I ran across several studies that seem to indicate that P5P is a
superior supplement to pyridoxamine for glycation prevention, contrary
to my expectations. First up is http://pubmed.gov/16470027, May 2006:
However, lipid glycation inhibitor has not been discovered yet because
of the lack of a lipid glycation model useful for inhibitor screening.
We optimized and developed a lipid glycation model considering various
reaction conditions (glucose concentration, temperature, buffer type,
and pH) between PE and glucose. Using the developed model, various
protein glycation inhibitors (aminoguanidine, pyridoxamine, and
carnosine), antioxidants (ascorbic acid, alpha-tocopherol, quercetin,
and rutin), and other food compounds (L-lysine, L-cysteine, pyridoxine,
pyridoxal, and pyridoxal 5'-phosphate) were evaluated for their
antiglycative properties. Pyridoxal 5'-phosphate and pyridoxal (vitamin
B(6) derivatives) were the most effective antiglycative compounds.
Above I think the claim is made for lipid and not protein glycation. The
next study however seems to be for protein glycation
(http://pubmed.gov/17449494, August 2007:
Streptozotocin (STZ)-induced diabetic rats were treated by oral
administration of PLP or pyridoxamine (PM), another active form of
vitamin B6, at a dose of 600 mg/kg/day for 16 weeks. ... PLP was
superior to PM in inhibiting accumulation of AGEs, expression of
TGF-beta1, type 1 collagen, and fibronectin, and the development of
diabetic nephropathy.
Finally, in this study, http://pubmed.gov/18004515,
Amino acids react with methylglyoxal to form advanced glycation end
products. This reaction is known to produce free radicals. In this
study, cleavage to plasmid DNA was induced by the glycation of lysine
with methylglyoxal in the presence of iron(III). This system was found
to produce superoxide as well as hydroxyl radicals. The abilities of
various vitamins to prevent damage to plasmid DNA were evaluated.
Pyridoxal-5-phosphate showed maximum protection, while pyridoxamine
showed no protection. The protective abilities could be directly
correlated to inhibition of production of hydroxyl and superoxide
radicals. Pyridoxal-5-phosphate exhibited low radical scavenging ability
as evaluated by its TEAC, but showed maximum protection probably by
interfering in free radical production. Pyridoxamine did not inhibit
free radical production.
Is there something I'm missing, or is P5P better at preventing AGE
formation?

Stephen