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Evolution and a longer life span

Evolution and a longer life span

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http://en.wikipedia.org/wiki/Telomere#Extending_telomeres

"A telomere is a region of highly repetitive DNA at the end of a linear chromosome that functions as a disposable buffer. Every time linear eukaryotic chromosomes are replicated during late S-phase, the DNA polymerase complex is incapable of replicating all the way to the end of the chromosome; if it were not for telomeres, this would quickly result in the loss of vital genetic information, which is needed to sustain a cell's activities. Every time a cell with linear genes divides, it will lose a small piece of one of its strands of DNA. This process has been referred to by James Watson and Alexei Olovnikov as the "end replication problem" (1971).

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Extending telomeres
The phenomenon of limited cellular division was first observed by Leonard Hayflick. Significant discoveries were made by the team led by Professor Elizabeth Blackburn at the University of California - San Francisco. In 1998, Geron Corporation developed techniques for extending telomeres, and demonstrated that this prevented cellular senescence.[citation needed]

Advocates of human life extension promote the idea of lengthening the telomeres in certain cells through temporary activation of telomerase (by drugs), or possibly permanently by gene therapy. They reason that this would extend human life. So far these ideas have not been proven in humans. In 2006, Geron corporation's web site indicated that it had at least two candidate drugs able to activate telomerase. [1]

However, it has been hypothesized that there is a tradeoff between cancerous tumor suppression and tissue repair capacity, and that by lengthening telomeres we might slow aging and in exchange increase vulnerability to cancer (Weinstein and Ciszek, 2002).

A study done with the nematode worm species Caenorhabditis elegans indicates that there is a correlation between lengthening telomeres and a longer lifespan. Two groups of worms were studied which differed in the amount of the protein HRP-1 their cells produced and, resulting in telomere lengthening in the mutant worms. The worms with the longer telomeres lived 24 days on average, about 20 percent longer than the normal worms. A side effect of the mutation was an increased resistance to the effects of heat exposure. The reasons for that effect are unclear. (Joeng et al., 2004).

Techniques to extend telomeres could be useful for tissue engineering, because they might permit healthy, noncancerous mammalian cells to be cultured in amounts large enough to be engineering materials for biomedical repairs.

However, there are several issues that still need to be cleared up. First, it is not even certain whether the relationship between telomeres and aging is causal. Although this is indeed probably so because changing telomere lengths are usually associated with changing speed of senescence, the relationship may well be the other way around, with telomere shortening a consequence of and not a reason for aging. That the role of telomeres is far from being understood is demonstrated by two recent studies on long-lived seabirds:

In 2003, scientists observed that the telomeres of Leach's Storm-petrel (Oceanodroma leucorhoa) seem to lengthen with chronological age, the first observed instance of such behaviour of telomeres[2]. In 2006, Juola et al. reported that in another, unrelated long-lived seabird species, the Great Frigatebird (Fregata minor), telomere length did decrease until at least c.40 years of age (i.e. probably over the entire lifespan), but the speed of decrease slowed down massively with increasing ages, and that rates of telomere length decrease varied strongly between individual birds. They concluded that in this species (and probably in frigatebirds and their relatives in general), telomere length could not be used to determine a bird's age sufficiently well. Thus, it seems that there is much more variation in the behavior of telomere length than initially believed, and more research into the topic is clearly warranted before any firm conclusions can be drawn or even practical applications tested.
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i wonder what the Iceman's telomeres look like?

hey, sonhouse, you got connections, can you score me some Geron juice?

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re lengthening lifespans in the 20th century due to better medical care, at what point in the past would people have reached greater average lifespans because they didn't move around so much, not spreading diseases that they didn't have vaccines for?

maybe methuselah really was 900 years old!

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http://en.wikipedia.org/wiki/Methuselah%27s_Children

"Methuselah's Children is a 1941 science fiction novel by Robert A. Heinlein, originally serialised in Astounding Science Fiction (July, August, September 1941). It was expanded into a full-length novel in 1958.

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Spoiler warning: Plot and/or ending details follow.
The Howard Families (the titular Methuselah's Children) are the product of a centuries-long eugenics scheme started in 1873 by a millionaire named Ira Howard, who found himself (presumably through a rare mutation) dying of old age in his forties. He therefore set up a trust fund to execute a long-term plan to selectively breed humans for longevity (thereby saving others from his fate). The plan encourages particularly long-lived people to produce children, by providing a large payment for any baby born to parents who each have four centenarian grandparents.

Several centuries later, a stable and peaceful world discovers the Howards, whose average life expectancy is now around 150.

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