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  • aka B6
  • Involved in many reactions of amino acid conversion and catabolism
  • e.g., transamination (aminotransferases), decarboxylation, dehydration, and desulfhydration
  • If a person is B6 deficient, all vitamins become essential, since transamination is necessary to make any other vitamin useful
  • pyridoxal phosphate is the coenzyme formed from vitamin B6
  • It is the active coenzyme form of Pyridoxin
  • Plays a role as a cofactor in several important enzymes of synthesis and amino acid metabolism
  • Transamination is a crucial vitamin B6-dependent reaction for conversion of protein to carbohydrate


  • Neurological symptoms of B6 deficiency arise from an impairment of γ-aminobutyric acid (GABA) synthesis
  • GABA is an inhibitory neurotransmitter
  • It requires pyridoxal phosphate for synthesis
  • Imbalance of GABA can lead to seizures or other brain nasties.

Sideroblastic anemia

  • Sideroblastic anemia is a possible consequence of B6 deficiency
  • Caused by defective heme synthesis
  • Δ-aminolevulinic acid synthesis requires pyridoxal phosphate
  • Δ-aminolevulinic acid is a precursor of heme
  • Therefore, B6 deficiency can cause sideroblastic anemia where immature iron-loaded red cells accumulate


  • B6 is an example of a water-soluble vitamin with documented evidence of toxicity due to overdosing
  • The popular belief was that water-soluble vitamins could not be overdosed on, since the excess would simply be purged from the body. This is wrong.
  • B6 is popularly advised for tingling, muscle spasms, numbness in the hands, and edema
  • Megadosing can occur at 2-6g / day
  • Causes peripheral neurological damage
  • The damage may be irreversible
  • The mechanism is "starvation in a sea of plenty"
    • excess pyridoxin overloads the conversion mechanism to the active enzyme, and uselessly occupies the sites on enzymes reserved for the coenzymes (pyridoxal and pyridoxamine phosphate)