22 thoughts on “Resetting The Clock”

  1. I first became aware of telomeres and their role from a science fiction book about Alpha Centauri going supernova (no, really!) (that howler was dealt with in the sequel, BTW).

    I’ve been hoping someone would make inroads on telomeres ever since. Making small stars explode, less so.

  2. Anyone read any good sf on the implications of age extension?

    Will we reach a curve where the increase is always more than our present age?

    Biblically, it was Satan that said, “you will not die.”

  3. Anyone read any good sf on the implications of age extension?

    The age extension part was secondary in the book I referred to (and aw crap, now I have to try to remember the name of it); in fact it was a side effect of the treatment being used experimentally against cancer.

    […]

    Okay, Wikipedia claims the first book was called Aftermath and the sequel Starfire, though I thought it was the other way around. Search Amazon for “Charles Sheffield” as the author of both books.

  4. Heinlein dabbles with it from several different directions.
    David Weber’s Honor Harrington books are primarily space/military/political, but there’s a variety of expensive ‘prolong’ procedures – stress between haves/havenots, refuseniks, genetic slavery, ‘what is human’, etc.
    Lois McMaster Bujold’s Miles Vorkosigan series is space/espionage/political. Genemods, ‘uterine replicator’, breeding programs, clones, several ‘culture clash’ aspects of above.
    Elizabeth Moon’s Herris Serrano/Esmay Suiza books space/military/political. The core of the political conflict is between ageists/rejuves.
    Elizabeth Moon’s Vatta’s War series is also space/military/political. A slice of the political conflict is about ‘humods’.

    Boiled down: Imagine being stuck with the unshiftable incumbents for more than a decade or two – but more like a century. Admirals-for-life, tycoon-for-life -> what in hell do the kids ‘inherit’ -> conflict.

  5. I find it difficult to believe that telomere shortening is the cause of aging. Telomere shortening is likely a bio-marker of aging, but not the cause. I think the cause is the build up of mutant mitochondria. Telomere shortening is how damaged cells shut themselves down in response to mitochondrial aging damage, or at least this is how I see it.

  6. The best SF with life extension in it is Peter F. Hamilton’s Commonwealth stories (Pandora’s Star, Judas Unchained). I really like these two novels.

  7. Imagine being stuck with the unshiftable incumbents for more than a decade or two – but more like a century. Admirals-for-life, tycoon-for-life -> what in hell do the kids ‘inherit’ -> conflict.

    Al, the solution is obvious – artificially select proles who simply won’t care about the Malthusian catastrophe. It would be the same as they’re doing now with regards to encroaching statism (i.e. import high-birth rate presumptively Democrat-voters, discourage libertarians from seeking increasingly socialized medical care, etc.)

  8. Relengthen teleomeres, and you will likely discover how short teleomeres have been suppressing cancer. 🙁

  9. So how is the mitochondrial DNA reset in the egg? Or does it not mutate seriously in the first place? (Eggs being created while still in the womb.) Still, the female body presumably has a way of mass producing relatively unmutated mitochondrial DNA.

    Cancer is generally less common among the youth, so presumably short teleomeres are not the only path to suppressing cancer. Also, our capacity to resist cancers is much greater now than it was many generations ago.

  10. Titus, that’s actually explored in the Honor Harrington series. David Weber’s view of statist society can only be described as “Mighty Dim.”

  11. “Relengthen teleomeres, and you will likely discover how short teleomeres have been suppressing cancer.”

    By that argument, one would think young people should be riddled with cancer. Short telomeres are more likely a response to oxidative damage. The six base telomeric repeat in humans is TTAGGG, and we know that guanine is the most easily oxidised of the bases. I speculate further that as telomeres shorten (for whatever reason) gene expression in the sub-telomeric region of the chromosome alters (the so-called TPE, or telomere position effect) and it is this changes expression, routinely seen in gene arrays, that produces much if not most of the changes in the cell that we associate with aging. I think it is suggestive that the p53 gene is in the sub-telomeric region of chromosome 17, which starts off with the shortest telomere in humans.

    If one could relengthen the telomeres before cell apoptosis checkpoints are triggered by DNA damage, then I would expect gene expression to again assume a more youthful phenotype.

    (And before anyone jumps on all this speculation, please note I did use the word: “speculate.” Plus I am only a simple minded rocket engineer, not a gerontologist. And yes, I do know that mice, who are cancer prone, have long telomeres. In their case, due to inbreeding, it is “too much of a good thing” where I think the mus telomere is less likely to be fully protected by Shelterin proteins, and thus more easily damaged. The damage is seen as double stranded breaks, and causes fusion to other chromosomes, leading to aneuploidy, and then to cancer.)

  12. By that argument, one would think young people should be riddled with cancer.

    No, because young people don’t have the progressive damage to their DNA that teleomere shortening helps compensate for.

    I do not expect there will be any simple fix for aging. If there were, evolution would already have found it.

  13. I do not expect there will be any simple fix for aging. If there were, evolution would already have found it.

    What is the evolutionary advantage of a long life?

  14. Paul – That turns out to be just plain wrong. A longer life means a greater proportion of available resources (which are always in short supply in primitive or natural conditions) being devoted to maintenance of your own body – which necessarily means less energy devoted to reproduction, and that reduces your likelihood of reproducing particularly in women.

    The reason why one doesn’t compensate for the other – at least not before the last 70 years or so – is that in primitive conditions infectious illness or injury are very likely to see you off before you get old.

    Women are the only mammals that go through menopause. This, and the anomalously long maximum lifespan of humans in general, may well be an adaptation that is “designed” to make it easier for people of reproductive age to get their offspring to adulthood. (Granny looks after the kids while you go out hunting or gathering.) A long lifespan also gives more of an opportunity for the young to learn from the experience of the old.

    But there are limits to this. Consider the extreme case; a human with a body so perfectly adapted that all cellular damage is repaired and because of that he is immortal until killed – and also because of that, there is no energy left for reproduction that he is sterile.

    What technology might just offer us is a way of avoiding the necessity of this tradeoff. And I hope it happens while it might do me, personally, some good.

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