoxine forms of vitamin B6 range from 5 to 75% of the total vitamin B6 content in fruits, vegetables, and grains.
The other vitamers, primarily pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate, are found in animal products. There is very little or none of the glycosylated pyridoxine form of vitamin B6 in animal products.
Vitamin B6 is soluble in water and stable to heat and acid. However, oxidation and exposure to alkaline conditions or UV light destroy vitamin B6.
As much as 50% of vitamin B6 is destroyed during cooking and processing.
Pyridoxal 5'-phosphate is involved in more than 100 biochemical reactions as a coenzyme. These reactions include the metabolism of glycogen and amino acids, the synthesis of nucleic acids, and the synthesis and metabolism of hemoglobin.
Pyridoxal 5'-phosphate is also involved as a coenzyme in the synthesis of sphingomyelin and other sphingolipids and the neurotransmitters serotonin, dopamine, norepinephrine, histamine, and gamma-aminobutyric acid.
Males 9 to 13 years 14 to 50 years 51+ years Females 9 to 13 years 14 to 18 years 19 to 50 years 51+ years
1.0 1.3 1.7
1.0 1.2 1.3 1.5
Pregnancy <= 18 years 19 to 30 years 31 to 50 years
1.9 1.9
Lactation <= 18 years 19 to 30 years 31 to 50 years
2.0 2.0 2.0
*Values are Adequate Intakes (AI), others are RDA.
There are no determinable Tolerable Upper Intake Levels (UL) for riboflavin due to lack of data of adverse effects in all age groups.
The symptoms of vitamin B6 deficiency are microcytic hypochromic anemia, seizures, seborrheic dermatitis, confusion, and depression.
Deficiency of vitamin B6 in children and infants results in seizure activity and electroencephalogram abnormalities.
Deficiency of vitamin B6 in adults results in cheilosis, glossitis, stomatitis, anemia, irritability, confusion, and depression.
Secondary deficiencies of vitamin B6 may result from vitamin B6 malabsorption, uremia, cancer, heart failure, and cirrhosis.
Pregnant adolescent females, the elderly, and alcoholics are at elevated risk for secondary vitamin B6 deficiency.
Other vitamin B6 deficiencies may result from chemical inactivation, excessive vitamin B6 excretion, or increased metabolic activity associated with the use of some medications (e.g. isonicotinic acid hydrazide, penicillamine, cycloserine, thionamide, hydralazine, and theophylline).
Although there are benefits from megadoses of vitamin B6 for certain individuals, the use of high doses of pyridoxine may have some risks. Adults chronically ingesting megadoses of 2 to 6 g/day pyridoxine may experience progressive sensory neuropathy. Excessive amounts of pyridoxine appear to cause the degeneration of dorsal root ganglia.
Infants who are born with low plasma concentrations of vitamin B6 and are breastfed may be at risk for vitamin B6 deficiency.
The elderly, who have a poor intake of vitamin B6, may also have accelerated hydrolysis of pyridoxal phosphate and oxidation of pyridoxal to pyridoxic acid. Additionally, in one study with healthy individuals aged 65 years or older, researchers found abnormal concentrations of vitamin B6 and riboflavin. The authors concluded that a high proportion of older adults might have suboptimal vitamin B6 and riboflavin status even when the recommended nutrient intakes are achieved through diet. 9
Alcoholics may be at risk for vitamin B6 deficiency due to the impaired conversion of pyridoxine and pyridoxamine to pyridoxal phosphate.
Maintenance dialysis causes an abnormal loss of vitamin B6, increasing the risk of vitamin B6 deficiency for renal patients.
Seven inborn errors of metabolism involve defects in the pyridoxal 5'-phosphate binding site. These disorders may be responsive to high doses of vitamin B6.
Isoniazid (INH), an antituberculosis drug, can increase vitamin B6 requirements. Patients receiving more than 10 mg/kg/day of INH should be supplemented with 50-100 mg of vitamin B6 per day to prevent peripheral neuritis. It is suggested that children receiving the medication do not need vitamin B6 supplementation unless they have nutritional deficiencies. It is recommended that children or adolescents with low meat and milk diets, symptomatic children with HIV infection, breastfeeding infants and women, and pregnant women take supplementation.
Cycloserine, an antibiotic used mainly for tuberculosis, can block the actions of vitamin B6 and increase renal excretion of the vitamin leading to anemia or peripheral neuritis. Vitamin B6 supplementation may be required in some patients receiving cycloserine.
The therapeutic effects of levodopa, an anti-Parkinsonian agent, can be compromised by vitamin B6 due to accelerated peripheral metabolism of the drug. Concomitant use of carbidopa with levodopa prevents the increase in this metabolism by vitamin B6. Patients using levodopa alone should not use vitamin B6 in doses greater than 5 mg/day.
Vitamin B6 has been shown to decrease serum concentrations of anticonvulsant medications, such as phenobarbital and phenytoin. Supplementation is not advised without first consulting with a physician or pharmacist.
Penicillamine, used for rheumatoid arthritis or Wilson’s disease, can increase vitamin B6 requirements.
Neurotoxicity from the chemotherapeutic drugs, altretamine or cisplatin can be reduced with vitamin B6; however, vitamin B6 may compromise therapeutic benefits of the drugs and should not be administered with altretamine or cisplatin.
Many antibiotics can destroy normal gastrointestinal flora leading to decreased production of the B vitamins in general. The clinical significance is unknown.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial.
The Vitamin Intervention for Stroke Prevention (VISP) was a randomized controlled trial evaluating whether high doses of folic acid, B12, and B6 reduced the risk of recurrent stroke in adults over a two-year period. Participants were selected from patients presenting with nondisabling cerebral infarction. Three-thousand-six-hundred-eighty adults were randomly assigned to receive once-daily doses of the high-dose formulation (25 mg of B6, 0.4 mg B12, and 2.5 mg of folic acid) or the low-dose formulation (200 mcg B6, 6 mcg B12, and 20 mcg folic acid). Modest reductions of total plasma homocysteine were found in both groups, but had no effect on risk for stroke, CHD, or death. A 2 micromol/L greater decrease in total plasma homocysteine was found for the high dose group compared to the low dose group. When stratified by baseline homocysteine levels, significant risk reductions were revealed for the low dose group. A 3 micromol/L lower baseline total plasma homocysteine concentration was associated with a 10% reduction in risk of stroke (P=0.05), a 26% reduction in risk for CHD (P<0.001), and a 16% reduction in risk of death (P=0.001). A nonsignificant trend toward reduction was also noted for the high dose group. These results indicate that a B vitamin supplement can reduce homocysteine concentrations and may reduce risk for further vascular events for those with lower baseline levels. 16
Low-dose vitamin B-6 effectively lowers fasting plasma homocysteine in healthy elderly persons who are folate and riboflavin replete.
A randomized, double-blind, placebo-controlled trial conducted with 22 healthy persons aged 63 to 80 examined low-dose vitamin B6 supplements for reduction of plasma homocysteine concentrations. Participants consumed 1.6 mg/day vitamin B6 or a placebo for 12 weeks after repletion with folic acid (400 mcg/day for 6 wk) and riboflavin (1.6 mg/day for 18 wk). Folic acid supplementation lowered fasting homocysteine by 19.6% (P < 0.001). Ten subjects were found to have suboptimal vitamin B6 levels. Vitamin B6 supplementation reduced plasma homocysteine levels by an additional 7.5% (P=0.008). The results of this study indicate that vitamin B6 lowers fasting total plasma homocysteine concentrations in healthy elderly people who are both folate and riboflavin replete. The significance of this reduction for cardiovascular health is not known. 5
Effect of homocysteine-lowering treatment with folic acid plus vitamin B6 on progression of subclinical atherosclerosis: a randomised, placebo-controlled trial.
A trial among 158 healthy siblings of 167 patients with premature atherothrombotic disease investigated the efficacy of folic acid plus vitamin B6 on progression of atherosclerosis. Participants consumed either 5 mg of folic acid plus 250 mg of vitamin B6 or a placebo daily for 2 years. Supplementation with folic acid plus vitamin B6 significantly decreased plasma homocysteine concentrations versus placebo (from 14.7 to 7.4 micromol/L versus from 14.7 to 12.0 micromol/L). Compared to placebo, the supplemented group was also associated with a significant reduction in risk for abnormal exercise electrocardiography tests (odds ratio 0.40 [0.17-0.93]; p=0.035), suggesting improvements in atherosclerotic symptoms. Overall, these data suggest that vitamin treatment aimed at lowering concentrations of total blood homocysteine can favorably influence the course of atherosclerotic disease. 6
A prospective study of folate and vitamin B6 and risk of myocardial infarction in US physicians.
Researchers from the Physicians Health Study at the Harvard School of Public Health examined plasma vitamin B6 and folic acid concentrations in 14,916 men aged 40 to 84 years. Participants were followed for 7.5 years. Men in the lowest 20% of vitamin B6 values had increased relative risk of 1.5 (95% CI: 1.0-2.2) for acute MI or death due to coronary disease. For men with the top 5% of homocysteine concentrations, the risk of MI increased three-fold. The results of this prospective trial suggest that low dietary intake of vitamin B6 and folic acid may have increased risk for acute MI or death due to coronary disease, although the results are not statistically significant. 8
Homocysteine lowering and cardiovascular events after acute myocardial infarction.
The Norwegian Vitamin Trial (NORVIT) evaluated the efficacy of homocysteine-lowering treatment with B vitamins for secondary prevention in patients who had had an acute myocardial infarction (MI). Three-thousand-seven-hundred-forty-nine men and women were randomly assigned to receive folic acid (0.8 mg), B12 (0.4 mg), and B6 (40 mg), folic acid and vitamin B12, vitamin B6 alone, or placebo. Patients were seen at a 2 month follow-up visit and at a final visit after 2 to 3.5 years. Despite a substantial reduction in plasma total homocysteine, intervention with B vitamins did not lower the risk of recurrent cardiovascular disease or death after an acute MI. In the group receiving all three B vitamins, there was a trend toward an increased rate of events. The researchers concluded that B vitamin intervention not be recommended after acute MI. 24
Homocysteine lowering with folic acid and B vitamins in vascular disease.
The Heart Outcomes Prevention Evaluation 2 (HOPE2) researchers evaluated whether therapy with homocysteine-lowering B vitamins reduced the risk of major vascular events in a high risk population. Participants, 5,522 patients aged 55 years or older with vascular disease or diabetes, were randomly assigned to a daily treatment with a B vitamin combination (2.5 mg folic acid, 50 mg B6, and 1 mg B12) or placebo for an average of 5 years. The results demonstrated that daily administration of the B vitamin combination significantly lowered homocysteine but had no beneficial effects on major vascular events in a high risk population with vascular disease. 25
Effect of folic acid and B vitamins on risk of cardiovascular events and total mortality among women at high risk for cardiovascular disease: a randomized trial.
In this randomized, placebo-controlled, double-blind trial, the efficacy of a B vitamin supplement to reduce risk for cardiovascular disease (CVD) was assessed in women with CVD or at high risk for CVD. The study enrolled 5,442 female U.S. health professionals 42 years or older with a history of CVD or with at least three risk factors for CVD. Participants were randomly assigned to receive either a placebo or a daily B vitamin supplement containing 2.5 mg folic acid, 50 mg vitamin B6, and 1 mg vitamin B12 for 7.5 years. During the trial, 406 CVD events (myocardial infarction, stroke, coronary revascularization, or CVD mortality) were reported for the vitamin supplement group while 390 CVD events were reported for the placebo group. Thus, the risk for CVD events was similar for both groups (relative risk [RR], 1.03; 95% confidence interval [CI], 0.90-1.19; P = 0.65). The B vitamin supplement was found to reduce the geometric mean plasma homocysteine level by 18.5% (95% CI, 12.5%-24.1%; P < 0.001) compared to placebo. The results of this large study indicate that B vitamin supplements do not reduce risk for CVD events in women with CVD or at high risk for CVD, despite significant reductions in homocysteine concentrations. 14
Mortality and cardiovascular events in patients treated with homocysteine-lowering B vitamins after coronary angiography: a randomized controlled trial.
A large randomized, double-blind, placebo-controlled trial at two hospitals in Norway assessed the effect of vitamin B6 or vitamin B12 plus folic acid supplements for secondary prevention in patients with coronary artery disease or aortic valve stenosis. A total of 3,096 adults undergoing coronary angiography were enrolled in the study. Participants were randomly assigned to one of four groups: 1) 0.8 mg folic acid, 0.4 mg vitamin B12, and 40 mg vitamin B6; 2) folic acid plus vitamin B12; 3) vitamin B6 only; or, 4) placebo. The trial was continued for approximately 38 months, but was terminated early due to concerns about the treatment resulting from another clinical trial. During the trial, a total of 422 participants (13.7%) experienced an event (defined as all-cause death, nonfatal acute myocardial infarction, acute hospitalization for unstable angina pectoris, or nonfatal thromboembolic stroke). Folic acid plus vitamin B12 was not found to be better than placebo or vitamin B6 alone for prevention of these events (hazard ratio, 1.09; 95% confidence interval, 0.90-1.32; P = 0.36). Vitamin B6 versus other treatments was also not found to be effective (hazard ratio, 0.90; 95% confidence interval, 0.74-1.09; P = 0.28). The results of this trial do not support use of B vitamin supplements for secondary prevention for people with coronary artery disease. 17
Premenstrual Syndrome:
Efficacy of vitamin B6 in the treatment of premenstrual syndrome: systematic review.
A review of nine randomized, placebo-controlled trials evaluated the efficacy of vitamin B6 in a total of 940 patients with premenstrual syndrome. Relative to placebo, the odds ratio for an overall improvement in premenstrual symptoms was 2.32 (95% CI 1.95 to 2.54). Relative to placebo, the odds ratio for an improvement in depressive symptoms was 1.69 (1.39 to 2.06) from four trials representing 541 patients. The results suggest that doses of up to 100 mg of vitamin B6 may be beneficial in treatment of premenstrual syndrome and premenstrual depression. 11
Role of bromocriptine and pyridoxine in premenstrual tension syndrome.
A placebo controlled trial investigated the efficacy of vitamin B6 supplements for reducing symptoms of premenstrual tension syndrome (PMS). Sixty women aged 20 to 45 years with PMS symptoms enrolled in the study. Twenty were assigned to receive 2.5 mg bromocriptine twice daily for three months; twenty were assigned to receive 100 mg vitamin B6 daily for three months; twenty received a daily placebo for three months. Participants were assessed monthly for three months. Significant reductions in PMS symptoms were found for those taking bromocriptine or vitamin B6 supplements. However, the vitamin B6 group reported fewer side effects and tolerated the supplements better than the bromocriptine group. 7
Ageing:
Reduction of plasma homocysteine and serum methylmalonate concentrations in apparently healthy elderly subjects after treatment with folic acid, vitamin B12 and vitamin B6: a randomised trial.
Plasma total homocysteine, a marker of suboptimal levels of vitamin B12, vitamin B6, and folate, and serum methylmalonic acid (MMA) which indicates vitamin B12 deficiency, were investigated in 209 community-dwelling individuals aged 70 to 93 years. Baseline levels of plasma homocysteine and serum MMA were assessed and then participants consumed daily supplements of 0.5 mg cyanocobalamin, 0.8 mg folic acid, and 3 mg vitamin B6 for four months. Plasma homocysteine was elevated at baseline in 65% of males and 45% of females. Serum MMA was elevated at baseline in 11% of participants. Deficiency of vitamin B12 was identified in 7.2% of the participants and folate deficiency was found in 11% of the participants. Supplementation significantly reduced plasma homocysteine concentrations (P<0.001) and serum MMA (P=0.009). By the end of the study, all but a few of the vitamin treated subjects showed metabolite concentrations within healthy limits. 22
B-vitamins reduce plasma levels of beta amyloid.
In a small placebo-controlled supplementation study, possible preventative effects of B vitamins against Alzheimer’s disease (AD) were investigated. Two-hundred-ninety-nine older males enrolled in the study. Participants were randomly assigned to receive either 2 mg folic acid, 25 mg vitamin B6, and 0.4 mg vitamin B12 or a placebo for two years. Previous studies have indicated that elevated homocysteine is a risk factor for development of AD; to evaluate risk for AD, this study measured circulating levels of A-beta protein 1-40 (A beta 40). After two years of supplementation, A beta 40 had increased by 4.9% in the supplemented group and had increased by 18.5% in the placebo group. These results indicate that this combination of B vitamins may reduce risk for AD, as indicated by attenuation of increases in A beta 40. 21
Dietary folate, vitamin B12, and vitamin B6 and the risk of Parkinson disease.
Potential associations between B vitamins and development of Parkinson’s disease (PD) were investigated in a prospective, population-based cohort study of people aged 55 years and older. A total of 5,289 people initially free of dementia enrolled in the study and were followed for an average of 9.7 years. Seventy-two cases of PD were identified. Comparing those with and without PD, higher dietary intake of vitamin B6 was found to be inversely associated risk of PD (hazard ratio per SD, 0.69 [95% CI 0.50 to 0.96]; for highest versus lowest tertile, 0.46 [0.22 to 0.96]). No associations were found for folic acid or vitamin B6. These intriguing results suggest that low vitamin B6 intake may be associated with development of PD. Further investigation is necessary to understand the underlying mechanisms and to validate these results. 26
Cancer:
Association of the B-vitamins pyridoxal 5'-phosphate (B(6)), B(12), and folate with lung cancer risk in older men.
A study was conducted within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study to test for associations between folate, vitamin B6, and vitamin B12 and incidence of lung cancer. Three-hundred participants with lung cancer and an equal number of matched controls were enrolled in the study. A statistically significant reduction of risk for lung cancer was found for males with the highest serum levels of vitamin B6. Men in the highest quintile of vitamin B6 had approximately one-half the risk for lung cancer when compared to those in the lowest quintile (odds ratio = 0.51; 95% confidence interval: 0.23, 0.93; p-trend = 0.02). This intriguing report is the first prospective study to find an association between low vitamin B6 concentrations and lung cancer. 13
Plasma folate, vitamin B6, vitamin B12, homocysteine, and risk of breast cancer.
This study investigated the associations between vitamin B6, vitamin B12, and folic acid with breast cancer in a group of women from the Nurses’ Health Study. A total of 712 breast cancer cases were identified from the 32,826 women enrolled in the Nurses’ Health Study. An equal number of matched controls were also included from the initial cohort. Vitamin status and homocysteine levels were determined from blood samples collected at baseline. Comparing the highest versus lowest quintiles of vitamin B6 revealed a relative risk for breast cancer of 0.70 (95% CI = 0.48 to 1.02; P(trend) =0.09). Comparing the highest and lowest quintiles of folic acid concentration revealed a significant reduction in risk for breast cancer (0.73, 95% confidence interval [CI] = 0.50 to 1.07; P(trend) =0.06). This trend was particularly significant for women who consumed at least one alcoholic beverage daily (multivariable RR = 0.11, 95% CI = 0.02 to 0.59 for highest versus lowest quintile). An inverse association was also found between breast cancer risk and vitamin B12 for premenopausal but not postmenopausal women. Results of this study revealed an inverse association between B6 and breast cancer risk in patients, with an especially strong association in post-menopausal women. 19
Plasma vitamin B6 and the risk of colorectal cancer and adenoma in women.
In a nested, case-control study of participants in the Nurses’ Health Study, possible associations between vitamin B6 and colorectal cancer or colorectal adenoma were investigated. The Nurses’ Health Study included 32,826 women; 194 cases of colorectal cancer and 410 cases of colorectal adenoma were identified. Vitamin B6 (as pyridoxal 5'-phosphate [PLP]) was measured in blood samples from all participants. When comparing the highest quartile versus the lowest of plasma PLP, an inverse association between PLP and risk for colorectal cancer was identified (RR = 0.56, 95% CI = 0.31 to 1.01; P(trend) = 0.07). A statistically significant association between PLP concentration with colon cancer was also revealed (RR = 0.42, 95% CI = 0.21 to 0.85; P(trend) = 0.02). Controlling for intakes of folate, multivitamins, and methionine strengthened these statistically significant associations (for colorectal cancer, RR = 0.48, 95% CI = 0.25 to 0.92; P(trend) = 0.03; for colon cancer, RR = 0.38, 95% CI = 0.18 to 0.80; P(trend) = 0.01). An inverse association between plasma PLP concentration and advanced distal colorectal adenoma was also identified (RR = 0.65, 95% CI = 0.37 to 1.11; P(trend) = 0.08). These data indicate that those with highest B6 levels had the lowest incidence of colorectal cancer and polyps. Total vitamin B6 intake was related to reduced risks for colorectal cancer starting at daily intakes of 3.3 mg and colorectal cancer risk was lowest in those consuming 8.6 mg daily. 23
Food, nutrient and heterocyclic amine intake and the risk of bladder cancer.
An epidemiologic study conducted in Spain investigated the associations between diet and bladder cancer. A total of 912 people with bladder cancer and 873 normal, matched controls were enrolled in the study. The study found an inverse association between fruit intake and bladder cancer for current smokers (OR (95% CI) for 5th versus 1st quintile: 0.5 (0.3-0.9), p trend=0.009). Inverse associations were also found for folic acid, vitamins B12, B6, and B2, and retinol. The strongest inverse associations were identified for vitamin B6 (OR (95% CI) for 5th versus 1st quintile: 0.5 (0.3-0.9), p trend=0.009) and for retinol (0.6 (0.4-0.9) p trend=0.004). These data suggest that further evaluation of the associations between vitamin B6 and bladder cancer are necessary. 18
Pregnancy:
Vitamin B-6 content of breast milk and neonatal behavioral functioning.
The amount of vitamin B6 in breast milk may influence an infant’s behavioral development. The major form of vitamin B6 identified in transition milk was pyridoxal. Dietary intake of vitamin B6 was associated with breast milk vitamin B6 content: mothers with intake greater than the median value had a significantly higher median pyridoxal level in their breast milk than those with intakes below the median value. Infants were evaluated with the Neonatal Behavioral Assessment Scale (NBAS). NBAS scores on habituation (r = 0.94, P < 0.05) and autonomic stability (r = 0.34, P < 0.05) subscales of the infants were positively correlated with milk pyridoxal values. Higher vitamin B6 levels in breast milk were associated with higher NBAS scores which indicate a better capability of the infant to deal with their environment. Pregnant and breast-feeding women should take a multivitamin to insure adequate amounts of vitamin B6. 15
Rheumatoid Arthritis:
Abnormal vitamin B(6) status is associated with severity of symptoms in patients with rheumatoid arthritis.
A cross-sectional study evaluated associations between vitamin B6 levels, disease activity, and severity in rheumatoid arthritis. Thirty-seven patients who met the American College of Rheumatology criteria for rheumatoid arthritis were enrolled in this study. Plasma pyridoxal 5'-phosphate levels were inversely correlated with the erythrocyte sedimentation rate, C-reactive protein level, disability score, morning stiffness, and degree of pain. This study revealed strong and consistent associations between vitamin B6 status and several clinical indicators and biochemical markers of inflammation. The results suggest that suboptimal vitamin B6 levels may be due to inflammation in rheumatoid arthritis. 20
The dietary supplement information contained on this site has been compiled from published sources thought to be reliable, but it cannot be guaranteed. Efforts have been made to assure this information is accurate and current. However, some of this information may be purported or outdated due to ongoing research or discoveries. The authors, editors and publishers cannot accept responsibility for errors or omissions or for any consequences from applications of the information in this site and make no warranty, expressed or implied, with respect to the contents herein.
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