The formation of these hydrates is indicative of the high reactivity of MGO, which is relevant to its biological behavior.

[4] Illustrative of the myriad pathways to MGO, aristolochic acid caused 12-fold increase of methylglyoxal from 18 to 231 μg/mg of kidney protein in poisoned mice.

Due to increased blood glucose levels, methylglyoxal has higher concentrations in diabetics and has been linked to arterial atherogenesis.

Damage by methylglyoxal to low-density lipoprotein through glycation causes a fourfold increase of atherogenesis in diabetics.

[13] Methylglyoxal binds directly to the nerve endings and by that increases the chronic extremity soreness in diabetic neuropathy.

[16] Research suggests that methylglyoxal contained in honey does not cause an increased formation of advanced glycation end products (AGEs) in healthy persons.