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Tumor-suppressing Gene Contributes to Aging 145

Posted by CowboyNeal
from the growing-old dept.
Van Cutter Romney writes "Scientists have discovered a tumor suppressing gene which also leads to aging in stem cells. The gene also known as p16INK4a when removed from 'knockout' mice resulted in older mice having organs as healthy as younger ones. However they didn't live any longer than normal mice. The new study was confirmed by three independent researchers from Harvard, UNC Chapel Hill and University of Michigan."
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Tumor-suppressing Gene Contributes to Aging

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  • Cancer, aging. (Score:4, Informative)

    by sporkme (983186) * on Thursday September 07, 2006 @09:51PM (#16063646) Homepage
    "I don't think aging is a random process - it's a program, an anti-cancer program,"
    Cancer, then, is an anti-aging program.

    The article basically states that when they turned off the flow of ink-4, embyyonic stem cells were free to divide without check. The mice without the ability to produce ink-4 developed cancer within a year and died. This behavior cannot be reliably reproduced in aged stem cells, and ink-4 production naturally increases exponentially with age.

    The main news I see here is either a possible avenue for cancer research, or a good supporting argument to lift bans on exploiting new strains of embryonic stem cells (over adult stem cells). This does not represent a specific breakthrough, but yet another amazing revelation of stem cell capabilites has come to light.

    I support the ban on cloning, I disagree with the ban on new stem cells, I am relatively opposed to mass abortion, but banning it would be stupid. I think this story's new information supports these views.


    • The article basically states that when they turned off the flow of ink-4, embyyonic stem cells were free to divide without check. The mice without the ability to produce ink-4 developed cancer within a year and died.

      There's a famous principle in Mathematics & Quantum Mechanics, first discovered by the British mathematician GH Hardy, and then refined by Heisenberg, which states that both a function & its Fourier transform cannot decay too rapidly [otherwise the function is identically zero].

      Or, as Mi
      • Re: (Score:3, Funny)

        So it sounds like The Designer of the Universe [a pretty intelligent Fellow, from what I hear] may have placed the very same restrictions on the stuff He created on Day 5 as He did on the stuff He created way back on Day 1.

        I forget, was it spaghetti or ramen he created on Day 5?
        • Re: (Score:3, Interesting)

          by Xichekolas (908635)
          Who the hell modded the parent down? That was totally on topic... just because your creator is a vengeful old dude in white robes and mine is the divine embodiment of my favorite meal doesn't mean it was off topic!
      • by SteveAyre (209812)
        Spooky. He sang that line at exactly the same time as I read that. :)
      • So, Mick Jagger [lyricsfreak.com] is an alien, QED.
    • by NotQuiteReal (608241) on Thursday September 07, 2006 @10:37PM (#16063823) Journal
      Cancer, then, is an anti-aging program

      Yes, when cancer works, you stop getting older.

      Q.E.D.

    • by TubeSteak (669689)

      "I don't think aging is a random process - it's a program, an anti-cancer program,"

      Sounds to me like Planned obsolescence [wikipedia.org]... that is, if you believe in a higher power.

      Cancer, then, is an anti-aging program.

      Why is it that back in Biblical times, people like Abraham & Moses used to live several hundred years? Did they all have cancer? (Assuming that cancer is an anti-aging program)

      • by sporkme (983186) *
        I was referring to the part of having cancer where you DIE, whereby aging ceases. Nice extrapolation though. Religious science is getting pretty keen nowadays. "Don't you worry Mrs. Smith. Moses had cancer too, and he lived nearly a thousand years!"
      • I think you're thinking of someone else. Abraham lived to be 175, and Moses lived to be 120, IIRC.

        Perhaps you're thinking of the antediluvian patriarchs. Noah was one of the younger ones at like 600.

      • Re:Cancer, aging. (Score:4, Interesting)

        by Fordiman (689627) <fordiman@gmGIRAF ... minus herbivore> on Friday September 08, 2006 @09:27AM (#16065622) Homepage Journal
        "Sounds to me like Planned obsolescence... that is, if you believe in a higher power."

        You don't have to believe in a higher power for that. Sounds to me like a natural function of the balance between being able to repair yourself and exploding into a ball of disorganized meat (ie: developing cancer in every cell). Based on the amount of damage your body takes, it automatically determines how much it needs to be able to redivide its cells.

        "Why is it that back in Biblical times, people like Abraham & Moses used to live several hundred years? Did they all have cancer? (Assuming that cancer is an anti-aging program)"

        Nah. I would guess it's because of a trans-generational game of 'rumour' that happened before any of it got written down. Don't get me wrong; much of Exodus actually happened (the plagues, parting, etc, are easily explained by a volcano eruption that happened as moses returned to Egypt; I can't blame him for using it as a way to extort pharoh and reinforce judaism - we all have our agendas, after all, and they're almost always good in our eyes). But Genesis... it all sounds a bit like stories passed from father to son that eventually got written out.

      • Re: (Score:3, Funny)

        by kalirion (728907)
        Why is it that back in Biblical times, people like Abraham & Moses used to live several hundred years? Did they all have cancer? (Assuming that cancer is an anti-aging program)

        It's really quite simple. The early people had nearly perfect genes (you know, made in God's image and all that), but since God only really created two (and the second one was basically a clone of the first one but with the Y chromosome taken out and the X duplicated again) there was a LOT of inbreeding going on. Which isn't
    • Re: (Score:3, Funny)

      by Explodicle (818405)
      I support the ban on cloning...
      Hey, the average Slashotter isn't reproducing the normal way... why you gotta be stomping on our only hope?
    • One key mistake in the parent's summary: Ink-4 limits the ability of adult stem cells to divide. The article suggests a theory that because damaged adult stem cells are prevented from dividing by Ink-4, unchecked tumor growth (cancer) is averted later in life.

      How this supports embryonic stem cell research is: we now have evidence that adult stem cells will not be effective when used as treatment because they will be naturally suppressed. Thus to get stem cells that will divide and provide therapy, we mus
      • by Noehre (16438)
        You can't draw that conclusion without knowing the pathways involved in expression of INK4.

        Extracellular signalling pathways, such as G-coupled protein receptor pathways, may be key to INK4 expression levels. If that is the case, embryonic stem cells would likely undergo the same INK4 suppression as adult stem cells, whether they be transplanted or naturally occuring.

        The key is then not the source of the stem cells but modulation of protein expression in the stem cells you have.
      • by ivan256 (17499)
        It is ironic that you are willing to make such enormous logical leaps given your user name.
  • Old news... (Score:3, Interesting)

    by elysian1 (533581) on Thursday September 07, 2006 @09:55PM (#16063662)
    Isn't this talking about the same thing as this article: http://science.slashdot.org/science/05/04/06/23302 49.shtml?tid=191&tid=14 [slashdot.org] which was posted here over a year ago? I guess this is pretty good for slashdot to go over a year without reposting a similar story.
    • Re:Old news... (Score:5, Informative)

      by juushin (632556) on Thursday September 07, 2006 @10:13PM (#16063726)
      No, it is different. In the story a year ago, a korean group found that if you suppress telomerase in cancer cells--an enzyme that makes cells 'immortal' by continually adding repeats of bases on to the ends of chromosomes--the cells die. the summary on the slashdot page is not exactly correct--telomerase is not an enzyme specific to cancer cells. In this present work, it is a gene that, in a way, computes a differential equation--weighing the importance of replacing cells using stem cells from its cache against the risk that the replication of cells will result in a cancerous cell. "To offset the increasing risk of cancer as a person ages, the gene gradually reduces the ability of stem cells to proliferate." it is a fundamentally different story and is interesting.
      • by Ungrounded Lightning (62228) on Friday September 08, 2006 @12:16AM (#16064123) Journal
        In this present work, it is a gene that, in a way, computes a differential equation--weighing the importance of replacing cells using stem cells from its cache against the risk that the replication of cells will result in a cancerous cell. "To offset the increasing risk of cancer as a person ages, the gene gradually reduces the ability of stem cells to proliferate."

        If I understand it correctly, this is a SLIGHT mischaracterization. It's not about risk of creation of cancer cells so much as it is about limiting tumor size - generally in malfunctioning differentiated cells - and limiting stem cells is an undesirable side-effect of how it's done (though it WOULD also limit a stem-cell tumor, if such exist).

        The mechanism (or set of mechanisms) is a limit on how many times a non-gamette cell may replicate. Thus when a cell mutates so that it, and its progeny, continue to replicate (ignoring their normal limits), the resulting tumor reaches a maximum size (say-pea sized) and stops growing. (It may even die off, as cells die TRYING to replicate with an "expired meter", or are no longer replaced fast enough to stay ahead of immune-system attacks).

        The smaller the tumor when it hits the limit, the better (and the less likely some cell within it will acquire the ADDITIONAL mutations necessary to escape this limit, founding an "immortalized" tumor cell line). But there's the downside that the limit also results in cellular senescence - inability of the body to replace tissue in late age, because the "counter" in the otherwise-fine cells is running out.

        So the limit apparently evolves with the typical lifespan of the population, allowing enough replication that cellular senescence doesn't begin to occur in normal inividuals until virtually all of them would be dead (or otherwise no longer an asset to the species) due to other causes. (I vuagely recall reports of research suggesting the typicall setting is something like twice as many cell replications as are necessary to avoid senescence by the age where about 95% of the population would be dead.)

        Meanwhile other protective mechanisms (such as the metabolically-expensive production of antioxidant enzymes) co-evolve to trade off keeping the cancer rate down against resource consumption, given the typical lifespan due to risks and the cell-reproductive limit setting. (THESE are the "twiddle settings" that trade off CREATION of a cancer cell against other life-shortening factors.)

        The settigs of these protective mechanisms apparently evolve quite rapidly, so they tend to closely track the lifespan-due-to-circumstances of most species that have been in their niche for a while. But the human lifespan has been drastically extended in a period that is evolutionarilly VERY short, thanks to weapons (protection against predation and improved hunting success), agriculture, animal domesitication, lore transmission, medicine, and other technological and cultural improvements in lifestyle. So plenty of people live to the "threescore and ten" or so years when the current setting of the cell replication limit tends to cause fatal system failures.

        Research such as this, identifying the details of the mechanisms, should lead to interventions to compensate for the now incorrectly-low setting of this "tuning knob" in the human genome.
        • Re: (Score:3, Interesting)

          by wulfhound (614369)
          Interesting point of view, but perhaps a bit optimistic:- human lifespan is already up at the top of the range for mammals -- even if the 'turning knob' can be fixed (double or triple the maximum cell division count, and suitably increase the metabolic / nutritional budget for tumor suppression to compensate), our evolutionary line has had an upper limit of a hundred years or so since the earliest mammals evolved 100m years ago -- nothing that we've evolved in that time has built for multi-century endurance
        • Re: (Score:3, Informative)

          The mechanism (or set of mechanisms) is a limit on how many times a non-gamette cell may replicate.

          This is known as the Hayflick limit, and is related to what the great-grandparent post brought up- telomeres. When normal differentiated cells divide, an issue with the way our DNA polymerase works causes a bit off the end of the DNA strand to not be replicated- your DNA gets shorter with each cell division. To counter this, there are sequences of repeating nucleotides at the end called telomeres. The te

      • by Fordiman (689627)
        Ok, so how difficult would it be to suppress all the ink-4 (stopping the cancerous property) and increasing the telomerase output of cells? Would that not make effectively immortal, noncancerous cells?

        Possibly. But they'd also be completely unable to repair themselves. You'd get a population much like the late Brunnen'gee.
  • by Meccanica (980734) on Thursday September 07, 2006 @10:00PM (#16063672)
    although it does not follow directly from this discovery, is the question: If you could change the balance at any point, what would it mean to be able to choose between heightened risk of cancer and some of the worse effects of old age? What a choice to have to make. (AFAIK, this is not even an issue, just something I thought of after hearing of it. I did not RTFA, but I heard this same discovery reported on the news recently.)
    • Re: (Score:3, Insightful)

      by zCyl (14362)
      If you could change the balance at any point, what would it mean to be able to choose between heightened risk of cancer and some of the worse effects of old age? What a choice to have to make.

      Ideally, you would be able to turn it on and off at will. Turn off aging when you reach a certain age. Then if you contract cancer, turn it on really quick to help kill off the cancer, and then when you recover from cancer, turn the "aging" process back off.

      Not that we could do anything of the sort anytime soon, but
  • Hmm. (Score:3, Interesting)

    by Lord Aurora (969557) on Thursday September 07, 2006 @10:13PM (#16063728)
    If the organs in the older mice were just as healthy as those in younger mice, how did they not live longer? It would seem to me that if your organs are perfectly healthy, you'll live. Wonder what the catch is.
    • Re: (Score:2, Funny)

      by Anonymous Coward
      The mice didn't live longer because they had to kill the mice to check if the organs were as healthy. :-)

      You say flawed methodology, I say.... progress!
    • Clarification: Yes, the mice in TFA all got cancer and died because of the whole risk-increase thing, but "What if they HADN'T gotten cancer?" was my line of thought. Failed to mention that critical detail. =D
    • Re:Hmm. (Score:5, Insightful)

      by ozmanjusri (601766) <aussie_bob@[ ]mail.com ['hot' in gap]> on Thursday September 07, 2006 @10:34PM (#16063812) Journal
      Wonder what the catch is.

      There is only one catch and that is Catch-22, which specifies that turning off p16INK4a for one's safety of your organs in the face of dangers that are real and immediate will cause cancer. Giving yourself cancer is not the process of a rational mind.

      The trick might be to turn off the expression of the gene temporarily to rejuvenate aging organs, then switch it back in again to suppress cancer. That way, maybe Yossarian can have is cake and eat it too...

      • And if they can rejuvenate aging organs consistently, maybe the dead man in his tent can be brought back to life.

      • The trick might be to turn off the expression of the gene temporarily to rejuvenate aging organs, then switch it back in again to suppress cancer.

        Only to be killed at a zebra crossing right after the procedure.
      • Re:Hmm. (Score:4, Insightful)

        by Grym (725290) * on Friday September 08, 2006 @12:10AM (#16064107)

        he trick might be to turn off the expression of the gene temporarily to rejuvenate aging organs, then switch it back in again to suppress cancer. That way, maybe Yossarian can have is cake and eat it too...

        Wishful thinking. As much as people would love to blame the cause of aging on one particular gene or process, the truth of the matter is that aging is a complex and multi-factorial phenomenon that can't be addressed that easily.

        Sure, stopping this particular gene might allow for more somatic cell repair but what does that do for the damaged mDNA due to free radicals in the mitohondria [nature.com]? And what about the telomeres protecting the ends of your chromosomes which would decrease with every replication [utah.edu]? And what about damaged cells whose replication could cause the very cancer this gene was probably "designed" to prevent?

        Not to be discouraging of this kind of research, but really it is just pie-in-the-sky type of stuff and should be regarded as such; the science just isn't there yet. And the irony of it all is that immortality most certainly won't be obtained in our lifetimes. Joseph Heller has to be smiling somewhere about that one.

        -Grym

  • From what I know about cancer, which isn't a whole lot, the immune system is supposed to be a supressor of tumors. It doesn't make any sense for just a gene to do it if it isn't one related to white blood cell manufacturing. To make a long story short, the "cancer supressing" powers of the gene are barely noteworthy, like putting on a spring jacket to stop frostbite at -40 F, and they wrote it in that biased way so it makes a dramatic headline that implies you may have to choose between living longer and
    • I think you fail to understand the possibilities of having multiple avenues for the body to prevent unchecked cellular reproduction. Built into each cell should be the codings to tell it how and how often to divide, and at what stages of life. When those checks fail due to any number of circumstances (mutations due to environment or flawed genes), a secondary check, the immune system, responds to a threat of unchecked cellular reproduction by destroying it if possible.

      Think of it like social behavior. Ideal
      • okay, I'll explain it a bit more. What I'm 99% sure they're referring to is a gene that affects how much of a certain mollecule (or maybe group of mollecules) is chopped off when a cell splits. It's a little barbel shaped thingy and every time a cell divides, it loses a little bit of it. Once it's out, the cell can't divide anymore and it dies. Cancer cells are defined by having unlimited barbels. They never run out so it divides over and over and never stops. Remove this gene and your cells can split
        • Re: (Score:3, Informative)

          No, this has nothing to do with telomeres, which is what I think you're talking about. The product of the gene p16-Ink4a is a protein which inhibits an enzyme called a cyclin-dependent kinase. What this cyclin-dependent kinase does is control a "checkpoint" between two stages in a cell's life cycle. A cell at this checkpoint can either be told to go ahead and replicate its own DNA, or it can be told to just sort of "pause." Due in large part to the action of this gene, p16-Ink4a, most of your adult cell
    • The gene probably slows metabolism. Slower metabolism means fewer chances of cell replication errors, reducing the risk and spread of cancer. It has been speculated for about the last 10 years or so that there is a trade-off between slowing of aging and cancer risk.

      This is probably why a handful of humans had deseases causing them to age far too prematurely, but NEVER the opposite (at least not on a signif scale). Thus, entropy is innevitable it appears. Errors happen. Either we slow down to death or get i
    • It's all the unremarkable things that will eventually add up to a tool to fight against, or a cure for cancer. DNA FTW.
    • by RsG (809189) on Thursday September 07, 2006 @10:34PM (#16063815)
      Actually, genetic safeguards are potentially more important than immune response in many ways.

      The immune system is handicapped by the fact that with at least some types of cancer, there is comparatively little difference between the malignant and healthy cells. If it can't tell them apart, it can't stop the cancer from developing or spreading. You're right in that the immune system can sometimes stop cancer, but from a survival standpoint it's better not to get it in the first place.

      So we have genes in place to limit cell replication. It's been suggested that aging is an inevitable side effect of these limits (take a look at telomeres for instance). Just the immune system by itself, or just the genetic protections by themselves, isn't enough; you really want both defenses.

      Oversimplified, the genetic element is why some cancers run in family lines, and the immune element accounts for why some cancers develop when the immune system is weakened (like KS in AIDS patients).
      • by tempest69 (572798) on Thursday September 07, 2006 @11:36PM (#16063997) Journal
        Higher organisms have genetic safeguards that are stopping cancer ALL THE TIME. Generally multiple systems in a cell need to fail before cancer can begin.

        The first thing that needs to fail is the proofreading enzymes, so that a gene or two are damaged without being repaired.

        Then the "self destruct" needs to fail to activate in a cell, The self destruct is almost always armed and ready to go, unless it gets knocked out by a "lucky" mutation.

        Even if the self destruct fails, the cell sensing needs to fail in order to grow beyond a few cells. Then the telemorase halting needs to fail in order for the cancer to reach something larger than a mole.

        The immune system is a last resort, and not a very good one in comparison.

        Storm

    • "Tumor suppressor" is the term for genes that act as inhibitors in growth pathways. It's a somewhat misleading term, at least in the way it's used nowadays, but they're not claiming that this gene has some magical anti-cancer properties. (the submitter probbaly didn't realize that, though.)

      That has very little to do with the immune respose issue you mention, which comes in significantly later, when tumors have actually started to form. The oncogene / tumor suppressor interactions are part of the balance tha

  • by qaffle (264280) on Thursday September 07, 2006 @11:09PM (#16063929)
    As organisms get older the chance that they will have a mutation that leads to some form of cancer grows (in a if every day you have the chance of something happening, after enough days go by you're likely to have had it happening sense).

    Does the same thing apply to a cell?

    In other words, as a cell ages is it more likely to have a cancerous mutation? And how does this likeliness compare to the chance of having a cancerous mutation through a cell's reproduction process? (these are for the biologists out there)

    If you have a greater chance to have the mutation a cell reproduces then you'd want cells to live along time so they have to reproduce less. If you have a greater chance as the cell sticks around (ages) then you'd want more reproduction and a shorter life span (even though this would be less energy and resource efficient, but maybe more efficient than fixing/killing cancerous cells).

    • by Anonymous Coward on Friday September 08, 2006 @12:24AM (#16064142)
      The assumption that you made incorrectly was that the probability for a mutation is constant. It is infact cumulative. While the chance that any one healthy cell will mutate is constant, a mutated cell will always produce another mutated cell. Thus the total number of expected mutations goes up everytime a cell divides.

      Look at this statistically.

      Everytime a cell divides there is probablitly P that the cell mutates.
      Everytime a cell ages 1 day there is a probability Q that the cell is damaged.
      Since we must maintain a constant number of cells we assume that everytime a cell divides the "Old" cell dies.

      If we make the simplified assumption that all cells must divide at the same time then we must choose to either (1)let the cells divide or (2)let the cells age one more day.

      There is an obvious strategy to keeping the greatest ratio of healthy cells in the body. We will choose whichever action results in the least expected number of unhealthy cells.

      If P Q (which it should be) the strategy would be to divide every chance you get until the probability of getting a mutation is greater then the probability of having cell damage. You will then alow the cell to age and the ballence will swing back in the other direction.

      As you continue this pattern you will find that it is optimum to have cells divide less and less frequently. Eventually the probability of mutation will be so high that the best strategy is to simply stop cell division all together although it is unlikey that anything will live long enough to reach thsi point.

      This is an oversimplification but the point is still valid. The best strategy for survival changes constantly.

    • (in a if every day you have the chance of something happening, after enough days go by you're likely to have had it happening sense).

      Perhaps OT, but your example doesn't accurately characterize what I think it is you're saying. Consider a coinflip. Assume the chance of the coin landing heads-up is 1:2, as is the chance of it landing tails up. Assume you're going to flip the coin once. What are the chances of a heads-side-up landing? 1:2, of course. What about if you flip 700 times? 1:2, still. The fallacy

      • Re: (Score:2, Insightful)

        by CTachyon (412849)

        No, your parent post deliberately sidestepped the Gambler's Fallacy. He clearly indicated that he meant "more likely" in the sense of "the odds of at least one tails after one flip is 50%; the odds of at least one tails after 8 flips is 99.6%", since the total number of tails/mutations accumulates. After a very long time, the probability of one or more mutations is nearly certain, even if the probability of each mutation occuring is constant.

        • by Skadet (528657)
          "the odds of at least one tails after one flip is 50%; the odds of at least one tails after 8 flips is 99.6%"
          The odds of at least one tails after one flip is 50% (1/2); the odds of at least one tails after 8 flips is 4/8 (1/2).
          • by CTachyon (412849)

            No... the odds of at least one tails flip (that is, the sum of exactly one tails flip, exactly two tails flips, exactly three tails flips, etc.) is the complement of exactly zero tails flips -- that is, all heads flips. The probability of 8 heads flips in a series of 8 flips is (0.5)^8 = 0.00390625; the probability of less than eight heads flips in a series of 8 flips (that is, the odds of one or more tails flips) is therefore 1-(0.5)^8 = 0.99609375. Please study some high school statistics.

  • I heard this on NPR today...I was wondering why they didn't say "Aging gene surpresses tumors"...
  • Imagine youthful looks and good health almost all your life, then dying of cancer before you hit 80.
  • In the western world old people are sitting in their big houses with backyards while young families with children are crowded into small apartments.

    Once the old people can no longer look after themselves, they will be put into a care home, and kept alive for decades using modern technology. I visited old folks homes for a while, and me playing chess with an old man for 1 hour a week was the highlight of his life, the highlight for another man was me rolling a ball back and forth on a table to his arthritic
    • Anti-ageing research is selfish

      Nobody will take you seriuosly unless you live by example. Will you willingly die before you hit `old age' and become a `burden on society'?
      • by Profound (50789)
        >> live by example

        I'm 26 - how should I do that? Take up smoking?
        • by TheLink (130905)
          That's not such a bad idea. Esp if the tobacco taxes are high. Then you'd be paying for your short illness and probably for one or two others too.

          A very commendable sacrifice Citizen!

          I don't know why Govs around the world complain about smoking etc, and worry about aging populations on the other.

          Just tax tobacco at a reasonably high rate, educate citizens on the dangers of smoking. And if people still want to smoke, why make it so hard for them?

        • by lachlan76 (770870)
          Smoking, overly large amounts of alcohol, medical studies.

          Or you could just donate your organs.
    • Re: (Score:2, Insightful)

      by Anonymous Coward
      Okay. A few problems with your thinking:

      1) Those old people are generally able to end their own lives if they really wanted to - but they don't. Your generalisation that old people "don't want to live" is inaccurate. Many studies (check on PubMed with a few salient keywords) have shown that elderly people are just as happy (if not more so) than younger people. There is also no magic point at which people suddenly decide that life is not worth living - the vast majority of people will always want to live lon
      • by Profound (50789)
        Other reasons: People become more invested in the status quo as they become older, and thus become more conservative.

        Babyboomers make up a significant proportion of the population. Thus, when they were young, they were listened to, and lots of changes (equality of women/non-white etc) occured. Now that they are old, almost all countries in the English speaking (winners of WW2) world have become very conservative.

        Evolution occurs when a new generation replaces the old. A society where the old outnumber the y
        • by Bozdune (68800) on Friday September 08, 2006 @07:00AM (#16065094)
          Actually, the majority is almost always conservative, no matter what generation you consider. We have had rather few progressive Presidents, wouldn't you say? Didn't matter whether the boomers were young or old. The Boomers were too young to vote for Kennedy. The choice in 1964 was between Goldwater, who wanted to expand the war in Vietnam, and Johnson, who claimed he didn't, but did. Johnson was a fluke. Nobody knew he had a liberal social policy agenda, he was a conservative Southern democrat who Kennedy put on the ticket in order to win Texas. After Johnson we elected Nixon, by landslides, just when the boomers started voting en mass. Then we chose Carter, a conservative, religious southern Democrat, over the half-dead Jerry Ford, hardly a progressive choice. Then 12 years of Reagan and Bush I -- our most conservative Presidents since Hoover -- during the prime years of 30-something Boomer voting! 8 years of Clinton, who cut welfare to the bone and accomplished nothing on any progressive agenda. Then 8 years of (gack) Bush II.

          John Stuart Mill said, "I never meant to say that the Conservatives are generally stupid. I meant to say that stupid people are generally Conservative. I believe that is so obviously and universally admitted a principle that I hardly think any gentleman will deny it." Mill goes on to say that since there are undeniably a lot of stupid people, the Conservatives will always be a very powerful party. Perhaps this is closer to the explanation you are looking for.
          • by DrCode (95839)
            I've known plenty of stupid lefties. Stupid people tend to follow the crowd. I wouldn't be surprised if many of the middle-aged, unthinking right-wing types today weren't unthinking left-wingers back in the 60's.
        • This is an interesting hypothesis, but it is not supported by the data [people-press.org] concerning party affiliation. According to Pew Research data, there are more Democrats than Republicans in every age category except 30-49. In fact, the spread (in favor of more Democrats) increases with age.
    • How about BOTH quality and quantity.

      Why is everything assumed to be a tradeoff, or subject to some sort of cosmic balance or fairness.
          Sometimes the very rich are also happy, smart, beautifull, wonderfull people.
      Sometimes the poor are ugly idiot assholes who desrve worse than thier short miserable lives.
          Life aint fair and sometimes you can have your cake and eat it too.

      Mycroft
    • by vertinox (846076)
      Once the old people can no longer look after themselves, they will be put into a care home, and kept alive for decades using modern technology.

      Ummm... If you were 80 years old and had the body and the mind of a 20 year old... Well... I don't think there is going to be a need for you to retire... EVER!

      Maybe a scary prospect having to keep a day job for the next 1,000 years, but I'd take that over having my mind rotting away and me crapping myself for a good 30 years in some rest home.
  • by Slashdiddly (917720) on Friday September 08, 2006 @12:38AM (#16064191)
    So, if I understand it correctly, if we were able to prevent cancer (by finding a root cause or otherwise), then that would change the risk equation balanced by this gene. This gene could then be turned off, the effect of which would be unabated rejuvenation of body organs, leading to indefinite lifespan.
    • by Descalzo (898339)
      The human body breaks down, it doesn't wear out. That is to say, we don't die, cancer kills us. We don't die, our heart kills us. It reminds me of the deacon's one-hoss shay [williamson-labs.com]. We get rid of all the things that kill us, and then what will happen?
    • by Khyber (864651)
      no indefinite lifespan. RTFA, or even TFS which states that "the knockout mice didn't live any longer than the normal mice." This isn't rejuvenation at any level, this is prevention.
    • Re: (Score:3, Insightful)

      by Peaker (72084)
      Cancer is not a disease.

      It is a whole class of diseases. There are many many types of cancer, each with its own causes, mutations or cell environment changes.

      If there is a "cure for cancer" its going to be a hell of a lot of cures.
      • by Noehre (16438)
        I find that almost nobody understands that there is no "cure for cancer."

    • by deuterium (96874)
      This was my immediate thought. If medical science can devise much more targeted and refined methods of removing cancer, it would enable us to turn off this broad, overkill method. The same goes for other systems. Overactive immune response is shaping up to be a much bigger culprit in heart disease and depression than previously thought. If we can modulate the immune response down while mitigating the legitimate hazards they attack, we could alleviate the systemic damage caused by the inflammation. Now that
    • So then, perhaps if the recent breakthrough on white-blood cell modifications to target cancerous cells can be improved, then we'll be in good shape?
    • by geekoid (135745)
      no, just a really healtth internal organs for your life.
      Not an expanded life.

      Imortalty would be nice, but this is good to.
  • by Ungrounded Lightning (62228) on Friday September 08, 2006 @12:53AM (#16064221) Journal
    "There is no free lunch -- we are all doomed," Dr. Sharpless said. But he quickly modified his comment by noting that a calorically restricted diet is one intervention that is known to increase lifespan and reduce cancer, at least in laboratory mice.

    Unfortunately, caloric restriction only raises the life expectancy of rodents in the laboratory, not when exposed to natural conditions. While it reduces risk of cancer, it also drastically reduces the effectiveness of the immune system at fighting off infection (and the resulting stresses which, in turn, re-raise the cancer risk.)

    This has been known for decades by those educated in food & nutrition science. Unfortunately, the news has apparently not spread widely in other fields.

    So while there is a strategy that reduces both of these TWO problems, it does it at the cost of creating a third. Again no free lunch.

    Though there may be useful insights from the lab results, life extention strategies based on caloric restriction in the real world seem unlikely to be successful.
    • ... it also drastically reduces the effectiveness of the immune system at fighting off infection (and the resulting stresses which, in turn, re-raise the cancer risk.)

      (Note that the main problem, of course, is death and disability from the infections, not the marginal cancer re-increase.)
    • Re: (Score:3, Funny)

      by zCyl (14362)
      Unfortunately, caloric restriction only raises the life expectancy of rodents in the laboratory, not when exposed to natural conditions.

      Well I know plenty of people who spend all day in the lab and barely take any time off to eat. But I'm guessing this will not increase their lifespan much. :)
    • by Steeltoe (98226)
      Unfortunately, caloric restriction only raises the life expectancy of rodents in the laboratory, not when exposed to natural conditions. While it reduces risk of cancer, it also drastically reduces the effectiveness of the immune system at fighting off infection (and the resulting stresses which, in turn, re-raise the cancer risk.)

      This has been known for decades by those educated in food & nutrition science. Unfortunately, the news has apparently not spread widely in other fields.


      It all depends how you
      • by 7-Vodka (195504)
        No kidding I would be so extremely depressed on a caloric restricted diet that I'd probably take my own life. I'll take fine foods, sex, booze, drugs and exercise over adding a few extra years to the shit end of my life anyday.
      • However, key to a good diet is enough proteins. Too many young girls start eating only pizza, salads, pasta, etc. and get malnutrition as a result from going "veggie". A veggie-diet without enough proteins and variation is no veggie-diet in my book. Correct veggie recepees have been used for thousands of years in the East, based on the Vedic Science of Ayur-veda (knowledge about life).

        Another risk is B12 deficiency - it is NOT found in plants, humans and their intestinal flora don't synthesize it, and perma
        • by Steeltoe (98226)
          I understand that the Vedic diets are NOT a protection against this. When they were developed in India the grain had enough insect parts and animal droppings to provide the required levels of B12. (Indeed, it still may.) But under US food inspection laws such contaminants are so vigorously suppressed (to prevent disease from bacteria and parasites) that these same diets become dangerously low in B12.

          There are many different thoughts on Ayurveda. Some ayurvedic doctors recommend eating meat (usually due to p
          • by Steeltoe (98226)
            I'd also just like to add, that vedic science, being a science based on logic, observation and testable results as well as intuitive knowledge (which maybe not so testable today because of our lack of consciousness), does not deal with dogmatic prescriptions: eat this, don't eat that. etc. This may change due to circumstances, so there's never one way to do things.

            It is originally more of a scientific description of cause and effect. That if you pull the trigger while pointing at your toe, it will hurt alot
    • by geekoid (135745)
      studies show that reducing caloric intake expands the life of humans as well.

      Don't confuse low caloric with malnutrition.

      Of course, if the only caloric intake you have is candy, pop and chips, you've missed the point.
  • Do these stemcells we're reading about include the telomeres [wikipedia.org] that act like "time to live" cell division countdown timers in cells' DNA? Do embryonic stemcells have more generations left in them than do more adult stemcells?
  • The summary says: However they didn't live any longer than normal mice.

    This isn't really surprising. I think that JSB Haldane provided the mathematical framework for showing why this is the case.

    First off, evolution is about amplification: the genes from an animal that has more children, younger, will be spread more than the genes from an animal that lives longer, so the successful strategy is to commit energy towards early maturation, rather than towards longevity.

    Secondly, and this is the part Haldane wo
    • by DrCode (95839)
      Sounds like something a friend told me he learned in medical school: Once we cure cancer and heart disease, people may very well start dying from even nastier problems.

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