When people have diabetes, their organs and tissues mimic those of much older individuals, meaning the disease appears to cause the body to age at an accelerated pace. Why should high blood sugar damage skin, nerves, eyes, joints and arteries?
Part of the answer appears to lie in glucose’s propensity, as it floats around in your bloodstream, to attach itself to proteins. That attachment is called glycation (or glycosylation). Scientists at Rockefeller University and other research centers have demonstrated that the process leads to irreversible cross-links between adjacent protein molecules. Cross-linking significantly contributes to the stiffening and loss of elasticity found in aging tissues.
If you want to know whether your blood sugar is generally elevated, ask your doctor to order a Hemoglobin A1c (glycosylated hemoglobin) laboratory blood test for you. It measures your blood glucose control over the last two to three months.
Anthony Cerami, M.D., the pioneer in this field, gave the new protein structures formed from this chemical collision an appropriate name: advanced glycosylation end-products, or AGEs1. Collagen, the flexible connective tissue that holds your skeleton together, is one of the first proteins to be affected. As collagen’s flexibility is destroyed, your skin sags and your organs stiffen. Your arteries also take a major hit, which explains in part the connection between diabetes and heart disease. AGEs attach themselves to LDL, or ”bad” cholesterol, and these LDL molecules then become more oxidated, causing severe damage to any arterial surface to which they become attached2.
AGEs are truly a main contributor to aging, so keep your blood sugar within the normal range so those glycating sugar molecules don’t gain a foothold on your body. High levels of blood sugar can also be present in pre-diabetes and in the metabolic syndrome.
Selected References
1. Cerami, A., Vlassara, H., Brownlee, M., “Hypothesis: Glucose as a Mediator of Aging,” Journal of the American Geriatric Society, 33(9), 1985, pages 626-634.
2. Lyons, T.J., “Glycation and Oxidation: A Role in the Pathogenesis of Atherosclerosis,” American Journal of Cardiology, 71(6), 1993, pages 26B-31B.
