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The Quest for Immortality
Peter Murphy
Massachusetts Academy of Math and Science
Throughout the course of history, there have been stories of humans attempting to
evade death and of immortal beings. We have always had a fear of death and have
remained fascinated with the subject since Sumerian times. We think about living forever
and we contemplate escaping death. Alchemical elixirs, endless reincarnation, eternal
afterlives, and personified death serve as a small sample of our intrinsic desire to conquer
death.
Gilgamesh, a Sumerian king, lived during approximately 2700 B.C.E. Myths
about his adventures were written down circa 2000 B.C.E.(Hooker, 1996). The Epic of
Gilgamesh was one of the first written stories and, as a major theme, focused on
Gilgamesh’s attempt to become immortal by eating a magical flower.In China, there was
a different culture towards death. Many alchemists believed that substances such as jade,
gold, and mercury would increases the lifespan of those around them (Radcliffe, 2001).
Alchemy in China focused almost exclusively toward creating an elixir of immortality.
Today there is a far greater comprehension of the mechanism of aging. There are
a several factors for the aging of an organism. The combination of these factors, called
senescence, is the deterioration of a biological entity after development. Senescence can
be divided into the categories of cellular senescence, organismal senescence, chemical
damage, and extrinsic mortality.
Cellular senescence refers to normal cells that are unable to divide after
approximately fifty cell divisions in vitro. This occurs because some cells become
senescent as a result of toxins or reproductive errors that result in gaps in the DNA helix.
This phenomenon results in a limit to how many times embryonic cells are capable of
division and is called the Hayflick Limit, named after Dr. Leonard Hayflick. He wrote
about how cells age and self-destruct, the latter being known as apoptosis, when damage
to DNA occurs. A major contributing factor to the Hayflick Limit are telomeres, caps on
the end of DNA strands that become shorter during duplication (Telomere Info., 2007).
The cell death and inability to divide mentioned above frequently occur when cells have
short telomeres.
Organismal senescence is the increasing risk of age associated pathology,
inability to handle stress, and homeostatic imbalance. This results from cellular
senescence and physical trauma. This form of senescence relates to the aging of an
organism in its entirety and is equivalent to the damage caused by continued living, one
example being a gradual loss of hearing. The ultimate result from organismal senescence
is death.
Chemical damage relates metabolism to the damage of DNA and structural
proteins. A chemical process of normal cellular aspiration results in the conversion of
oxygen into toxic superoxide ions and other highly reactive compounds. These
compounds can pull elements out of bonds, disrupt cellular integrity, and potentially
cause cancer. Hence, as a result of oxygen and sugars in the body, damage can occur to
strands of DNA.
Extrinsic mortality describes how a member of any species is progressively more
likely to die as it ages. This form of mortality results from statistical probability of death
caused by accident, injury, or predation. Species that are not threatened by predators are
less likely to have extrinsic mortality as a high cause of death and typically have a longer
lifespan. Species with many predators, such as rabbits, are heavily influenced by extrinsic
mortality and may have evolved to increase propagation by emphasizing reproduction
rather than lifespan (Butler, Miller, Olshansky, & Perry, 2006).
Resulting from an increased understanding of the mechanism of aging, there are
now many theories of how to prevent, nullify, or counteract aging. Ideas such as cloning
and body part replacement, mentally uploading the human conscious onto computers, and
decreasing chemical damage by reducing calories to be burned, are all considered in the
quest to increase lifespan.
Recently, a potential approach to decreasing senescence, named Strategies for
Engineered Negligible Senescence (SENS), has developed potential factors that will
theoretically be necessary to slow or halt the effects of again (An Engineering Approach,
2008). The concept is akin to maintaining a system through engineered intervention.
There are three areas of research in SENS: metabolism, damage, and pathology. These
are treated with gerontology, which focuses on preventing damage, engineering, which
involves the manual repair of damage, and geriatrics, which serves to assist those already
suffering from effects of advanced senescence. The SENS project lists: cell loss,
senescent cells, protein cross-linking, extracellular build-up, non-degradable build-up,
mitochondrial mutations, and cancerous cells as the seven major contributing factors for
senescence and details methods to nullify these factors.
There are numerous ramifications of living in a world in which a sizable
population does not noticeably age. One of the most prominent would be the threat of
overpopulation. The decrease in mortality rates, coupled with anything less than a
decrease in child birth, would result in populations swelling. Another important point
would be the decrease in age related illness, such as Alzheimer’s disease or dementia.
Another drastic change would be retirement age; someone with an indefinite lifespan
would need to work indefinitely. Widespread delivery of senescence treatment would
result in a cultural paradigm shift in the way people view death and, as people would be
able to work for longer periods, likely lead to an increase in the rate of technological
development.
Literature Cited
An Engineering Approach to Curing Aging (2008). Retrieved December 10, 2008,
from http://www.mfoundation.org/index.php?pagename=sens_index
Butler, R., Miller, R., Olshansky, S., and Perry, D. (2006). In pursuit of the
Longevity Dividend, retrieved December 9, 2008, from
http://www.edmontonagingsymposium.com/files/eas/Longevity_Dividend.p
df
Hooker, R. (1996) Mesopotamia Gilgamesh. Retrieved December 11, 2008, from
http://www.wsu.edu/~dee/MESO/GILG.HTM
Radcliffe, J. (2001) Alchemy and Daoism. Retrieved December 10, 2008,
fromhttp://homepages.ihug.com.au/~panopus/jeannie/alchemy%20&%20d
aoism.html
Telomere Information Center (2007). Retrieved December 10, 2008, from
http://websites.afar.org/site/PageServer?pagename=IA_b_tel_home