Our cells need oxygen to create energy to function. However, as we process oxygen, we also produce toxic molecules, called free radicals, along the way. These can damage DNA, proteins, and mitochondria, the so-called "powerhouses" of cells.

Free radicals (and the oxidative damage they cause) are believed to be major factors in much of the cellular and tissue deterioration that occurs with aging. For example, skeletal muscle loses bulk and strength as we and other mammals age. The mitochondria in skeletal muscle cells show greater amounts of oxidative damage as animals age²⁷, and it is speculated that the increased oxidative damage is responsible at the level of the cell for the loss of function at the level of the muscle.^28,29

And just as there are negative consequences from natural oxygen metabolism, there are similar problems as we process needed sugars. When excess sugars react with some proteins and nucleic acids, the sugars can cause irreversible changes to these genetic building blocks. Research has shown that such "glycated" compounds increase with age and also may be responsible for age-related deterioration of cellular structure and function.

Caloric restriction is believed to slow aging in animals at least in part by retarding oxidative and glycation damage. In one study, researchers compared mice placed on a calorie-restricted diet with mice fed at will. They studied the mice's skeletal muscle mitochondria throughout the their lives and into (mouse) old age, up to 30 months. The free feeding mice showed marked evidence of oxidative damage, while the calorie restricted mice had very little³⁰. The studies are consistent with the notion that mitochondrial oxidative damage is a consequence of aging and that caloric restriction's effect on increasing longevity may be due in part to reducing that oxidative damage.

Studies are beginning in primates to examine the effect of oxidative damage in their mitochondria³¹.