Monday, August 21, 2006

An End To Old Age?

Taking a radical departure from the political topics that have dominated my blog recently, this post introduces a topic that I consider much more important. However, to a certain degree, this post builds on my previous post concerning President Dubya's misguided opposition to funding for embryonic stem cell research. To wit, can medical science find a cure for old age? If so, when? According to Dr. Michael Fossel of Michigan State University, old age may soon be as curable as polio, notwithstanding a lack of funding for embryonic stem cell research.

Since I was a small child in grade school, I was intrigued by the thought that the aging process was somehow genetically programmed into our DNA, and I anticipated a day when medical science could unravel the human genome and figure out a way to halt and/or reverse the aging process. And during my undergraduate studies in anthropology, I discovered the field of senescence, which (at the time) seemed to have an explanation for why aging occurs, but didn't yet seem to know how to halt or reverse the process. In sum, for reasons that were once quite mysterious, the specialized cells that constitute the vast majority of cells in the human body became post-mitotic, meaning that they could no longer replicate themselves to replace other specialized cells that had been damaged. This phenomenon was known as the Hayflick Limit, and it was contrasted by the relative immortality of stem cells and cancer cells.

While there is not yet a consensus as to why specialized cells become post-mitotic, one theory (championed by the aforementioned Dr. Fossel) is that this phenomenon is caused by the fact the telomeres in specialized cells get shorter every time one of these cells undergoes cellular mitosis and makes a copy of itself. These telomeres are at the end of DNA strands, but they don't carry any genetic information. Rather, telomeres function as aglets -- i.e., the tips of shoelaces - and protect the integrity of the genetic information contained within DNA strands; as telomeres shorten, gene expression is affected in various ways, and when the telomeres on DNA strands become too short to protect the integrity of said DNA strands, the process of cellular mitosis comes to a screeching halt.

Nobody actually dies of old age. Rather, as people get older, their cells become post-mitotic, and they can no longer heal the way that they could when they were younger. Consequently, older people can succumb to minor trauma and diseases that would be trivial to a younger person. Even a small paper cut can be fatal to a centenarian. However, if the telomeres on old cells could be lengthened, the process of cellular mitosis could presumbably resume, and people of advanced age could become young again and have an indefinite lifespan. Indeed, laboratory researchers have already succeeded in lengthening telomeres in DNA strands and rejuvenating old but otherwise healthy cells and tissue. Ironically enough, this was first accomplished by researchers attempting to shorten the length of telomeres in cancer cells, hoping to make those cancer cells self-destruct.

In the final analysis, the regulation of telomere length is probably the key to both health and longevity. Even if this sort of medical treatment becomes commonplace, people would probably still die from a wide variety of causes, but they would be much healthier overall and would no longer require the expensive medical care that elderly people typically require nowadays in their last decade of life. Meanwhile, new medical and social issues will start to emerge as people with access to telomere therapy start to live lives measured in centuries rather than decades even as old and unresolved medical and social issues such as birth control and genocide come into sharper focus.


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