Pyridoxamine inhibits Advanced Glycation End products (AGE)
and Advanced Lipoxidation End products (ALE) which are
implicated in the progression of diabetic health problems.
                                   

1.   Pyridoxamine   inhibits formation of advanced glycation end products (AGE)

2.   Pyridoxamine   may be useful in diabetes & atherosclerosis

3.   Pyridoxamine   protects against vascular damage

4.   Pyridoxamine   may be useful for treating diabetic retinopathy

5.   Pyridoxamine   inhibits renal disease and decreases hyperlipidemia in diabetic rats

6.   Pyridoxamine   and progression of nephropathy in the diabetic rat

7.   Pyridoxamine   reduces oxidative stress and AGE formation

8.   Pyridoxamine   inhibits superoxide radicals and prevents lipid peroxidation

9.   Pyridoxamine   inhibits chemical modification of proteins

10.   Pyridoxamine   restores beta cell function in diabetic hamster

11.   Pyridoxamine   inhibits retinopathy and neuropathy in diabetic rats

Recent clinical trials have supported facts about pyridoxamine that do not appear to be present in the more commonly available B6 vitamins.

One of the most noticeable features of pyridoxamine is the fact that it is the most potent natural substance to inhibit glycosylation. This process (also known as cross-linking) inhibits the actions of proteins to go about there functions, it is formed when sugar (normally as glucose) meets oxygen and protein.

More glycated proteins leads to more incidences of aging disorders such as cataracts, hardened skin, tough collagen (thereby more inefficient cell and arterial walls) and it is a well know fact that diabetics have large numbers of glycated proteins, a prominent feature of the diabetic disease.

In animal models, pyridoxamine has inhibited both development and progression of diabetic nephropathy for type 1 and 2 diabetes. Human trials are ongoing but show promise at doses of 50 mg. twice daily, and whilst some patients have taken as much as 300 mg daily, they have not shown any signs of serious side effects or contraindications.

Glycation, particularly as Advanced Glycated End products (AGE) has been associated with aging for many years and forms a fundamental theory of aging. There are a number of stages, both early and late, in the formation of AGE’s and whilst excellent anti-glycators such as Aminoguanidine show excellent ability to prevent early-stage glycation, it is not so effective in post or late stage glycation. This is where pyridoxamine has been shown to be most effective. One study, (Booth AA, Khalifah RG, Todd P, Hudson BG, In-vitro kinetic studies of formation of antigenic advanced glycation end products. Novel inhibition of post-Amadori glycation pathways, Journal of Biological Chemistry, Feb 28;272(9):5430-7), stated that; “…[pyridoxamine] may compliment others, such as Aminoguanidine, known to either prevent initial sugar attachment or scavenge highly reactive dicarbonyl intermediates.”

Apart from inhibiting AGE formation, pyridoxamine also “traps” advanced lipoxidation end-products (ALE’s). This fact has not escaped researchers interested in atherosclerosis, because this is viewed as an age-related disease and the presence of an excess of ALE’s seem to set the stage to affect the structure and function of the vascular wall. In animal experiments, pyridoxamine is noted to help reduce the formation of ALE and has therefore been suggested that it could help prevent (or slow) the formation of atherosclerosis, which would naturally assist in the avoidance of heart disease.

Further interesting animal experiments with pyridoxamine have shown improvement for kidney disorders, in particular helping to prevent the formation of kidney stones.