Washington, Dec 3 (IANS) Chimpanzees and great apes have lifespans that barely exceed 50 years, in spite of their genetic similarity to humans. The difference is that humans evolved genes that enabled them to better adjust to levels of infection, inflammation and to the high cholesterol levels of their meat-rich diets.
Caleb Finch, gerontology professor at the University of Southern California (USC) says that a major contributor to longevity is human 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 (ApoE3), which also regulates inflammation and many aspects of ageing 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.

However, the minor allele apoE4, when expressed in humans, can impair neuronal (nerve cell) development, as well as shorten human lifespan by about four years and increase the risk of heart disease and Alzheimer’s disease manifold. (Minor allele is either of a pair of alternative forms of a gene).

ApoE4 carriers have higher totals of blood cholesterol, more oxidised blood lipids and early onset of coronary heart disease and Alzheimer’s disease, says a USC release.

“ApoE4 may be a prototype for other genes that enabled the huge changes in human lifespan, as well as brain size, despite our very unape-like meat-rich diets,” Finch said. “Drugs being developed to alter activities of apoE4 may also enhance the lifespan of apoE4 carriers.”

These findings were published in the December issue of PNAS Early Edition.