Early theories of evolution, by Darwin, considered apes to be our ancestors. Scientifically, it has been proven that apes, chimpanzees and humans have genetic correspondence. However, apes have relatively shorter life span than human. They seldom bypass 50 years of age despite the close similarities. So the question is why?
According Professor Caleb Finch, USC David School of Gerontology, human’s genes have evolved, in a direction that permits better adaptation and adjustment to inflammation and infection as well as high level of meat and cholesterol intake. The rich composition of diets has eventually positively altered our DNA sequencing, whereby human beings have become more vulnerable to disease of aging such as heart disease, cancer and dementia in contrast to our counterparts.
The change in DNA sequencing increasing our genes’ ability to cope with inflammation is the reason for our longer lifespan than apes, according to Finch, the ARCO & William F. Kieschnick Professor in the Neurobiology of Aging and a distinguished University Professor.
Constantly consuming raw meat affected by parasites prior to cooking fuels infection and inflammation, which according to Finch, is the reason for typical diseases.
The significant difference in the diet between humans and primates is that the former have developed a distinct cholesterol transporting gene called apolipoprotein E. ApoE3 is according to Finch a “meat-adaptive gene” that accounts for the longevity of human in contrast to apes and primate. Moreover, ApoE3 is also responsible for the control of inflammation and aging (aging of arteries and brain).
Moreover, the allele; apoE4, can eventually cause severe damage to the development of neurons. This can reduce human lifespan by as much as four years by augmenting the potential risk of diseases such as stroke and Alzheimer. The composition of apoE4 consists of more blood cholesterol, oxidized blood lipids which causes Alzheimer and heart disease.
On the other hand, chimpanzees are less prone to Alzheimer and Heart disease. They have more of the apoE, the good allele apoE3. Empirically, chimpanzees kept in captivity experience a tremendously low rate of heart or Alzheimer disease while aging.
The conclusion drawn by Finch was that apoE4 which is positive in early life is hostile to aging. The gene counter-attacks diseases in youth and turns out to act antagonistically as the body grows older.
It the apoE can prove to have significant contribution in determining life span. It might even have an effect on our brain size and capabilities. Despite our rich meat diet, drugs that improve the function of apoE4 might prolong life span by alleviating shortcomings that apoE4 has at late life. The National Institution on Aging as well as Ellison Medical Foundation support the fact that finding about apoE4 accounts for significant advancement in the field of gerontology and longevity.
Reference:
http://www.sciencedaily.com/releases/2009/12/091202153802.htm
Wed, Dec 9, 2009
Bioscience, Gerontology, Health And Aging, Longevity