User:Tgdetto345/sandbox

References

Posted in the Sarcopenia Talk Page.

Evolutionary Considerations[edit]

I am a student at Case Western Reserve University interested in the evolutionary considerations of sarcopenia and muscle loss. The following is a sample of what I plan on adding to the article under the subtitle "Evolutionary Considerations." "Myostatin is a substance that the body produces in order to keep muscles from getting too large. Myostatin inhibitors will result in the success of muscle growth and may soon be used as a way to help people with muscle-wasting diseases. The two roles of myostatin are in embryo to limit formation of muscle fibers, and later in life to limit the growth of the muscle . There are a few hypotheses relating to why myostatin is genetically inherent." Furthermore, I will discuss the two opposing hypotheses on muscle-wasting as related to the proximate cause of myostatin in an ultimate, evolutionary, context. Tgdetto345 (talk) 18:18, 5 November 2013 (UTC)

Evolutionary Considerations addition to Sarcopenia Page. Aging may seem to be a mystery.Senescence, the bodily process of deterioration that occurs as age increases, can be found in many species. Senescence decreases (biology)Fitness (biology) more than all other forces of selection combined. The theory that Natural selection has not yet had the opportunity to eliminate the Genes linked to senescence is challenged by the idea that the forces of natural selection become weaker as age increases. [7] Proximate causes of muscle wasting is Oxidative stress. These reactive molecules damage any tissue which comes in contact with them. The body has developed defenses, Superoxide dismutase, which neutralizes free radicals before the damage is done. Nature seems to fix this problem by synthesizing SOD, because muscle wasting is proximately related to abnormal levels of SOD[8] . This is two-sided argument in that damage by free radicals is a proximate cause of sarcopenia, but alternatively, it is a demonstration on how natural selection works to adjust defenses. [7] There are medical implications in that the mechanism of muscle wasting may be a trade-off equalized by natural selection. The genes involved often contain a vital function. These genes do not become deleterious until after reproductive age, thus making them not a focus of natural selection. Continued research in senescence and muscle wasting diseases is hopeful that prevention or postponing disease will allow the aging process to be comfortable and offer a higher quality of life to the end. [7]