Prompt #3 3/23/13 The Effects of Aging on the Individual,
and the Human Species
Dr. Moalem introduces aging and the idea of planned biogenic
obsolescence in Chapter 8. Perhaps
humans were programmed to die in order to make way for new models, creating
room for change (Big Idea #1-evolution), and protecting the group by
eliminating individuals who are disease ridden (p. 191). He discuses the rare
and quite tragic disease called Hutchinson-Gilford progeria syndrome, which
causes premature, accelerated aging in humans. This aging starts right after birth and someone suffering
from this genetic disorder usually does not live past the age of 30. Researchers discovered that the gene
that caused this disorder produces a protein called lamin A. People with this disorder do not
produce functional lamin A, and as a result, their cells deteriorate at an
accelerated pace. Furthermore, lamin A deteriorating was linked to normal human
aging. (p. 183-184) Later on, Dr. Moalem discusses studies that scientists are
exploring to slow the aging process and reverse the cellular damage caused by
progeria. Although the scientists
haven’t been able to reverse progeria in humans yet, we can be assured that
they are working towards this and towards other ways to reverse or slow the
normal aging process (p. 192).
Questions: With all this new research going into preventing
or slowing down aging in humans, how does it affect the individual? The
species? Might slowed aging in humans actually hurt the evolutionary process by
not making room for “new and improved” models?
Rachel Chang (rchang4@students.d125.org)
Our bodies possess many complex properties and every property is there for a reason. Whether its getting a fever to get rid of an infection or shivering to warm our bodies, these properties are all necessary. This is important because we have to understand that our bodies age and become less and less capable of certain functions as we grow older. This is all normal. Now, through the process of natural selection, the environment always seeks to weed out those who are incapable of surviving and reproducing with those who can outperform and outlast. So, it would make sense that to live longer is something that is beneficial. This increases our chances of reproducing and passing our genes on to our offspring. On the contrary, our bodies are genetically wired to die. As we've learned in Chapter 16 of the textbook and as Dr. Moalem explains on pages 185-186, our cells can only divide X number of times before they stop functioning. Every time a cell divides, the daughter chromosomes end up with shorter and shorter ends. This happens because when a RNA primer is removed from a replicating DNA strand, it leaves a 5' end open and is unable to be filled due to the absence of a 3' end for DNA polymerase to attach nucleotides to. Sooner or later cells reach what is called the Hayflick limit. This happens when our telomeres, which are located at the end of our chromosomes, run out. Telomeres are non coding regions of DNA attached to the ends of DNA strands to combat this loss of nucleotides after each cell division.
ReplyDeleteGoing back to our bodies having specific functions for a reason, we can look at the addition of telomeres to the end of chromosomes as our body's adaptation to live as long as it can. This relates to Big Idea 3. These telomeres allow us to live longer and to age slowly.
In the article "Geneticists claim ageing breakthrough but immortality will have to wait" by Ian Sample, Sample investigates how ageing can be slowed in humans. Scientists have successfully slowed the ageing process in mice and single celled organisms by isolating the Sir2 and SCH9 gene. Sample states that, "By blocking the gene [Sir2], the cells were essentially tricked into believing food was scarce and switched them into a survival mode." Dr. Longo explains that this decreases ageing because the cells are programmed differently causing the cells to believe that they need to live longer in order to reproduce; just not now because the cells do not have the necessary resources. While the tests were successful in mice, some issues were noticed such as infertility and muscular defects. This meant that the Sir2 gene is necessary for normal development.
Seeing that these problems occurred in an ageing breakthrough, this type of anti-ageing proved to be ineffective. Therefore, not only would this cause humans to live longer, but it would cause a myriad of problems and in the end reducing their chances of surviving and reproducing. Overall a species would experience a large drop in the population since reproduction is impossible. Anti-aging can hurt the evolutionary process greatly by not allowing our bodies to normally develop and it could stop the evolutionary process entirely.
Although, drugs are currently being created to slow the ageing process. The article "Anti-aging drug breakthrough" from Science Daily examines multiple drugs that can act on an enzyme, SIRT1, which can cause our bodies to work more efficiently. SIRT1 was shown to increase the physical ability in mice, allowing them to run farther and live 15 percent longer. This is looking promising but its full effects are unknown. Until wide range testing for other anti ageing techniques are completed, we will have to watch our own habits and maintain our health to live as long as we can.
(Sources: http://www.sciencedaily.com/releases/2013/03/130308111312.htm, http://www.guardian.co.uk/uk/2005/nov/18/genetics.science)
(Ted Nowak tnowak4@students.d125.org)
The process of aging is a natural mechanism that helps facilitate evolution. As cells divide, the ends of their chromosomes called telomeres become shorter. Eventually cells will reach a Hayflick limit, the point at which their telomeres become too short and the cells can no longer reproduce. Once an organisms cells can no longer divide and reproduce, the organism will slowly deteriorate, unable to repair itself. Scientists are currently examining stem cells, as these cells are unable to reach the Hayflick limit. Since stem cells have the ability to make any cell and continually divide, there are many potential medical applications for these cells.
ReplyDeleteTed researched the anti-aging drugs that are currently being developed. These drugs act on the enzyme SIRT1, which has many potentially anti-aging applications. I researched how these drugs affect the SIRT1 enzyme. A ScienceDaily article found that Hydrogen Sulfide can activate the SIRT1 enzyme, as well as upregulating (increasing the sensitivity of) the gene klotho (2013). Klotho has been linked to the slowing down of aging and an extended lifespan. Hydrogen sulfide has also been linked to possibly slowing down cancer and neurological disorders such as Parkinson's and Alzheimer's.
While these anti-aging medications are certainly promising, they pose a potential threat to the gene pool of humans. By allowing humans to live longer, we are artificially selecting those with money for these medical treatments rather than those with "better" genes. Instead of allowing natural selection to potentially eliminate these diseases, we may instead pass them down to future generations if we also allow these people to reproduce at a later age. Furthermore, the logistics of "living forever" should be carefully thought about. With millions of people in the world already suffering from malnutrition and lack of resources, we should be more concerned about the overpopulation of Earth and it's potentially catastrophic effects on the environmental. Allowing humans to live longer will further increase the birth:death ratio, making this problem even worse.