Metabolically speaking, we're all on fire. Current thinking in the biology of aging suggests that the normal processes cells use to burn fuel, providing energy for life, indirectly lead to much of the disease and disability that characterize aging in humans and other animals. Chemically unstable by-products of cellular oxidation--especially free oxygen radicals--can initiate the deterioration of cell membranes and macromolecules. As small "hits" causing cellular injury accumulate, the results can range from uncorrected mutations and cancers to forms of tissue damage leading to vascular pathology and Alzheimer's disease.
Oxidative damage remains a central player in the drama Fitch unfolds, but now it shares the stage with several lesser-known, equally important accomplices: inflammation, damage during development, and the hazards of overnutrition.
Finch proposes that increases in brain size and the human life span over the past million years occurred in concert with changing nutritional priorities, slower developmental rates, and a tolerance for inflammation in "dirty, invasive, and stingy" prehistoric environments. The integration of more meat into the human diet, he argues, provided protein needed for larger brains but involved new physiological and genetic trade-offs between fitness and liability for long-term damage. This scenario provides a satisfying rationale for why variants of some genes for metabolizing animal fat that are linked to a human predilection for atherosclerosis, some cancers, and the amyloid plaques characteristic of Alzheimer's disease (such as those of the ApoE gene family) are not shared by our closest primate relatives.
Monday, March 03, 2008
The Fires of Aging
Donna Holmes offers an interesting review with the title of this post, of Caleb Finch's new book "The Biology of Human Longevity." Here are a few edited clips from that review: