Vitamin B6 is a water-soluble vitamin that exists in three major chemical forms: pyridoxine, pyridoxal, and pyridoxamine. It performs a wide variety of functions in your body and is essential for your good health. For example, vitamin B6 is needed for more than 100 enzymes involved in protein metabolism. It is also essential for red blood cell metabolism. The nervous and immune systems need vitamin B6 to function efficiently, and it is also needed for the conversion of tryptophan (an amino acid) to niacin (a vitamin).
Hemoglobin within red blood cells carries oxygen to tissues. Your body needs vitamin B6 to make hemoglobin. Vitamin B6 also helps increase the amount of oxygen carried by hemoglobin. A vitamin B6 deficiency can result in a form of anemia that is similar to iron deficiency anemia.
An immune response is a broad term that describes a variety of biochemical changes that occur in an effort to fight off infections. Calories, protein, vitamins, and minerals are important to your immune defenses because they promote the growth of white blood cells that directly fight infections. Vitamin B6, through its involvement in protein metabolism and cellular growth, is important to the immune system. It helps maintain the health of lymphoid organs (thymus, spleen, and lymph nodes) that make your white blood cells. Animal studies show that a vitamin B6 deficiency can decrease your anti-body production and suppress your immune response.
Vitamin B6 also helps maintain your blood glucose (sugar) within a normal range. When caloric intake is low your body needs vitamin B6 to help convert stored carbohydrate or other nutrients to glucose to maintain normal blood sugar levels. While a shortage of vitamin B6 will limit these functions, supplements of this vitamin do not enhance them in well-nourished individuals.
Clinical signs of vitamin B6 deficiency are rarely seen in the United States. Many older Americans, however, have low blood levels of vitamin B6, which may suggest a marginal or sub-optimal vitamin B6 nutritional status. Vitamin B6 deficiency can occur in individuals with poor quality diets that are deficient in many nutrients. Symptoms occur during later stages of deficiency, when intake has been very low for an extended time. Signs of vitamin B6 deficiency include dermatitis (skin inflammation), glossitis (a sore tongue), depression, confusion, and convulsions. Vitamin B6 deficiency also can cause anemia. Some of these symptoms can also result from a variety of medical conditions other than vitamin B6 deficiency. It is important to have a physician evaluate these symptoms so that appropriate medical care can be given.
Individuals with a poor quality diet or an inadequate B6 intake for an extended period may benefit from taking a vitamin B6 supplement if they are unable to increase their dietary intake of vitamin B6. Alcoholics and older adults are more likely to have inadequate vitamin B6 intakes than other segments of the population because they may have limited variety in their diet. Alcohol also promotes the destruction and loss of vitamin B6 from the body.
Asthmatic children treated with the medicine theophylline may need to take a vitamin B6 supplement. Theophylline decreases body stores of vitamin B6, and theophylline-induced seizures have been linked to low body stores of the vitamin. A physician should be consulted about the need for a vitamin B6 supplement when theophylline is prescribed.
A deficiency of vitamin B6, folic acid, or vitamin B12 may increase your level of homocysteine, an amino acid normally found in your blood. There is evidence that an elevated homocysteine level is an independent risk factor for heart disease and stroke. The evidence suggests that high levels of homocysteine may damage coronary arteries or make it easier for blood clotting cells called platelets to clump together and form a clot. However, there is currently no evidence available to suggest that lowering homocysteine level with vitamins will reduce your risk of heart disease. Clinical intervention trials are needed to determine whether supplementation with vitamin B6, folic acid, or vitamin B12 can help protect you against developing coronary heart disease.
1. Vitamins May Reduce Risk of Colon Polyps
Vitamins C, B6, D and folate appear to reduce risk of colon adenoma in both smokers and non-smokers, whereas beta carotene may only have a protective effect in non-smokers and an adverse effect in smokers, according to a study published in the October issue of the Journal of Nutrition (135:2468-72, 2005).
French scientists investigated the effect of dietary vitamins and beta-carotene on the risk of adenomas and a potential interaction with smoking status as part of a case-control study of environmental factors associated with the risk of colorectal adenomas and cancers. The researchers compared nutrient intakes in polyp-free controls (n = 427) and adenoma cases (n = 362), globally and using models stratified by smoking status, adjusted for age, sex, BMI, and energy and alcohol intakes. Folate, vitamin C and vitamin B6 were inversely related to adenoma risk, whereas vitamin D tended to be inversely associated with risk. There was a significant interaction between beta-carotene and smoking. In nonsmokers, beta-carotene was inversely associated with adenoma risk, especially that of colon adenomas; whereas in past or current smokers, beta-carotene was not associated with a significant increase in the risk of colon adenomas.
The research findings support a chemoprotective effect of folate, vitamin C and vitamin B6, irrespective of smoking habits, and a protective effect of beta-carotene in non-smokers only. Based on the adverse effect of beta-carotene in smokers, researchers concluded smokers should be cautious about taking high doses of this micronutrient.
2. B Vitamins May Prevent Strokes
Taking high doses of B vitamins including folic acid, B6 and B12 may help reduce the risk of a second stroke and heart attacks, according to a new study titled "Vitamin Intervention for Stroke Prevention Trial - An Efficacy Analysis," published in the Nov. 1 issue of Stroke.
Canadian researchers J. David Spence, MD, FRCPC, FAHA and colleagues from the Stroke Prevention and Atherosclerosis Centre and other organizations found that "for the combined end point of ischemic stroke, coronary disease, or death, there was a 21% reduction in the risk of events in the high-dose group compared with the low-dose group.
The new findings were contradictory to previous studies. One study conducted by researchers at the University of Tromsų, Norway found treating patients who had a heart attack with high doses of B vitamins did not lower the risk of getting another heart attack or stroke, although homocysteine levels, which have been associated with an elevated risk of heart disease, were lowered after the treatment.
Even worse, harmful effects were observed among those patients with high levels of homocysteine at the start of the trial, or with impaired renal function, or with other vitamin supplements being taken in addition to the study medication.
The findings of the current study were also contradictory to a previous study of the same authors who wrote, "treatment with a combination of folic acid, pyridoxine (vitamin B6) and cobalamin (vitamin B12) reduces plasma H(e) levels in most cases, restores endothelial function, and regresses carotid plaque, but there is no evidence that such treatment will reduce clinical events. The study titled Vitamin Intervention for Stroke Prevention (VISP) trial: rationale and design was published in the Feb. issue of Neuroepidemiology.
Dr. Spence and colleagues wrote in their current report that "reasons for lack of efficacy may have included folate fortification of grain products, inclusion of the recommended daily intake for B12 in the low-dose arm, treatment with parenteral B12 in patients with low B12 levels in both study arms, a dose of B12 too low for patients with malabsorption, supplementation with nonstudy vitamins, and failure of patients with significant renal impairment to respond to vitamin therapy."
In the current study of 2155 patients, the authors excluded those with low and high B12 levels at baseline (637 pmol/L, representing the 25th and 95th percentiles), as they were likely to have B12 malabsorption or to be taking B12 supplements outside the study or to have significant renal impairment.
3. Huang YH, Wang GS. Vitamin B6 Deficiency Decreases the Glucose Utilization in Cognitive Brain Structures of Rats. J Nutr Biochem. 1999 Sep;10(9):525 -31.
The effects of vitamin B(6) deficiency on metabolic activities of brain structures were studied. Male Sprague-Dawley weanling rats received one of the following diets: (1) 7 mg pyridoxine HCl/kg (control group); (2) 0 mg pyridoxine HCl/kg (vitamin B(6)-deficient group); or (3) 7 mg pyridoxine HCl/kg with food intake restricted in quantity to that consumed by the deficient group (pair-fed control group). After 8 weeks of dietary treatment, rats in all three groups received an intravenous injection of 2-deoxy-[(14)C] glucose (100 microCi/kg). Vitamin B(6) status was evaluated by plasma pyridoxal 5'-phosphate concentrations. The vitamin B(6)-deficient group had significantly lower levels of plasma pyridoxal 5'-phosphate than did the control and pair-fed groups. The local cerebral glucose utilization rates in structures of the limbic system, basal ganglia, sensory motor system, and hypothalamic system were determined. The local cerebral glucose utilization rates in each of the four brain regions in the deficient animals were approximately 50% lower (P < 0.05) than in the control group. Results of the present study suggest that serious cognitive deficit may occur in vitamin B(6)-deficient animals.
4. Rimm EB, Willett WC, Hu FB, Sampson L, Colditz GA, Manson JE, Hennekens C, Stampfer MJ. Folate and Vitamin B6 from Diet and Supplements in Relation to Risk of Coronary Heart Disease Among Women.
Context: Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6. However, prospective data relating intake of these vitamins to risk of coronary heart disease (CHD) are not available.
Objective: To examine intakes of folate and vitamin B6 in relation to the incidence of nonfatal myocardial infarction (MI) and fatal CHD.
Design: Prospective cohort study.
Setting and Patients: In 1980, a total of 80082 women from the Nurses' Health Study with no previous history of cardiovascular disease, cancer, hypercholesterolemia, or diabetes completed a detailed food frequency questionnaire from which we derived usual intake of folate and vitamin B6. MAIN OUTCOME MEASURE: Nonfatal MI and fatal CHD confirmed by World Health Organization criteria. RESULTS: During 14 years of follow-up, we documented 658 incident cases of nonfatal MI and 281 cases of fatal CHD. After controlling for cardiovascular risk factors, including smoking and hypertension and intake of alcohol, fiber, vitamin E, and saturated, polyunsaturated, and trans fat, the relative risks (RRs) of CHD between extreme quintiles were 0.69 (95% confidence interval [CI], 0.55-0.87) for folate (median intake, 696 microg/d vs 158 microg/d) and 0.67 (95% CI, 0.53-0.85) for vitamin B6 (median intake, 4.6 mg/d vs 1.1 mg/d). Controlling for the same variables, the RR was 0.55 (95% CI, 0.41-0.74) among women in the highest quintile of both folate and vitamin B6 intake compared with the opposite extreme. Risk of CHD was reduced among women who regularly used multiple vitamins (RR=0.76; 95% CI, 0.65-0.90), the major source of folate and vitamin B6, and after excluding multiple vitamin users, among those with higher dietary intakes of folate and vitamin B6. In a subgroup analysis, compared with nondrinkers, the inverse association between a high-folate diet and CHD was strongest among women who consumed up to 1 alcoholic beverage per day (RR =0.69; 95% CI, 0.49-0.97) or more than 1 drink per day (RR=0.27; 95% CI, 0.13-0.58).
Conclusion: These results suggest that intake of folate and vitamin B6 above the current recommended dietary allowance may be important in the primary prevention of CHD among women.
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