bility that treatment with antioxidants might slow the development of AGEs is under investigation.

The issue of whether modifications observed in plasma and tissue proteins in patients with diabetes are due to an oxidative stress or a stress from reactive carbonyls has been discussed by Baynes and Thorpe (1999). A number of studies have tried altering the pathobiology of diabetes by treating patients with either single antioxidant-type compounds or combinations of compounds with antioxidant properties. The results have been inconclusive, which may reflect the fact that the underlying pathology is not caused exclusively by an oxidative stress, but by an inability to metabolize and inactivate reactive carbonyls appropriately. Under these circumstances, the oxidative damage may be exacerbated, resulting in an increase in many of the markers associated with oxidative stress but not caused directly by oxidative stress (Baynes and Thorpe, 1999).

Aging

Aging is not in itself a chronic disease, but rather is characterized by the active or passive presence of a chronic disease (cardiovascular disease, cancer, cataracts, Alzheimer's disease, etc.). It is not clear if an accumulation of chronic insults and weakened defenses renders the aging individual more susceptible to various diseases. Do antioxidants play a role in preventing aging or prolonging life? There is no direct evidence in humans for such an effect, although vitamin E supplementation appears to improve some immune responses in the elderly (Meydani et al., 1997). There have been suggestions that supplementing older animals with antioxidants may improve various physiological functions (Hagen et al., 1999), but the only experimental intervention that has resulted in prolongation of the life span of the animals has been the drastic reduction of food consumption (Pariza and Boutwell, 1987). Whether such a protocol would delay aging in humans has not yet been studied. Whether dietary antioxidants can lead to healthier aging remains to be proven.

CONCLUSIONS

There is little doubt that an imbalance in the production of free radicals and other reactive species and the natural protective systems available to organisms can lead to the production of oxidized products of lipids, nucleic acids, and proteins. These oxidation products, or biomarkers of this imbalance, may be related to early



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