Human genes have adapted to inflammation, but we are more susceptible to diseases of aging
In spite of their genetic similarity to humans, chimpanzees and great apes have maximum lifespans that rarely exceed 50 years. The difference, explains USC Davis School of Gerontology Professor Caleb Finch, is that as humans evolved genes that enabled them to better adjust to levels of infection and inflammation and to the high cholesterol levels of their meat rich diets.
In the December issue of PNAS Early Edition, Finch reveals that these evolutionary genetic advantages, caused by slight differences in DNA sequencing and improvements in diet, make humans uniquely susceptible to diseases of aging such as cancer, heart disease and dementia when compared to other primates.
Finch, the ARCO & William F. Kieschnick Professor in the Neurobiology of Aging and a distinguished University Professor, argues that a major contributor to longevity for humans is the genes that adapt to higher exposure to inflammation.
"Over time, ingestion of red meat, particularly raw meat infected with parasites in the era before cooking, stimulates chronic inflammation that leads to some of the common diseases of aging," Finch said.
In addition to differences in diets between species of primates, humans evolved unique variants in a cholesterol transporting gene, apolipoprotein E, which also regulates inflammation and many aspects of aging in the brain and arteries.
ApoE3 is unique to humans and may be what Finch calls "a meat-adaptive gene" that has increased the human lifespan.