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Carnosine (L-Carnosine)

Carnosine - Protection from Age Related Diseases
(Prevention of Glycation)

"...Because of its anti-glycation actions, carnosine may be useful in preventing and treating diabetic complications such as cataract, neuropathy, arteriosclerosis and kidney failure. It can also be helpful to all of us since AGES age us all, although not a rapidly as diabetics..."

Most recent research suggests that the most important action of carnosine is its anti-glycation effect (Aldini et al 2002a, 2002b, Yeargans and Seidler 2003).

Then what is this glycation?

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Let me try to explain it to you in a simple way.

Every second, a destructive process called glycation occurs throughout the body. Glycation can be described as the binding of a protein molecule to a glucose molecule resulting in the formation of damaged, nonfunctioning structures. Glycation alters protein structure and decreases biological activity. Glycated proteins, which accumulate in affected tissue, are reliable markers of disease. Many age-related diseases such as arterial stiffening, cataract and neurological impairment are at least partially attributable to glycation.

Carnosine, which prevents glycation, may also play a role in the disposal of glycated protein. Carnosinylation (the process where carnosine combines with denaturated molecules) tags glycated proteins for cell removal.

Glycation, also known in biochemistry as the Maillard reaction, occurring between proteins and glucose, is recognized as a major contributor to aging and perhaps cancer, as well as the complications arising from diabetes. Glucose provides the fuel for glycation, the insidious protein/glucose combination that (following several steps including the oxidation process) results in the formation of an advanced glycation end product or AGEs.

Once AGEs are formed, they interact with neighboring proteins to produce pathological cross linkages that toughen tissues. It has been speculated that no other molecule has the potential toxic effects on proteins as advanced glycation end products. Diabetic individuals form excessive amounts of Ages earlier in life than non-diabetics, a process that disrupts the normality of organs that depend on flexibility for function. It has been shown that it is glycation hardens the arteries of a diabetic individual.

Ages trigger a cascade of destructive events as Ages cling to cellular binding sites. One of the consequences of Ages is a 50-fold increase in free radical formation. As diabetes, a condition of accelerated aging, spawns a harvest of Ages, the arteries, the lens and the retina of the eye, peripheral nerves and the kidneys are under specific attack. By opposing glycation, glomerular damage and the resulting inflammation and renal degeneration is reduced. Diabetic rats, not treated with glycation inhibitors, show a twofold increase in glomerular staining for advanced-glycation end products compared with a similar group of diabetic rats receiving treatment (Forbes et al., 2001).

Cataracts (another complication common to diabetics) are also likely to form as a result of glycation, while glycation inhibitors, like carnosine and calcium pyruvate protect against the damage. Supplementation with glycation inhibitors enable humans to prevent many of the adversities that accompany aging. Because carnosine structurally resembles the sites that glycating agents attack, it appears to sacrifice itself to spare the target. Carnosine also bolsters proteolytic pathways, i.e., the disposal of damaged and unneeded proteins.

Because of its anti-glycation actions, carnosine may be useful in preventing and treating diabetic complications such as cataract, neuropathy, arteriosclerosis and kidney failure. It can also be helpful to all of us since Ages age us all, although not a rapidly as diabetics.

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