Pyridoxin

Basics

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 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)