VITAMIN B6 (PYRIDOXINE)

 VITAMIN B6 (PYRIDOXINE)
Vitamin B6 is a mixture of 6 inter-related forms of pyridoxine, pyridoxal, pyridoxamine and 5'-phosphates. Interconversion is possible between all forms.

The enzyme pyridoxal phosphate plays an essential role in the metabolism of many amino acids, and the deficiency of this coenzyme can lead to many manifestations. Clinical symptoms include delayed development, acrodynia, alopecia, skeletal changes and anemia, changes in neurotransmitter levels, such as dopamine, serotonin, norepinephrine (noradrenaline), tryptamine, tyramine, histamine, GABA and taurine, brain function and can lead to seizures and convulsions.

The active form of the vitamin is pyridoxal phosphate, which is a coenzyme required to function more than 60 enzymes. Pyridoxine is present in the feed in its free form and as a glucoside. The glucoside may undergo partial hydrolysis in the gut lumen or can be absorbed intact, and thus eliminated mainly in the urine without hydrolysis.

The metabolism of tryptophan depends on the status of vitamin B6, due to an enzyme that requires pyridoxal phosphate. Vitamin B6 is involved in the metabolism of amino acids containing sulfur (methionine, taurine and cysteine).

The majority of the body's vitamin B6 is linked to the muscle glycogen phosphorylase enzyme. When muscle glycogen stores deplete due to prolonged fasting, the vitamin is released from the muscles. However, pyridoxal muscular phosphate is not released in response to the B6 deficient diet so that muscle reserves cannot be considered as a form of vitamin storage.

The main concern associated with excessive intake of vitamin B6 is damage to the nervous system. The initial observations were derived from studies in experimental animals, but more recent studies in volunteers and patients reported cases in humans as well.

Data on human neurotoxicity due to vitamin B6 administration are primarily related to a series of case reports of patients with severe effects associated with extremely high dosage. An essential aspect of these cases is the duration of intake before the symptoms develop. Data showed that clinical cases of neuropathy occur after about 12 months or more of treatment with doses of 2 g/day or less, and neuropathy may develop in less than 12 months at doses greater than 2 g / day.

Deep peripheral limb damage is seen in adult patients after massive doses of vitamin B6; unsteady gait and numbness in the legs, profound positional weakness and vibration sensation, and sensations of touch, temperature and pain were less affected. Also, pyridoxine-related neuropathy was described in 16 patients in another study with patients experiencing symmetrical distant esthetic loss and absence of sensory nerve potential absent.

Photosensitivity has been described as another undesirable effect associated with pyridoxine uptake as well as skin lesions reported in a woman who received enormous doses (4 g/day) for 4 years.

The toxicity of pyridoxine that is of concern is neurotoxicity, which has been clearly demonstrated in animals and humans. Other effects reported in animals that occur at high doses have not been investigated in humans because the main effect in animals is in spermatogenesis and the primary use of high doses in humans is a premenstrual tendency.

Daily doses of about 500mg are necessary to prevent severe neurological effects. Dose-response data in humans, which form the basis for determining the upper level, are predominantly derived from women with premenstrual syndrome.

Pyridoxine neuropathy develops very slowly in humans even at high doses where ingestion is required for 12 months or more for neurotoxicity at doses of 2 g per day or less.

Maximum levels of intake for children are based on body weight differences compared to adults:
 
Age (years) Tolerable Upper Intake Level (UL)
(mg per day)
1-3 5
4-6 7
7-10 10
11-14 15
15-17 20
Adults 25
 
There is a wide margin between the maximum tolerable level of 25 mg daily intake and food intake alone, and there are no safety concerns about vitamin B6 intake from food. The combined intake of food and supplements is generally below the allowable limit.

Supplements are available that contain significantly higher amounts than those of the above level per tablet. The highest level of intake does not apply to people who take vitamin B6 under medical supervision.

Neurotoxicity has been reported only after prolonged treatment periods at high doses. Pyridoxine deficiency has a significant effect on neuronal growth, but there is no data on the toxicity of excessive pyridoxine during the development of the nervous system.
 
 Reference:
  1. SCF (2000) Opinion of the Scientific Committee on Food of the tolerable upper intake level of vitamin B6. Scientific Committee on Food. European Commission Health & Consumer protection. Directorate General, Brussels, 28 November 2000.
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