Sources and Physiologic Functions Sources: Poultry, fish, liver, and eggs are good sources of this vitamin; meat and milk contain lesser amounts. Pyridoxine in animal sources is 96% bioavailable. Vitamin B6 can be made by intestinal bacteria in healthy persons. Plant foods such as legumes, peanuts, potatoes, yeast, bananas, corn, cabbage, yams, prunes, watermelon, and avocados also contain this vitamin.
Populations at risk: As this vitamin is widely distributed, deficiency is rare except in chronic alcoholics and among women taking oral contraceptives. Elderly persons and infants of preeclamptic mothers or mothers deficient in B6 are at risk. Patients on Cycloserine, hydantoin, hydralazine, isoniazid, and penicillamine should be given B6 supplementation. High protein diet increases the needs of this vitamin.
Severe deficiencies of vitamin B6 are rare, but mild deficiencies are extremely common. Dietary data from Second National Health and Nutrition Examination Survey (NHANES II) in 11,658 adults aged 19-74 y showed that 71% of males and 90% of females consumed less than the 1980 recommended dietary allowance (RDA) of vitamin B6. Vitamin B6 is the most common deficient water soluble vitamin in elderly. Single drug and drug combinations taken by elderly individuals may impose nutritional risk. Unwanted outcomes of drug-food and drug-nutrient interactions can be minimized by instructing elderly men and women and their caregivers to avoid timing errors in drug-taking behavior and toxic reactions due to food incompatibility. In addition, drug-induced nutritional deficiencies can be avoided by advising drug-taking elderly on the appropriate levels of nutrient intake. In a study which compared the nutrient intakes of American children aged 2 to 10 years, vitamin B6 was found to be below the RDA in more than 50% of the population.
Birth control pill usage and occupational exposure to carbon disulfide induce vitamin B6 deficiency and/or enhance vitamin B6 requirement. Both compounds cause adverse psychological/neurological disorders such as extreme irritability, manic depressive tendencies, headaches, and other variables, but related disorders presumably by disrupting normal vitamin B6 metabolism and vitamin B6 administration has been found to alleviate their adverse psychological symptoms. Further studies are needed to experimentally evaluate this interrelation. Conjoined exposure to OCs and CS2 may result in an enhanced disruption of tryptophan metabolism which may in turn cause exaggerated psychological sequelae associated with CS2 exposure.
Signs and Symptoms of Deficiency: In infants, convulsive seizures and hyperactivity are the usual presenting symptoms. Diarrhea is also common. Anemia and peripheral neuritis are seen in tuberculosis patients on isoniazid who develop pyridoxine deficiency. 20-30% of homocystinuric patients with dislocation of the lens of the eye, osteoporosis (brittle spine), mental retardation, and a tendency for spontaneous blood clots that can lead to heart attacks and death, respond to vitamin B6 therapy.
Biochemistry: Vitamin B6 isa collective term for pyridoxine, pyridoxal, and pyridoxamine, all of which serve as precursors of the biologically active coenzyme, pyridoxal phosphate. Pyridoxal phosphate functions as a coenzyme that catalyze reactions in protein metabolism, conversion of tryptophan to niacin, fat metabolism, carbohydrate metabolism, folic acid synthesis, glandular and endocrine functions, and for the nerve and brain energy. Vitamin B6 has a clear benefit in lessening the severity of homocystinuria, a rare disease that usually results from a defect in an enzyme used for degrading homocysteine.
Safety: Deficient and excess intakes of pyridoxine can produce neurologic disturbances. Most cases of sensory neuropathy have resulted from intakes of over 600 mg/day, but some evidence suggests that it may result from doses as low as 300-500 mg/d and that the total exposure over time is the determinant of toxicity. There is one report that a daily intake of 117 mg/day (on average) for 2.9 years may be related to some toxicity. In the same study however, the control group that did not get any neuropathy had an average intake of 116 mg/day for an average of 1.6 years, and some women in both groups had been taking as little as 50 mg/day, questioning the accuracy of the telephone survey method used to determine neuropathy.
Vitamin B6 is toxic at doses that are 1000 times the RDA. Daily doses of 2 to 5 g of pyridoxine can produce difficulty in walking and tingling sensations in the legs and soles of the feet. Continued consumption of the toxic dose results in further unsteadiness of walking, difficulty in handling small objects, and numbness and clumsiness of the hands. Where vitamin B6 supplementation is stopped, recovery begins after 2 months. Complete recovery may occur after 2 to 3 years of discontinuing consumption of the vitamin B6 supplements. One study showed development of pure central-peripheral distal axonopathy with pyridoxine abuse. Pyridoxine dose was 0.2 to 5 g/d, and duration of consumption before symptoms was inversely proportional to the daily intake. In all patients with adequate follow-up, improvement followed discontinuation of pyridoxine.
Is pyridoxine safe for long-term use in large segments of the population, including children? It would appear from retrospective analysis of several studies that pyridoxine is safe at doses of 100mg/day or less in adults. In children, there is not enough data to make any sort of suggestion. Because the major neurologic complication is a 螯合療法 peripheral neuropathy, and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition. Family histories, drugs, alcohol, nutritional status, and toxic exposure at home or in the work place may all be predisposing factors which, in combination with pyridoxine, produce the peripheral neuropathy that is not seen in other patients taking the same dosages. The duration of exposure that causes neuropathy is still a major question. Extremely high doses cause neurologic injury within a few days, and chronic low doses seem relatively safe.
Deterioration of acne vulgaris or eruption of an acneiform exanthema was demonstrated during treatment with vitamin B6 and/or vitamin B12 in 14 patients. Females were, by far, the more frequently affected. The appearance of skin symptoms, even outside the age groups typically affected by acne vulgaris, is characteristic. The clinical appearance of acneiform exanthema occurring during treatment with vitamin B6 or B12 consists of loosely disseminated small papules or papulopustules on the face (especially on the forehead and chin), on the upper parts of the back and chest, and spreading to the upper arm. The pathogensis of the change is not yet certain. The acneiform rash generally fades within a short time after vitamin B6 or vitamin B12 treatment has been stopped.
Recommendations: RDA in mg.
- Infants birth to 6 mos – 0.3mg
- Infants 6 mos to 1 yr – 0.6mg
- Children 1 yr to 3 yr – 1.0mg
- Children 4 yr to 6 yr – 1.1mg
- Children 7 yr to 10 yr – 1.4mg
- Adolescent males 11yr to 14 yr – 1.7mg
- Adolescent females 11 yr to 14 yr – 1.4 mg
- Adolescent males 15 yr to 18 yr – 2.0mg
- Adolescent females 15 yr to 18 yr – 1.5mg
- Adult males 19 yr to 50 yr – 2.0mg
- Adult females 19 yr to 50 yr – 1.6mg
- Adult males 51 yr plus – 2.0mg
- Adult females 51 yr plus – 1.6mg
- Pregnant Women – 2.2mg
- Lactating Mothers (1st 6 months) – 2.1mg
- Lactating Mothers (2nd 6 months) – 2.1mg
Food Source Serving Size/Amount # of mg/serving
Chicken (dark meat) 3.5 oz 0.37 mg
Chicken (light meat) 3.5 oz 0.63 mg
Atlantic Salmon (wild, raw) 3.0 oz 0.70 mg
Tuna (canned in water) 3.0 oz 0.30 mg
Liver (beef braised) 3.5 oz 0.91 mg
Live (veal braised 3.5 oz 0.91 mg
Navy beans (boiled) 1 cup 0.30 mg