Washington, Jan 27 (ANI): In a new study, researchers at the USC Davis School of Gerontology have found why humans outlive apes.
The genetic adaptation that increases human lifespan is also responsible for making us uniquely susceptible to diseases of aging such as cancer, heart disease and dementia, revealed the study.
Caleb Finch, ARCO and William F. Kieschnick Professor in the Neurobiology of Aging, compared the life spans of humans with other primates.
And they explained that slight differences in DNA sequencing in humans have enabled us to better respond to infection and inflammation- the leading cause of mortality in wild chimpanzees and in early human populations with limited access to modern medicine.
Specifically, humans have evolved what Finch calls "a meat-adaptive gene" that has increased the human lifespan by regulating the effects of meat-rich diets.
ApoE3 is unique to humans and is a variant of the cholesterol transporting gene, apolipoprotein E, which regulates inflammation and many aspects of aging in the brain and arteries.
"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," said Finch.
However, another expression of apolipoprotein E in humans -- the minor allele, apoE4 -- can increase the risk of heart disease and Alzheimer's disease by several-fold, explained Finch.
ApoE4 carriers have higher totals of blood cholesterol, more oxidized blood lipids and higher rates of early onset coronary heart disease and Alzheimer's disease.
"The chimpanzee apoE functions more like the "good" apoE3, which contributes to low levels of heart disease and Alzheimer's," Finch said.
Chimpanzees in captivity have unusually low levels of heart disease and Alzheimer-like changes during aging when compared to humans.
Finch hypothesizes that the expression of ApoE4 in humans could be the result of the "antagonistic pleiotropy theory" of aging, in which genes selected to fight diseases in early life have adverse affects in later life.
"ApoeE 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. Drugs being developed to alter activities of apoE4 may also enhance lifespan of apoE4 carriers," said Finch.
The study has been published in a special PNAS collection on "Evolution in Health and Medicine". (ANI)