An Opus for the Ages
In his new book, USC professor Caleb Finch covers the link between inflammation and the evolution of the human lifespan.By Athan Bezaitis
July 1, 2007
Ranked in the top half-percent of the world’s most cited scientists, University Professor Caleb Finch studies the genes that control aging in mammals.
In his latest book, The Biology of Human Longevity: Inflammation, Nutrition and Aging in the Evolution of Lifespans (Academic Press, 2007), Finch synthesizes 10 years of research on the biology of aging.
The 640-page opus is the follow-up to Longevity, Senescence and the Genome (University of Chicago Press), published in 1990, widely considered a landmark contribution to biomedicine and aging.
The Biology of Human Longevity incorporates findings from several disciplines, including gerontology, genomics, neuroscience, immunology and nutrition. Finch, the ARCO/William F. Kieschnick Chair in the Neurobiology of Aging, asserts that as humankind shifted from herbivore to a meat-rich diet, the gradual transition extended longevity by reducing levels of inflammation.
“Inflammation is a core feature in normal aging and in diseases such as atherosclerosis, Alzheimer’s disease, even cancer,” said Finch, who holds appointments in USC College’s biological sciences, anthropology and psychology departments as well as in the USC Davis School of Gerontology. “In the evolutionary past, the genes of inflammation also played a role in the evolution of humans as they developed longer life spans than their great ape ancestors.”
Inflammation, according to Finch, comes from two sources: chronic acute infections and the environment. Advances in hygiene, reductions in infectious diseases and medical treatments have greatly reduced chronic acute infections such as measles and gastrointestinal conditions.
In the last 200 years, one year of extra lifespan has been added for about every four years of historical time. Even more remarkable, life expectancy has doubled from roughly 40 to nearly 80 years since the industrial revolution.
However, environmental inflammation, caused by what people eat and breathe, could threaten this trend. Overpopulation, the spread of diseases through global travel, higher levels of dust from deforestation and what Finch calls the “obesity epidemic,” are all contributors to environmental inflammation.
“No state had more than 15 percent obesity 20 years ago,” Finch said. “Now every state has an obesity level of at least 15 percent.”
Being overweight, according to Finch, is a pro-inflammatory state in which fat tissues secrete inflammatory molecules called cytokines that contribute to chronic inflammation and conditions like heart disease and diabetes. With poor dietary habits and pollution on the rise, Finch predicts that increased levels of environmental inflammation could lead to shorter lives.
Other topics explored in the book are the effects of inflammation in the fetus on disease later in life and the role of inflammation in compounding free radical damage in cells, linked to a range of disorders that include cancer, arthritis, atherosclerosis, Alzheimer’s disease and diabetes.
Finally, a relationship between inflammation and diet might be a key to unlocking the full potential of human longevity, which Finch believes could increase considerably for those with the right resources such as funding and access to top-level medical resources.