The same evolutionary genetic advantages that have helped increase human lifespans also make humans susceptible to diseases of aging such as cancer, heart disease and dementia says a study published in a special Proceedings of the National Academy of Sciences collection on "Evolution in Health and Medicine". Comparing the life spans of humans with other primates, Caleb Finch, ARCO & William F. Kieschnick Professor in the Neurobiology of Aging in the USC Davis School of Gerontology, explains 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.
The same evolutionary genetic advantages that have helped increase human lifespans also make humans susceptible to diseases of aging such as cancer, heart disease and dementia says a study published in a special Proceedings of the National Academy of Sciences collection on "Evolution in Health and Medicine".
Comparing the life spans of humans with other primates, Caleb Finch, ARCO & William F. Kieschnick Professor in the Neurobiology of Aging in the USC Davis School of Gerontology, explains 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.
This is not the only variable that may affect lifespan. The Galapagos tortoise or Galapagos giant tortoise is the largest living tortoise and have lived as old as 175 years as well as the giant Redwood tree that have been reported to be as old as 2000 years.
!ADVERTISEMENT!Humans, of course, live an average of about 75 years though it varies depending on local environmental and nutritional conditions. As compared to other primates such as chimpanzees and gorillas, humans are quite long lived.
In spite of their genetic similarity to humans, chimpanzees and great apes have maximum lifespans that rarely exceed 50 years. Even in higher mortality modern hunter forager lifestyles, human life expectancy at birth is still twice that of wild chimpanzees.
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. This gene appears to be 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," Finch said.
However, another variation of the same gene in humans can increase the risk of heart disease and Alzheimer's disease by several fold, Finch further explained. Such 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 in captivity, in comparison, have unusually low levels of heart disease and Alzheimer like changes during aging when compared to humans.
Finch hypothesizes that this is "antagonistic pleiotropy theory" in action. Antagonistic pleiotropy refers to the action results of a gene ending in multiple competing effects, some beneficial but others detrimental to the organism.
One such example in male humans is the gene for the hormone testosterone. In youth, testosterone has positive effects including reproductive fitness but, later in life, there are negative effects such as increased susceptibility to prostate cancer. Another example is the p53 gene which suppresses cancer, but also suppresses stem cells which replenish worn out tissue.
Unraveling how long we can live will be a complex undertaking with some factors that may prove to be potentially counterproductive.
For further information: http://www.eurekalert.org/pub_releases/2010-01/uosc-who012510.php
