Vitamin B6 deficiency
Deficiency of vitamin B6 severe enough to lead to clinical signs is extremely rare, and unequivocal deficiency has only been reported in one outbreak, during the 1950s, when babies were fed on a milk preparation that had been severely overheated during manufacture. Many of the affected infants suffered convul-sions, which ceased rapidly following the administra-tion of vitamin B6.
The cause of the convulsions was severe impair-ment of the activity of the pyridoxal phosphate-dependent enzyme glutamate decarboxylase, which catalyzes the synthesis of the inhibitory neurotrans-mitter γ-aminobutyric acid (GABA), together with accumulation of hydroxykynurenine as a result of impaired activity of kynureninase, which is also pyri-doxal phosphate dependent.
Moderate vitamin B6 deficiency results in a number of abnormalities of amino acid metabolism, espe-cially of tryptophan and methionine. In experimental animals, a moderate degree of deficiency leads to increased sensitivity of target tissues to steroid hormone action. This may be important in the devel-opment of hormone-dependent cancer of the breast, uterus, and prostate, and may therefore affect the prognosis. Vitamin B6 supplementation may be a useful adjunct to other therapy in these common cancers; certainly, there is evidence that poor vitamin B6 nutritional status is associated with a poor prog-nosis in women with breast cancer.