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Science

Age A Byproduct of Cancer Defense? 298

Posted by Hemos from the vectors-of-prevention dept.
A reader writes "The International Herald Tribune has an article which says, in brief: they have discovered that aging in mice seems to be a byproduct of the chemicals that prevent cancer" If true, that's quite a double edged sword - avoid death, to cause it later.
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Age A Byproduct of Cancer Defense? More

Age A Byproduct of Cancer Defense?

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  • wording (Score:1, Interesting)

    by torqer ( 538711 )
    From the post:

    If true, that's quite a double edged sword - avoid death, to cause it later.

    Shouldn't that be to cause it sooner?

    • Re:wording (Score:2, Insightful)

      by Decimal ( 154606 )
      From the post:

      > If true, that's quite a double edged sword - avoid death, to cause it later.

      Shouldn't that be to cause it sooner?

      No, the poster was right. Cancer will kill you faster than old age*. So even though aging also kills you, growing old allows you to live longer. Quite preferable to the alternative, if you ask me.

      * Assuming you don't get it when you are old. If you get cancer at the age of 95, you're pretty much screwed no matter what.

  • There goes one industry down the toilet! (Score:5, Funny)

    by pgrote ( 68235 ) on Thursday January 03, 2002 @06:44PM (#2781793) Homepage
    Man o man are these guys in for a surprise:

    http://www.google.com/search?q=anti-aging+pills

    Especially these folks:

    http://www.pure-milk-calcium.com/immunocal.htm

    This product is supposed to prevent cancer by extending your life :-)

  • Makes sense (Score:3, Insightful)

    by corporatemutantninja ( 533295 ) on Thursday January 03, 2002 @06:49PM (#2781833)
    In the environment where we did most of our evolving very few people lived to "old age" before succumbing to a number of other dangers, so something that kept cancer at bay for a while at the price of guaranteeing death after a few decades probably seemed like a good deal. Kind of like the 640k limit. "That ought to be enough for everybody."
  • I wish these scientists would figure this stuff out about human beings instead of mice. I guess Douglas Adams was right in the HHGTTG, the mice are running the show here on Earth. That's why they get the most scientific interest -- of course all of this scientific investigation is the way mice get to observe us.

    "Nuts to your white mice" -- Zaphod Beeblebrox

  • Aging and Cancer (Score:3, Interesting)

    by Renraku ( 518261 ) on Thursday January 03, 2002 @06:50PM (#2781839) Homepage
    Chemicals that prevent or help prevent cancer usually tamper with cell division. If cellular division is in some way interrupted or affected by anti-cancer agents, then aging more than normal can easily occur. It goes back to one's preference. Long, suffering life or short, fulfilled life?

    • Re:Aging and Cancer (Score:2, Interesting)

      by Wire Tap ( 61370 )
      Almost reminds me of two different stories:

      1) Blade Runner (the movie, I never read the book)

      As the androids were limited to a fantastic life of being capable of much more than most ordinary humans were, but only had 4 years to live.

      2) Ender's Shadow

      Ender was doomed to expereicnce exponential growth and a life span of only 20 or so years, but before that his life would be full as he could make it. He had talents: a perfect memory, a dedicated spirit, etc... He was perfect, except for his genes.

      I suppose it is becoming a valid tradeoff now, although I hope researchers can find a way around that scary double-edged sword. It would be a shame to be able to only choose one.
    • That's what I thought too, but the stuff was highly active in the womb when a baby is growing fastest, which seems to indicate that it dosen't directly slow cell replication. Or at least, not all cells.

  • Wow (Score:5, Interesting)

    by TheGreenLantern ( 537864 ) <thegreenlntrn@yahoo.com> on Thursday January 03, 2002 @06:51PM (#2781851) Homepage Journal
    This sort of puts a whole new spin on this whole "Cure for Cancer" thing. The study seems to suggest that cancer is inevitable, and any attempts by our body to avoid it result in our own death.

    Seems to me that if this is the case, it would have some serious repurcussions on how we currently understand how our bodies work. What is it about our physiologies that makes cancer such an irresitible force?

    • Re:Wow (Score:5, Funny)

      by Tackhead ( 54550 ) on Thursday January 03, 2002 @07:14PM (#2782041)
      > This sort of puts a whole new spin on this whole "Cure for Cancer" thing. The study seems to suggest that cancer is inevitable, and any attempts by our body to avoid it result in our own death.

      Well, of course it should. These scientists are in contravention of the GMCA - Genetic Modification Copyright Act.

      God licenses His creatures to operate a DNA-replication machine for a certain number of years, depending on the sort of DNA involved. Mayfly licenses are good for a day or two. Giant redwood licenses have expiry dates measured in millennia.

      This is merely the DNACCA (DNA Copyright Control Association) invoking "self-help" on behalf of its client (JHVH-1, a.k.a. "God") whenever a licensee reverse-engineers its DNA with the intent of circumventing the digital rights management technology supplied with each organism.

      (Just great, now we're gonna have to put up with 1000 years of Jack Valenti and Hilary Rosen and Michael Eisner saying they're not about making money, they're only doing God's work on a human scale...)

    • Yeah, wow on my end, too. It makes me think that if we find the cure for cancer, we find the key to immorality.

      That's a scary thought. Are we ready for immorality? (Are we ready for cloning?)

      • Re:Wow (Score:5, Funny)

        by Daniel Dvorkin ( 106857 ) on Thursday January 03, 2002 @07:32PM (#2782163) Homepage Journal
        We've been doing immorality for quite a while now. I'd say we're not only ready for it, we're very good at it.

        Immortality, now, that's another question ...

      • Re:Wow (Score:2, Informative)

        by mgv ( 198488 )
        It makes me think that if we find the cure for cancer, we find the key to immorality.

        Its not that simple I think. (From memory I think I posted about this alot 2-3 months ago on /.)

        You can rest assured that there are many ways to die other than cancer however. These include accidents and trauma (mean time to death many hundred years), infections (major cause of death before antibiotics), vascular disease (still the leading killer), alzheimers (a good 10-15% of those who live long enough), respiratory failure (we get about 150 years worth of lung function at birth, accelerated decline with smoking etc). Not to mention non lethal problems such as cataracts and lens failure (age related long sightedness - presbyopia), macular degeneration - and these things only send you blind.

        Not that I would want to stop you hoping. I'm hoping too. Its just that I am starting to get a feel for how complex the whole problem is - our entire bodies were selected to get us to old age, which was probably mid 50's back when average life expectancy was in the mid 20's. And precious little lasts alot longer than that.

        I do believe that most of these problems are technical in nature, however, and there is hope in that.

        Michael

    • Re:Wow (Score:3, Informative)

      by Otter ( 3800 )
      This sort of puts a whole new spin on this whole "Cure for Cancer" thing. The study seems to suggest that cancer is inevitable, and any attempts by our body to avoid it result in our own death.

      You have it backwards -- controlling runaway growth is vital, and our bodies have it at the cost of aging and senescence. Attempts to halt or reverse aging would likely result in runaway cancer.

      What's new here, by the way, is the effect of p53. The tradeoff between aging and cancer has been clear for a while and suspected for decades -- Hemos reported on a project that supposedly beat the problem [slashdot.org] back in 1998.

    • How Cancer Works (was Re:Wow) (Score:2, Insightful)

      by Anonymous Coward
      Cells are dividing into more cells in our body at every given moment (e.g., skin sloughs off and more is "remade"). For a cell to divide, it's DNA must be replicated (i.e., copied). The molecular mechanisms that replicate DNA are very precise, but not perfect, even with the so called "error-correcting enzymes". This leads to maybe 1 error every 100,000 base pair copied.

      Don't worry, most mistakes, or mutations, are trivial, or if dangerous, will cause that cell to die or be unable to reproduce, so that mutation never gets passed on. But because so much DNA replication is going on in the body, somewhere, somehow, a mistake will lead to a mutant cell that has a slight advantage. This new cell might be able to divide fast, or resist molecules that check for fast dividers, or be able to live without being next to similar cells.

      In fact, many cancers seem to require a few distinct mutations before it can grow fast, split off, swim around in the bloodstream and still live, and finally be able to live off of whatever new cells it attaches to -- this endstage is called metastasized cancer, cancer that has traveled to the rest of the body.

      So the reason why we get cancers is almost because of Darwinan selection in the body: eventually, the most fit mutations will be able to survive and grow irregardles of how our normal body wants to function, and thus that cancer overtakes and drains our body's normal resources.

      So it actually makes sense that the longer you live, the more likely you will die of cancer, even without this new discovery of a potential mechanism. In fact, for adults over 55 years of age, the most common cause of death is cancer (even greater than heart disease, which is second). There is a subset of cancers known as "childhood cancers" that affect children, usually because of a genetic defect at birth that dooms them early. For "genetically normal" people, it is the stochastic process of accumulated mutations that, almost inevitably, resolves in cancer. In other words, everyone will get cancer if they lived long enough to get it.

    • Re:Wow (Score:2)

      by krmt ( 91422 )
      Ok, the whole "cure for cancer" deal isn't really what people are working for. What we're doing is looking to treat cancer, rather than cure it. First thing to note is that there's a whole lot more money in treatments than cures for any affliction, so many people will naturally look there first.

      The major point though is that it's a hell of a lot easier to treat something than to cure it. Take the flu for example. We can sink millions of dollars in to antiviral drugs to get rid of the sickness, or we can give you some antihistamines to treat the symptoms and let your body handle the work. It's a whole lot easier on everyone this way.

      The same sort of idea goes for cancer. Treating cancer by slowing its growth is the target of many researchers doing things like antiangiogenesis. The tumor itself isn't deadly (hence, benign tumors), it's the fact that it replicates like mad, spreads throughout your body, and eventually destroys so much of your tissue that you can't handle it. If you can treat the cancer by stopping it's spread, you'll have a much better method of saving lives. As many have mentioned, cancers have to route around mechanisms in place to stop a cell from dividing, but you can't very well stop all the cells in your body from dividing, you'd die within the week.

      As for cancer as irresistible force, I think it's a very interesting question when you start to dig in to it. Cancer is the ultimate in unregulated positive feedback, and I think its prevelance as a disease is demonstrative of the need for massive amounts of positive feedback in out bodies that are necessary for life. I think that if cells didn't have a natural tendency to keep dividing, and had to constantly be told to grow, that it would put a large damper on cell division, and thus evolution. Look at bacteria, which divide like crazy whenever there's enough food present. Because they do this, the can evolve defenses against drugs by the sheer weight of their numbers (note that this is a real problem, and is likely the next big one we face in terms of disease). While this doesn't directly affect humans in quite the same way, our own multicellular complexity may be a result of it. I think the natural tendency of our cells to divide allows for the greater benefits of growth and evolution that outweigh the negative possibility of cancer.

  • Evolutionary balance? (Score:5, Insightful)

    by pdqlamb ( 10952 ) on Thursday January 03, 2002 @06:52PM (#2781860)
    "Too much p53 and you get this aging effect. Too little and you get cancer. My guess is that evolution has evolved just the right level."

    Would somebody explain to me how evolution would play in this finely-tuned scenario? In the U.S. our average lifespan is over 70 years, yet most women pass menopause around age 45. There's a 25 year lifespan discrepancy, in which evolution has no effect, because the population (at least of women) can't reproduce!

    • Think of the children (Score:4, Informative)

      by mblase ( 200735 ) on Thursday January 03, 2002 @06:56PM (#2781912)
      The average lifespan is only that long thanks to modern advances in medicine, disease cures, etc. Without them, the average human could expect to live maybe 50 years, although menopause might also come a little earlier.

      But you can't think of those years as being wasted. After all, if a woman has children as late as 40, she'd certainly like to raise them to adulthood (and then help them learn to raise their own children) before she dies.

      • Re:Think of the children (Score:5, Informative)

        by geekoid ( 135745 ) <dadinportlandNO@SPAMyahoo.com> on Thursday January 03, 2002 @07:28PM (#2782134) Homepage Journal
        wrong.
        The "average" life span is increasing do to the lowering of the infant mortality rate.
        if took the aerage life span of anybodoy who at least lived until they where 5, would would findg that the average age has increased slightly.

        • Re:Think of the children (Score:5, Insightful)

          by MarcoAtWork ( 28889 ) on Thursday January 03, 2002 @07:55PM (#2782299)
          Do you have any links/info that corroborate your assertion?

          A *lot* of people I know would have died much earlier than they did (or they aren't dead yet, me included) due to illnesses they contracted after age 5...

          Considering all of the people older than 5 going in hospitals for heart surgery, appendicectomies, assorted cancer removals etc. that go on living for decades afterwards (rather than dying), I find it counter intuitive that a lower infant mortality is the only reason why the average lifespan has increased so much during the past decades.

          Note that I don't necessarily think it's wrong, mind you, just very counter intuitive, that's why I'd like to know if you have some sort of proof to back your statement with.
      • > The average lifespan is only that long thanks to modern advances in medicine, disease cures, etc.

        Actually, most people die of old age now, that's historically unusual- Cancer is a disease of old age, mostly; as is heart disease.

        The reason that the average old age is as it is, is believed to be evolutionary.

        In human history, and to a far lesser extent now, The human body has a certain amount of energy and other resources to play with; ultimately there's only so much food available; and the body has to balance growth, reproduction and repair (repair including genetic repair to head off cancer).

        The ideal amount of repair is linked to how long you expect to live- what's the point in repairing the body so that it would survive to 500, if by doing, say, 50% less repair you can live to be 85, when life expectency is only 35-50 anyway due to war, disease, accident etc. Evolution would change the genome to spend the energy reproducing a little more; as that way the genes will survive more often.

        Right now, we've messed with life expectancy. That means that, unless we do something, the human genome is going to tend to become longer lived, over the next few thousand generations (since, obviously, people who age more slowly will have more children; and their genes will spread.)

        This will involve changes to prevent cancer in other ways than this on the p53 gene, as well as changes to many other genes to ensure survival past the point we live to now.
        • People who age more slowly will have more children? What are you smoking? (Sorry to flame you, but I though you had already lit up...) The number of children one has nowadays is almost 100% related to personal choice. (well, it always has been, but now avoiding sex isn't the choice; birth control is.) If a woman wants to have 2 kids (or 1 or 4, whatever) and has her tubes tied after that, it doesn't matter how slowly she ages, or how long she would have been fertile (without having her tubes tied), she's not likely to have more kids. You're theory MIGHT work for, say, cattle, which are pretty much going to have a calf once a year from the time they are able until they aren't, as long as a bull is in the same pasture with them. People have more choice than that, and I think the evolutionary tact there isn't going to work.
          • I don't really agree with your analysis, but even if you are right the men can still father more children. If a man looks younger for longer, he can divorce and remarry fertile women more easily. The men that have the slower aging genes can thus spread them more widely. The women may WANT to bear his children.

    • Re:Evolutionary balance? (Score:5, Interesting)

      by zulux ( 112259 ) on Thursday January 03, 2002 @07:01PM (#2781949) Homepage Journal
      There's a 25 year lifespan discrepancy, in which evolution has no effect, because the population (at least of women) can't reproduce!

      In most primate cultures, old females still help with rearing the young. There is a hypothesis that this is the reason that females live longer than males - an old male is useless as a 'hunter' while an old femail is moderatly usefull as a child raiser.
      • an old femail is moderatly usefull as a child raiser.

        Older females are bloody marvelous at raising children and don't ever forget it.

        Don't make me talk to your Mama 'bout this.

      • In most primate cultures, old females still help with rearing the young. There is a hypothesis that this is the reason that females live longer than males

        Can I get a couple of extra years if I promise to help take care of the kids?

        -

    • Re:Evolutionary balance? (Score:4, Interesting)

      by Reality Master 101 ( 179095 ) <RealityMaster101@gmail. c o m> on Thursday January 03, 2002 @07:08PM (#2782007) Homepage Journal

      There's a 25 year lifespan discrepancy, in which evolution has no effect, because the population (at least of women) can't reproduce!

      That's an oversimplification of evolution. Evolution cares about maximizing survival of the species. Reproduction is only one factor in that. If reproduction were everything, we would never have split into male/female, since that obviously reduces the ease with which we reproduce.

      There are many things that people can do after child bearing to help propagation, such as protection, food production, education or labor.

      • Re:Evolutionary balance? (Score:3, Interesting)

        by Arrgh ( 9406 )
        Evolution has nothing to do with the differential survival of species, and everything to do with that of genes (individual organisms and close relatives, by extension).

        Here's a nice quote on the subject from something I just Googled up [missouri.edu]:

        Recall "suicidal" lemmings. Early biologists believed that lemmings (a) practice mass suicide and (b) that this trait is an adaptation benefiting the group. They reasoned that if the lemming population exceeds the carrying capacity of the local environment (if they exhaust food supplies) that the group will become extinct. To prevent group extinction, lemmings kill themselves. The gene for mass suicide is an adaptation benefiting the group to the disadvantage of the individual.

        This explanation has several problems. First, lemmings don't kill themselves. They migrate to new areas. They are excellent swimmers. By swimming across fjords in groups, an individual lemming is less likely to be swallowed by predators (safety in numbers).

        Second, a gene for suicide will not persist. Vehicles (lemmings) with the suicide gene do not reproduce?they kill themselves. In a population of lemmings with suicide genes, consider that a non-suicidal mutation would be very successful. If some lemmings refrain from killing themselves, they would be reproduce more than suicidal individuals and nonsuicidal genes would quickly predominate.

        Richard Dawkins has written about this common misconception at length.

        • Evolution has nothing to do with the differential survival of species, and everything to do with that of genes (individual organisms and close relatives, by extension).

          I'm not quite sure what you mean by "differential" survival, but I don't see how your quote contradicts what I said. All it says is that he believes suicide genes are not a successful strategy for a species. Which is interesting, but beside the point.

          Put it this way -- Any species that don't have survival as a goal don't last very long, by definition. Any species that is still around has survived through adapting to their local environment in some novel way. Reproduction is the easy part -- continuing to reproduce in normally hostile environments is the tricky part.

        • IANAGM (i am not a genetics major) - But - Couldn't a gene for suicide persist if it were manifested as a recessive trait?

          --jeff
        • According to the alt.folklore.urban FAQ, Disney caused people to believe that Lemmings suicide in march to sea. During the filming of the 1958 Disney nature documentary White Wilderness, the film crew induced lemmings into jumping off a cliff and into the sea in order to document their supposedly suicidal behavior.
      • Evolution doesn't care about maximizing survival of the species.

        To me it seems reasonable that species survive because so far they've been doing/being enough of the right things and not too many of the wrong things. Between the two there's a fairly broad spectrum of what they can do or be (given various other factors - environment etc).

        In an easy environment a species can do a lot of inefficient and ridiculous stuff and yet still survive. Whereas in a harsher environment ( artic, antartic), "no nonsense" species have a far better chance of survival.

        So it's far from maximising. It's more like good enough.

        Maximising could be something out of Aliens or The Thing ;).
    • I mean... isn't it sorta obvious?

      A person with too much p53 ages too fast to reproduce.
      A person without enough p53 gets cancer and dies before reproduction. These too extremes are quickly dropped from the gene pool.

      Where aging is loss of muscle tone, brittle bones, loss of coordination, skin elasticity, etc.

      If you're asking about our lifespan vs the age of menopause?

      If people only lived to the age of 50, then the genes that retard menopause to 60 never ever express themselves. They never really get selected for except at chance.

      Enter medical science and improved lifestyle. People now regularly live to 70, meaning that only women with the genes to retard menopause until 55 can bear children at age 50. If there is any benefit for bearing children at 50, such as increased resources, then there's a positive effect on those genes that retard menopause. As more people chose to delay (if people choose to delay) childbirth due to economic reasons, then more selective pressure is placed on menopause retarding genes, until eventually the lifespan discrepancy disappears.

      In the meantime, we prescribe drugs and lifestyle changes to women suffering from menopause.
  • die while I'm living than be dead while alive....Bring on the Prime Rib, the Marlboros, a good Shiraz. I may die sooner than later, but at least I will have lived..
  • When I look at pictures of my grandparents as they were my age, I have to wonder what they were like in person. What if I could meet them today, with them looking like that instead of some old people?

    I believe that eventually the aging process will be conquered, only to have more complex problems eventually cause our deaths (such as cancer).

    Imagine living to 100, but had stopped aging at 30. That would be so incredible, and would make a lifetime much more enjoyable overall. Yet, there is probably no way we could live forever, because something would eventually kill us. Heart failure or cancer would be the most likely candidates, because those are pretty much inevitable.

    Right now, I would give up everything I have to stop aging. At 22, I fear getting old...
    • It'll happen, but only for transcendant humanity (in the Alpha Centurai sense).

      Of course, you may not be able to appreciate how well preserved they are until you join them.
      .
    • If all of the world's six billion people were each guaranteed a 99.9999999% chance of surviving every year, six thousand people would die in the first thousand years. About six million people would be dead in a million years. In a billion years, 3.8 billion would be dead. In ten billion years, only about 270,000 of the original six billion would remain. The probability of anyone being alive after one hundred billion years is about 0.0000000000000000000000000000000002.

      One hundred billion years is a loooooong time, but this example shows that if you really want to live forever, you need to make damn sure you don't get into any accidents.

  • I wonder... (Score:3, Insightful)

    by TheGonzoKid ( 544822 ) <bpmatt1.cs@com> on Thursday January 03, 2002 @06:55PM (#2781899) Homepage
    Does this mean that since modern day man has increased contact with carcinogens, evolution will now favor those with higher cancer resistance and therefore shorter life-spans?
  • Stretching a bit here (and of course playing the devil's advocate), but are we seeing perhaps a result of how tampering with the natural process can affect us adversely?

    If we assume cancer is a naturally occuring phenomena (aside from cases caused by smoking, life habits, environment, etc..) against which we defend ourselves, is it not also possible that nature has found a way to defend ITSELF by hastening the death of the organism which is attacking it?
    • Anthropomorphism of Nature never seems to give reliable results.

      Nature isn't finding a way to do anything. It just is. We can't attack nature, all we can do is make our environment uninhabitable.. and nature won't (can't) care. Remember, jupiter is in an entirely natural state. Not a pleasant place to live, I'll grant, but entirely natural.

  • I know a woman who has stopped aging... (Score:3, Funny)

    by Rude Turnip ( 49495 ) <valuation.gmail@com> on Thursday January 03, 2002 @07:02PM (#2781951)
    she's been 35 years old for about 10 years now.

  • This just in! (Score:5, Funny)

    by Papa Legba ( 192550 ) on Thursday January 03, 2002 @07:02PM (#2781956)
    It has now been discovered that the leading cause of cancer in labratory mice is.....

    Scientists!

    Please take note and live you life accordingly.
    • We don't need better medicine we need better mice!

  • Opposite ends of the spectrum (Score:3, Insightful)

    by nick_burns ( 452798 ) on Thursday January 03, 2002 @07:07PM (#2781998)
    You could think of death as the end of cell growth, whereas cancer is cell growth gone out of control.

  • The more progress I see... (Score:3, Insightful)

    by Zen Mastuh ( 456254 ) on Thursday January 03, 2002 @07:10PM (#2782014)

    ...the stronger my belief in a creator. Over the last century we have been in a race to end death through bio-chemistry/bio-engineering. Now we are getting closer to the imaginary finish line and many people believe now that all cancer will be curable or preventable within a few years. Now we find that aging may fend off cancer.

    Silly mortals! I propose that whomever designed us intentionally created these apparent paradoxes to force all doubters to eventually believe.

  • If I recall correctly a lecture I heard back in 1995 or so presented research results according to which cancer cells, unlike other body cells, can exist (or reproduce? I dont recall.) without time limit in lab conditions. There seems to be no built-in time bomb for cancer cells.

    So it shouldn't be too surprising if further evidence shows for strong links between the aging process and natural cancer prevention.
  • Maybe it's a little bit more like this:

    Age In Mice A Byproduct of Cancer Defense

    Age In Humans A Byproduct of A Dodgy Marriage, Three Whining Kids, A Mortgage, A Dead End Job.

    :)

  • Interesting news, but not totally unexpected (Score:3, Informative)

    by jafuser ( 112236 ) on Thursday January 03, 2002 @07:39PM (#2782217)
    In biology, we were taught that each chromosome ends in a telomere (almost like those little plastic cylindrical thingies on the end of shoestrings) which doesn't do anything useful, but each time the cell divides, the telomere gets shorter. I'd imagine once the telomere is gone, the end of the chromosome would begin to "fray" as well, resulting in something equilvalent to a mutation, or maybe just a simple death of the cell (without the ability to divide further)

    I've read that in cancerous cells, the telomeres don't shorten each time the cell divides, so there's no system in place to stop the cell from dividing forever (and all of it's children cells, etc.).

    A reasonable hypothesis for why controlled growth through telomeres is necessary is to prevent mutations from a long series of copies (copies of copies, etc). This way, a "series" of cells only last for a fixed number of generations. After so many, the series stops. Then the stem cell(s) can take over and start a new "first generation" cell which can be the start of a new series of cells.

    As we get older, perhaps the stem cells themselves start to degrade or become mutated (possibly causing cancer), and are no longer able to produce good "first generation" cells. As an example, this could be why we develop skin blemishes as we get older. Just imagine what's happening to other genetic attributes.

    It's my personal theory that the process of aging is actually just the process of various parts of our body mutating to a small degree. For example, one little DNA pair mutated in a skin stem cell, and suddenly you have a freckle.

    I always figured that given the knowledge that's taught in regular high-school biology, most people could figure out that the tradeoff of preventing aging is the increased risk of cancer (since cancer cells could go on forever if supplied with the nutrients necessary for cells to live).

    *shrug* I dunno...

    • at the same time, many of the carcinogens are also the same compounds that cause aging. A familiar class of these compounds include free radicals and anything else that causes oxidation.
      It has been shown that organisms unable to manage certain environmental toxicants (as in knockout mice that can no longer tolerate heavy metals) age more quickly, and are immunosuppressed.

      Toxicants cause mutations directly in DNA, or interferes with protein assembly. The presence of toxicants also shift a cell's energy utilization since the cell must now use more energy to either remove or break down the toxicant. Many toxicants (such as heavy metals) can neither be removed nor processed. Higher energy utilization means energy production increases, and that increases oxidative stress (as in oxidation of sugars, etc.). Thus, the cell can not do its "job" correctly, because it has to deal with all the other crap being thrown at it. Finally, after age 21, you stop growing, so all the cells in your body are there to maintain homeostasis. When cells can no longer do their jobs efficiently, stuff starts breaking (as in cartilage breakdown in joints to cause arthritis, or fibroblasts can no longer maintain rigid cytoskeletons and cause wrinkles and muscle cells lose their tone; nephrons become unable to repair themselves and kidney failure results; neurons can no longer flush out incorrectly produced proteins and alzheimer's sets in).
    • I love when people with high school level education in anything think they understand how to solve something as difficult as cancer or aging.

      My first question to your personal theory is that if mutations are random (which they are), and aging is a result of said random mutations, then why is it that all humans age in a predictable manner? Why do they all get wrinkles, bad eyesight, etc? Granted, some effects of aging are different in different people, but overall it is a well known general degredation. Random mutations in actual genes(which aren't that frequent) do not happen in a predictable manner across the species like that.

      I don't honestly know much about the telomere thing other than what you've said here, but I am not inclined to believe it. I think apoptosis is far more important because it's so common. Sure, the telomeres could trigger apoptosis, but I somehow doubt it's the primary method of cell death, when there's so many other ways to trigger it. We are multicellular organisms, and most everything has to take in to account interactions between cells. The telomere-as-internal-clock idea pretty much ignores this. I wouldn't be surprised if it's possible, but I don't think that it's any explanation for aging.

      My other problem with your theory is that it goes straight to the DNA, and totally forgets the entire living environment within the cell (not to mention among cells). The state of a cell changes. It's not a binary system of life and death, a cell can do any number of things. Aging, to me, is the system of the cell changing, not at the genetic level (kids born to old parents would have these problems if it was) but at the molecular level. It happens via a change in gene expression, rather than mutation. This is a whole other can of worms, and it becomes way way more complex at this point, which makes a lot more sense to me given the complexities of a cell.

      Note that this doesn't even begin to get in to cancer, which is just as difficult. Yes, figuring out that cancer and aging are related is not too tough, the problem is finding the actual link between cancer and aging so that they can be separated somehow. Not everyone who ages gets cancer, and not everyone who gets cancer is old. Cancer is such a heterogeneous term that it can't be pinned down by simply saying "it's due to aging." This is why it's so difficult, and it's why there is so much work being done in the field.
  • Single cell organisms pretty much live forever
    until they are eaten, starve, or encounter an
    enviromental hazard. Multi-cellular bodies,
    pre-programmed death, and sex pretty much evolved
    together about 700 million years ago.

    • No They Didn't (Score:3, Insightful)

      by krmt ( 91422 )
      Single cell organisms pretty much live forever until they are eaten, starve, or encounter an enviromental hazard.
      Care to back that up? I have never seen any kind of data supporting the assumption that single cell organisms live forever, given those kinds of conditions, and without any kind of data, I won't believe it.

      The reason being that thermodynamics (or chaos theory, or whatever) says that you're wrong. Any system as complex as a living cell, even something so simple as a yeast cell or E coli can not maintain that level of organisation for long. The cell is very thrifty with its organization, to be sure, but it is not infinitely so. That's why reproduction and evolution are so critical, because no single system can survive by itself for too long, so it must rebuild itself from scratch. Yes, you can put these systems in to hibernation, but that isn't really life functioning in any way shape or form until it's revived.

      And of course pre-programmed cell death wasn't present in single cell organisms, it'd be counterproductive for an E coli to simply kill itself. Preprogrammed cell death does not kill the entire organism, and it obviously be detrimental if it did.

      And as for sex and evolution evolving together, there are single celled organisms that have sex via plasmids. Granted, it might not be the "one chromosome from each parent" that we are used to in humans, but it is still genetic exchange by conjugation. There is no apoptosis here either.
      • Well, I'm not really supporting his point so much, but take your standard average single-celled organism and tell me how old it is. You could tell me how long it's been since it last divided, but division isn't a process where one cell Ceases to Be and two appear out of nothing. In many ways it's still the same cell it was a million years ago. No cell in the world has been rebuilt from scratch for billions of years. Thermodynamics isn't meaningful here because the biosphere has a constant influx of usable energy.

        Of course, this is an interesting point of debate, kind of like wondering whether a computer in which every single piece has been upgraded at some point is really the same computer as it once was. Then again, I think I've heard that supposedly all the matter in a human body gets replaced within about seven years, so there you go.
        • You make a lot of good points. In a way, the cell was built from scratch. In many ways, you're right, it is still the cell it was millions of years ago, but it is different. It's a "daughter cell" now, which isn't really the same thing. Which cell is the original? The original doesn't exist any more, there are only daughter cells. If you don't let a cell divide, and provide it with enough nutrients and no predators, etc., will it live forever? I don't know, but I don't believe it.

          This leads us to a great truism in biology, that life is actually a process, not a state. As a process, you've got to ask why it has to replicate itself. If the parent was right, it wouldn't really need to, but all life does, even semilife like viruses must replicate. In large part, I think that it's competition, and having more on your side as it were, will increase your genetic odds. But I think the other reason is that processes tend to degrade, even with the influx of new energy. All these small interactions within a cell work to produce very fine systems, but these systems will eventually reach a chaotic point and will no longer function. They're very very very good at preventing this, but no complex system can escape chaos forever. Living systems must replicate and create fresh offspring to work around this problem. The process starts over (from scratch, as it were) and life begins anew.

          Perhaps "from scratch" really was a poor choice of words, but I think the point remains. The process has to restart, and the only way it can do this is with fresh materials.
  • The Atlantic Monthly had an article that documented research that stated that human biology is set up to maximize a person's health at age 20 at the expense of later years.

    Certain trade-offs are made that sacrifice the health of the future you just to keep the "child-bearing" you at 110%.

    This suggested that an individual human would live significantly longer if these trade-offs were not made, but a population group would surive longer and have more/better children otherwise.

    This research seems to be more of the same.

  • Read the real sources! (Score:5, Informative)

    by bradbury ( 33372 ) <Robert DOT Bradbury AT gmail DOT com> on Thursday January 03, 2002 @08:53PM (#2782601) Homepage
    One of the things that continually disappoints me about /. is the degree to which people will comment on things without slightest knowledge of the subject under discussion. One of the things that I find appealing is when someone who actually knows something provides a useful interpretation that abstracts useful data for people who aren't particularly well informed in an arcane knowledge base.

    I'm speaking here as founder and president of what was the 2nd largest biotechnology company in the U.S. focused on the molecular biology of aging during the mid-'90s. So we will assume for the sake of improving the discussion I'm moderately well informed in this arcane branch of knowledge.

    Point #1: If you read something scientific or technical in the "popular" press, never assume that they managed to interpret it properly. If reporters don't have an education in a particular discipline, they are not likely to understand the subtleties of what is being discussed. Always go back to the most scientific sources you can get access to. Most of the readers are presumably qualified to evaluate arguments on technical merits (this is the /. forum!). Learn the jargon and if you don't understand something find an expert and ask questions (or post to the forum -- you never know when an expert might be lurking).

    Point #2: Never assume a /. poster knows what they are talking about (or has verified what they may have copied or concluded from popular press). Case in point: "aging in mice seems to be the byproduct of the chemicals that prevent cancer". The material under discussion is a mutant p53 protein which is the byproduct of a modified p53 gene. It is not by anyone familiar with discussions in this field a "chemical". The p53 protein weighs tens of thousands of daltons and has multiple "active" functions -- most molecules considered "chemicals" weigh less than a few thousand daltons and have few, if any, "active" functions.

    From the Nature news report [nature.com]: "they created mice with a chunk missing from one copy of the gene". Translating this into "programmer" terms -- this is in effect replacing 1 of 2 instantiations of an essential subroutine in an ~30,000 subroutine system with a subroutine that has had some of its lines deleted. How do you draw conclusions as to what is going on in that situation? Unless you know what lines were deleted and what the purpose of those lines was you have relatively little hope of drawing conclusions that would allow you to debug the system (at least IMHO). You certainly cannot discuss what the situation means in any intelligent fashion.

    All of that being said, I'll provide my "spin" on the results. The normal p53 protein is a "gatekeeper" protein. Its purpose is to determine whether or not DNA damage is present (i.e. whether your program has been corrupted). If too much damage is present it induces cells to commit apoptosis (cellular suicide). If less damage is present, it delays cellular replication (copying) until the damage that is present can be repaired (calling the ECC subroutines). So it acts as a brake on the replication of mutated/damaged DNA and an executioner for cells that are so far beyond the error-correction subroutines that they represent a threat to the entire organism. In larger organisms (which have more cells and are therefore at greater risk of developing a "mutant" program and therefore cancer [which is unregulated cellular replication]) it is important to constrain replication. So humans, in contrast to mice may have a p53 which strongly constrains cellular replication. { Alternatively they may have "redundant" subroutines like telomere shortening (mice have very long telomeres, humans do not) which function as "backup" programs that function to limit cellular division and therefore the development of cancer. (This is based on the concept that short telomeres inform cells to "stop dividing" just as "damaged DNA" [through the p53 protein] cause cells to stop dividing.) } The extent to which short telomeres may resemble "damaged" DNA (and therefore activate the p53 "subroutines") is unclear (to me) at this point. [This is a fairly hot topic of scientific debate.]

    If we view cancer and aging as complementary ends of the see-saw -- allow too much cellular replication and one gets cancer -- allow too little cellular replication and those parts that wear out are not replaced, resulting in aging, and one may be able to interpret the results of this study. The part of the p53 gene that was deleted probably served to function to "remove" the block against replication or "enable" the replication function. So what may be occuring is that the mutant p53 gene may be detecting damage, blocking replication, but then when the damage is repaired the defective p53 may not be allowing replication to proceed. Thus you have very effective anti-cancer properties but as one gets older there are fewer and fewer cells available to replace those that are lost. Net result: accelerated aging.

    Now, this result need not be pessimistic. As Tom Kirkwood, one of the world's leading gerontologists pointed out in the Nature article, "We could be able to pick a path through the molecular mechanisms of ageing without making cells more tumour-prone. 'There's no reason why you shouldn't get greater defence against cancer and greater longevity.'"

    As a once upon a time programmer -- I encourage people in the software industry -- "View genomes as programs -- lets figure out where the bugs are and then lets go fix them."

  • Lifespan and Human Ego (Score:2, Interesting)

    by slinted ( 374 )
    The article in question skirts the edge of the changing paradigm in bioscience. The "goals" of western medicine for thousands of years has been to fight disease, be it internal or caused by external agents. This has lead to longer lifespans and for many individuals born with defective proteins from mutation, cures to debilitating diseases. These are still major concerns for drug development, and are straightforword since most could potentially (ignorning for the moment delivery/targeting) be solved through the presence of a functioning protein when the body itself can't produce it. But the modern study of cancer and heart/stroke disease has brought a new understanding of the "sources" of disease.


    For a population genetics class I took in school, I wrote a draft research grant for a project studying if there were age limiting factors positively selected by nature to limit the age of certain populations. Although my professor did get a good chuckle before "d"ing me, he did say something that caught my ear as blatent established science ego. "That anything would act to limit age goes against the whole understanding of life, that those who live the longest win, produce more young, provide better for them and reflect more of their own genes through greater numbers of offspring". Ok...well, now lets look at cancer. Although the greatest hype (and greatest understanding) of cancer findings revolve around "defective" proteins that cause greater occurances of cancer, the base assumptions about the manner in which cancer forms lies far from the "defective/working copy" model of the body's working.


    Copying DNA causes errors, and the body can fix an amazing number of them (end rates: 1 error per 10^9-10^10 bases), although it can't ever fix them all. The more times a cell needs to reproduce to replace damaged or non-functional cells, the more likely it is to lose function in a portion of its working copy of DNA. Cancer forms when these errors occur in specific places, but the general principle is that eventually a certain cell line will accululate enough errors to make it non-functional towards its intended purpose. Does P53 prevent cancer, sure, it lowers the error rate, but as the article mentions, too much p53 and you have other effects. The balance exists and has been selected for because it makes a working body capable of reproducing and caring for its young and then goes away. The premise that there is this one thing, this one chemical or protein or substance that will "unlock" another 50 years of human life is based on the premise that everything else in the human body will remain functioning were it not for that one thing. Evolution has crafted our bodies for their purposes, and none of it has been "tested" after 100 years. So where are we? We prevent a "disease", if you can call something like cancer or heart disease the same as a bacterial infection, only to find...Lo! there's something else that doesn't work after its been churning through our bodies for 80 years.


    Geneticists especially are learning the lesson of our war against disease, stemming in large part from the telomerase hype. Hey, look what I found, the cellular time bomb! If we can keep these puppies long, we'll have immortal cells and we'll all live forever! Well, guess what, cell death isn't why we die. Also research into menopausal woman is showing us the same path. Replace estrogen when the body stops making it and we prevent osteoperosis, but estrogen's presense raises rates of heart disease, breast and ovarian cancer. In the end, its all the same message... we die from our bodies falling apart, functioning way past their warranty. And we're just now begining to realize this as we find more and more reasons why one substance doesn't do it all.

  • These things are called "engineering tradeoffs", and they apply to biological organisms as much as to a processor chip. However, this particular tradeoff may not be inevitable: one of the most fundamental engineering tradeoffs in biological organisms is allowing for food scarcity. This not only puts us at risk for obesity, it also means that bodies have to be careful about wasting energy on repairing themselves. With unlimited food available, you may be able to live long, avoid cancer, and not even get fat. How? By having the body more aggressively replace possibly damaged cells, cells that right now are allowed to hang around because it would require too much energy to replace them.

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