Physiological Roles and Food Sources Vitamin B12 is found in moderate amounts in poultry, fish, liver, and eggs, with lower concentrations in meat and milk. The bioavailability of pyridoxine from animal products is 96%. In healthy people, vitamin B6 is produced by the gut bacteria. You can get this vitamin from various plants, including beans, peanuts, potatoes, yeast, bananas, corn, cabbage, yams, prunes, watermelon, and avocados.
Populations at Risk Because this vitamin is so common, deficiencies are uncommon, especially in long-term alcoholics and women using oral contraceptives. Those at higher risk include the elderly and newborns born to moms with B6 deficiencies or preeclampsia. B6 supplementation is recommended for patients on Cycloserine, hydantoin, hydralazine, isoniazid, and penicillamine. Vitamin B12 requirements rise with dietary protein intake.
Although severe vitamin B6 shortages are unusual, minor deficiencies are pretty frequent. According to the Second National Health and Nutrition Examination Survey (NHANES II), 71% of males and 90% of females did not get enough vitamin B6 in their diets compared to the 1980 RDA. Most seniors are weak in vitamin B6, a water-soluble vitamin. Individual drugs and drug combinations for the elderly can pose a nutritional risk. Instructing the elderly and their caretakers to avoid mistakes in drug timing and toxic reactions owing to food incompatibility might help lessen the adverse effects of drug-food and drug-nutrient interactions. The elderly who use drugs could benefit from advice on maintaining healthy vitamin levels in their diets and avoiding drug-induced nutritional deficits. Vitamin B6 intake was below the RDA in more than half of the population in a study comparing the nutrient intakes of American children aged 2 to 10 years.
Vitamin B6 insufficiency and increased need can result from birth control pills or exposure to carbon disulfide at work. Extreme irritability, manic depressive tendencies, headaches, and other variables are all caused by both substances. Still, vitamin B6 administration has been found to alleviate these symptoms and prevent further damage to the brain. To experimentally assess this correlation, more research is required. The psychological aftereffects of CS2 exposure may be amplified when combined with OCs because of the increased disruption of tryptophan metabolism.
In babies, the symptoms of deficiency are typically convulsive convulsions and hyperactivity. Likewise standard is diarrhea. Pyridoxine deficiency manifests clinically as anemia and peripheral neuritis in tuberculosis patients on isoniazid. Vitamin B6 therapy is effective for 20-30% of patients with homocystinuria who suffer from cataracts, displacement of the lens of the eye, osteoporosis (brittle spine), mental retardation, and a propensity for spontaneous blood clots that can cause heart attacks and death.
Biochemists refer to the precursors of the biologically active coenzyme, pyridoxal phosphate, as “vitamin B6,” which includes pyridoxine, pyridoxal, and pyridoxamine. There are several different reactions that pyridoxal phosphate catalyzes, including those involved in protein metabolism, tryptophan conversion to niacin metabolism, fat metabolism, carbohydrate metabolism, folic acid synthesis, glandular and endocrine function, and nerve and brain energy. Homocystinuria is an uncommon disorder caused by a lack of an enzyme that breaks down homocysteine. Vitamin B6 has been shown to alleviate the symptoms of this condition.
Pyridoxine is safe, but too little or too much can cause neurological problems. Toxic effects are determined by cumulative exposure, which can occur at much lower concentrations than the 600 mg/day linked to most sensory neuropathy occurrences. One study suggests that a daily dosage of 117 mg (on average) for 2.9 years might be harmful. The accuracy of the telephone survey method used to identify neuropathy is called into doubt by the fact that the control group that did not develop neuropathy had an average consumption of 116 mg/day for an average of 1.6 years and that some women in both groups had been taking as little as 50 mg.
Vitamin B6 is harmful at 1,000 times the recommended daily allowance. Walking impairment and foot and leg tingling have been reported in people taking 2–5 grams of pyridoxine daily. If the dangerous dose is used repeatedly, the user will experience worsening symptoms, including shaky legs, clumsy hands, and trouble with fine motor skills. When vitamin B6 supplements are withdrawn, symptoms often improve within two months. Full recovery is possible after 2–3 years of not taking the vitamin B6 pills. Pure central-peripheral distal axonopathy was found to develop in a pyridoxine addiction investigation. Pyridoxine dose ranged from 0.2 to 5 g/d, with symptom duration inversely related to the amount. Eliminating pyridoxine was followed by improvement in all patients with sufficient follow-up.
Is there any evidence that long-term usage of pyridoxine, even in youngsters, is unsafe? A meta-analysis suggests that daily doses of 100 mg or less of pyridoxine are safe for adults. There is not enough information to make any recommendations about children. Pyridoxine may cause neuropathy only in patients with a preexisting predisposition to this condition, as peripheral neuropathy is the predominant neurologic consequence and its numerous causes. Peripheral neuropathy not seen in other patients receiving the exact dosages of pyridoxine may be caused by a combination of pyridoxine and predisposing variables such as family history, drug use, alcohol use, nutritional status, and hazardous exposure at home or work. It’s still unclear how long exposure causes neuropathy. Neurological damage can occur in as little as a few days at extremely high dosages, whereas chronically low concentrations appear to be safe.
Treatment with vitamin B6 and B12 improved the condition of 14 patients with acne vulgaris or prevented the development of an acneiform exanthema. Women were hit more frequently than men. Acne vulgaris symptoms manifest on the skin at any age, not just those most susceptible. Acneiform exanthema is characterized clinically by the development of many minute papules or papulopustular all over the body, but most noticeably on the face (mainly the forehead and chin), upper back, upper chest, and occasionally the upper arm. There is still uncertainty about the change’s pathogenesis. The acneiform rash typically clears up quickly when vitamin B6 or vitamin B12 medication is discontinued.
Children aged 0-6 months: 0.3mg
Children from 6 months to 1 year: 0.6mg
1.0mg for children aged 1-3 years
Kids aged 4 to 6: 1.1mg
7-10-year-old kids: 1.4mg
11- to 14-year-old boys – 1.7mg
11- to 14-year-old girls – 1.4 mg
Male adolescents 15–18 years old: 2.0mg
Female adolescents aged 15–18 years: 1.5 mg
Males between the ages of 19 and 50: 2.0mg
Women aged 19-50 years: 1.6mg
Males over the age of 51: 2.0mg
Women aged 51 and up: 1.6 milligrams
Women Who Are Pregnant: 2.2mg
For the First Six Months of Breastfeeding, 2.1mg
Pregnant Women (Second Trimester) – 2.1mg
B6 Pyridoxal
Source of Food Amount Served per Serving Number of Milligrams
3.50 ounces of dark chicken meat 0.37 mg
White-meat chicken (3.5 ounces) 0.63 milligrams
3.0 ounces of raw, wild Atlantic salmon 0.70 milligrams
3.0 ounces 0.30 milligrams of tuna (in water)
3.5 ounces of beef liver (0.91 milligrams)
Eating veal live (3.5 ounces braised 0.91 mg
1 cup of boiling navy beans = 0.30 mg
Dry-roasted peanuts (1 ounce) 0.07 mg
Boiling a Potato: 1 Medium, 0.40 mg
One medium banana, 0.66 milligrams
Dried Prunes (10 of them) 0.22 mg
One cup of watermelon has around 0.23 milligrams of sodium.
Asparagus, One Medium, 0.48mg
Homocysteine
Vitamin B6, folate, and cobalamin deficits have been linked to hyperhomocysteinemia, an atherosclerotic risk factor. The risk of sudden cardiac chest pain or myocardial infarction was shown to be 27% higher in patients who had been given vitamin B6 for the treatment of carpal tunnel syndrome and other degenerative disorders. Dr. Ellis observed that the average age of death from myocardial infarction was eight years later in his senior patients who took vitamin B6 compared to those who did not. Increased synthesis of pyridoxal phosphate, the coenzyme needed for degradation of the atherogenic amino acid homocysteine, may explain vitamin B6’s protective effect on coronary heart disease progression.
Pregnancy difficulties, neural tube defects, mental disorders, and cognitive impairment in the elderly are all linked to total serum homocysteine (tHcy) levels. Moreover, a high tHcy level is a prevalent cardiovascular risk factor, supported by over 80 clinical and epidemiological investigations. Fasting tHcy is not reduced by oral treatment with pyridoxine at doses up to 300mg/d in healthy persons or vascular patients. However, with the addition of folic acid, nearly all patients achieve an average post-methionine tHcy level after treatment with pyridoxine (10-250 mg/d).
In a randomized study, Pyridoxine reduced ADP- or epinephrine-induced aggregation by 48% and 41%, respectively (p 0.001). It also increased the time it took for blood to leak and clot. The HDL-cholesterol level was increased while the overall plasma lipid and cholesterol levels were dramatically decreased due to pyridoxine. Therefore, it appears that vitamin B6 prevents platelet aggregation in healthy people when taken orally.
There was a substantial decrease in systolic (p 0.01) and diastolic blood pressure (p 0.005), as well as plasma NE (p 0.005) and E (p 0.05), in patients with hypertension who were given pyridoxine for four weeks. These individuals were assigned a pyridoxine dosage of 5 milligrams per kilogram of body weight each day. Therefore, pyridoxine might help with hypertension.
It’s been established that pyridoxine is a necessary cofactor in synthesizing neurotransmitters. Because of this, it has been considered a therapeutic adjuvant in a wide range of illnesses where abnormalities in neurotransmitters are either established or strongly suspected. Diseases like epilepsy, Parkinson’s, depression, chronic pain, headaches, atypical adult and child behavior, and peripheral neuropathy are all in this category. The therapy of premenstrual syndrome and carpal tunnel syndrome are two further clinical applications of pyridoxine. Because of pyridoxine’s neurotoxicity, it’s crucial to record vitamin consumption as part of a patient’s medical history.
Diabetic neuropathy is often treated with vitamin B6. It was previously believed that a lack of vitamin B6 was responsible for the neuropathy seen in diabetics. ACCORDING TO SEVERAL STUDIES, vitamin B6 supplements may not be helpful for these people. Eighteen patients with diabetic neuropathy symptoms were randomly assigned to receive either a placebo or pyridoxine in one of these investigations. Fasting plasma glucose, motor nerve conduction velocity, and ophthalmologic examination at the start and end of the trial showed no significant differences between the two groups after four months of follow-up. Based on these findings, vitamin B6 deficiency probably does not have a role in the development of diabetic peripheral neuropathy.
A relative pyridoxine shortage was suspected in a study of 14 pregnant mothers with gestational diabetes. Oral glucose tolerance was significantly enhanced after being treated with vitamin B6 (pyridoxine) 100 mg daily for 14 days. Gestational diabetes has been linked to increased xanthurenic-acid production, which has been theorized to occur naturally due to pregnancy. Vitamin B6 treatment increases oral glucose tolerance and normalizes xanthurenic-acid generation in women with gestational diabetes by re-establishing the body’s tryptophan metabolism.
There is some evidence that pyridoxine can help treat kidney stones, but it is inconclusive. Twelve individuals with hyperoxaluria and recurrent stone formation were treated with pyridoxine-HCl (10 mg/day) for 180 days. By the 90th day of therapy, urinary oxalate had decreased significantly (p less than 0.05), demonstrating the therapeutic effectiveness of low-dose pyridoxine (10 mg/day) for hyperoxaluric stone formers.
The benefits of vitamin B6 alone, magnesium alone, and in combination were studied in a meta-analysis of four therapeutic crossed-sequential double-blind trials, including 60 children with autism. Children’s conduct improved marginally when magnesium and vitamin B6 were administered but not when either was given separately.
Vitamin B6 acts as a cofactor in the neurological system, which may affect how the brain develops and functions. RECENT ANIMAL STUDIES HAVE SHOWN vitamin B6 deficiency during pregnancy and lactation to affect the activity of receptors with potential roles in learning and memory. Although the precise process is unknown, it is known that a lack of vitamin B6 during brain development leads to neurochemical and morphological changes that manifest as tremors, irritability, motor function impairments, and spontaneous seizures in affected individuals. Many studies have shown that pregnant and breastfeeding women may not get enough vitamin B6 from their diets, which can affect their children’s vitamin B6 status. Infants of unsupplemented breastfeeding moms have been shown to have vitamin B6 levels in their milk that are below 100 g/L, a number at which they are at risk for developing seizures. This level of vitamin B6 in milk may affect a child’s normal development, even if it may not necessarily cause clinical signs of severe vitamin B6 insufficiency. An Egyptian study found that children whose mothers had vitamin B6 levels in milk below 85 mg/L exhibited behavioral problems.
As a result, pyridoxine may be effective in treating a wide variety of neurological disorders in the clinic. The discovery that pyridoxine can increase serotonin levels and that serotonin shortage is shared by individuals suffering from headaches, chronic pain, and depression expands the treatment choices available to treat these conditions. When compared to amitriptyline, which is also used to treat headaches, it looks to be nearly as effective. However, amitriptyline may have more adverse effects. Supplementation in early life may prevent the occurrence of hyperactivity and violent behavior, a theory advanced by some medical authorities who have gone so far as to imply that many cases of the behavioral disorder are caused by “toxic” exposures to chemicals that are pyridoxine antagonists.
Some individuals receiving isoniazid (INH) medication require vitamin B6 (pyridoxine) supplementation to avoid the development of peripheral neuropathy. The coenzymes produced from pyridoxine in living organisms metabolize many different compounds, including the amines in the brain. It appears that INH affects pyridoxine’s role in several metabolic processes by acting as a competitive inhibitor. Regular pyridoxine supplementation is suggested for people at high risk of developing peripheral neuropathy.
Patients with a vitamin B6 deficiency often suffer from carpal tunnel syndrome and other related illnesses, which can be effectively treated with vitamin B6 supplementation. Higher plasma pyridoxal 5′-phosphate (PLP) concentrations were linked in a study to less pain/discomfort, tingling, and nighttime waking, especially among men who did not take a PLP supplement. In contrast, other analyses have linked elevated vitamin C levels or a relative deficit of plasma PLP relative to the plasma vitamin C (higher ASC/PLP ratio) to longer sensory latencies or more frequent symptoms. Because of this, it’s plausible that taking vitamin C supplements while deficient in vitamin B6 could be harmful to the median nerve and hasten the onset of CTS symptoms in the hands and wrists. Therefore, plasma vitamin levels are significantly related to both aspects of CTS (symptoms and median nerve slowness). When it comes to signs, the link between plasma PLP and ASC stands out as crucial. As a result, vitamin B6 is often suggested as a treatment for CTS.
The favorable effects of vitamin B6 in the treatment of premenstrual syndrome were only marginally supported by a meta-analysis of 12 randomized controlled trials. The trials’ primary flaw is their small sample size. In a recent, carefully conducted trial, one hundred and twenty women were randomly assigned to receive either the natural medicine or a placebo. Symptom reduction with pyridoxine at 300 mg/d was no better than with a placebo.
Possible involvement of vitamin B6 in the body’s reaction to exercise. When creating energy for physical activity, vitamin B6 is crucial. Exercise performance may suffer from insufficient vitamin B6. There is some evidence that taking a vitamin B6 supplement during and immediately after exercise raises plasma growth hormone levels. Muscle gain and fat loss are hypothesized results of these alterations, although their physiologic importance has not been investigated. Vitamin B6 deficiency is possible among female athletes and those participating in sports emphasizing light body weight (such as dancers, wrestlers, gymnasts, and runners).
There is some evidence that vitamin B6 can help with asthma, although it is not strong. After five months of treatment with pyridoxine (200 mg daily), 76 children with asthma showed considerable improvement in their symptoms and required less bronchodilator and cortisone. The findings show that long-term treatment with high dosages of pyridoxine helped these children with severe bronchial asthma because of a metabolic block in tryptophan metabolism. Another randomized controlled trial compared the effects of pyridoxine 300 mg daily with a placebo in treating asthma in 31 individuals who were already on steroids (oral or inhaled). Oral pyridoxine medication did not enhance outcome factors in patients needing steroid asthma treatment during a 9-week follow-up.
There is some evidence that vitamin B6 can help with depression, although it is not strong. In a well-conducted trial, researchers evaluated the effectiveness of adding 10 milligrams of vitamins B1, B2, and B6 to the tricyclic antidepressant regimens of 14 elderly inpatients suffering from depression. Ratings of sadness, cognitive function, and serum nortriptyline levels tended to improve more in the vitamin treatment group than in the placebo group. Therefore, supplementing with B complex vitamins may help treat elderly depression.
Protein, lipid, carbohydrate metabolism, folic acid synthesis, and glandular and endocrine function rely on pyridoxine. Because it produces serotonin, dopamine, and other neurotransmitters, it is a vital nutrient for maintaining normal cognitive and emotional functioning.
Atherosclerosis, ADD, autism, alcohol withdrawal, diabetes, fibrocystic breast disease, carpal tunnel, chemotherapy, HIV patients, nephrolithiasis, osteoporosis, photosensitivity, retinopathy, and canker sores are just some of the conditions that vitamin B6 has been said to help.
There is compelling evidence that vitamin B6 can slow the development of coronary artery disease. While vitamin B6 supplementation did not reduce fasting plasma homocysteine levels, it did minimize post-methionine load tHcy, which may explain its cardioprotective impact.
It has been demonstrated to be as effective as amitriptyline in treating chronic headaches in well-designed studies. Vitamin B6 therapy may help treat several clinical disorders, including chronic pain and depression due to serotonin insufficiency. Seizures, Parkinson’s disease, adult and childhood behavioral disorders, and peripheral neuropathy are only some illnesses for which this crucial component in manufacturing numerous neurotransmitters may be considered a therapeutic adjunct. Carpal tunnel syndrome in vitamin B6 deficient patients respond well to therapy with vitamin B6. Vitamin B6 supplements have been shown to boost athletic performance.
Chronic alcoholics, women on oral contraceptives, patients taking isoniazid, and athletes are just a few of the populations that may benefit from vitamin B12 supplementation. Vitamin B6 is essential for the healthy growth of the central nervous system and brain and the prevention of improper behavioral development in infants and children of pregnant and breastfeeding mothers.
Due to low-level indications of toxicity at 50 mg/d, we advise a lower dose of 40 mg/d for adults. Vitamin B6 intakes between 10 and 300 milligrams per day are considered safe. Adverse neurological effects have been reported at doses greater than 300 mg/day, which are uncommon but concerning. Consumption in pregnant and nursing women should not exceed 100 mg daily. When therapy-related sensory neuropathy, including hand and foot numbness and trouble walking, develops, vitamin B6 intake should be discontinued immediately.
Read also: Tips On How To Control Diabetes Type-2/Symptoms As Well As Complications And Best Meals For Diabetes
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