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Age A Byproduct of Cancer Defense?
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.
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
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."
Actually, I was trying to be Insightful, not Funny.
"Nuts to your white mice" -- Zaphod Beeblebrox
Strange women lying in ponds distributing swords is no basis for a system of government.
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?
Job? I don't have time to get a job! Who will sit around and bitch about being broke and unemployed then?
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?
It hurts when I pee.
Is Alex Chiu's miracle Eternal Life Device going to give me cancer now? I can't believe it! The man is a fraud!
This goes against everything I've ever been taught. I'm beginning to put more and more stock in that time cube thingy every day....
"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!
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...
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?
"when the going get's wierd the wierd turn pro." -hst
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?
"Moving through the masses like a fish through water." syrup
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.
she's been 35 years old for about 10 years now.
Bill Clinton: Pimp we can believe in. - The Shirt!!!
It has now been discovered that the leading cause of cancer in labratory mice is.....
Scientists!
Please take note and live you life accordingly.
Papa Legba come and open the gate
You could think of death as the end of cell growth, whereas cancer is cell growth gone out of control.
Silly mortals! I propose that whomever designed us intentionally created these apparent paradoxes to force all doubters to eventually believe.
"What is the sound of one belly slapping?"
It isn't that hard to create the proverbial. Longevity Vaccine. How effective it is, however, is a different story. What if we all had injections (or a gland of some type implanted) that gave us all the minerals/vitamins we needed every day, so all we'd have to do is eat a bit to take up some nutrients? Wouldn't that make us live longer? We could have that by the end of this year or next if we wanted.
Job? I don't have time to get a job! Who will sit around and bitch about being broke and unemployed then?
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.
:)
Ancient texts with people thousands of years old are explained by the lack of digital watches.
:)
Seriously, its the product of an oral tradition. Ever play the telephone game?
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...
Please consider making an automatic monthly recurring donation to the EFF
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.
.
I think we've pushed this "anyone can grow up to be president" thing too far.
The earlier report has been discounted.
Shark cancer, however, is uncommon.
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.
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.
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: "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."
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.
GPL Deconstructed
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.
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.
"I may not have morals, but I have standards."
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.
___
It's the end of my comment as I know it and I feel fine.
That report's logic is fallacious. Consider the case of case of two similar individuals: one who lives to a to a bit less than 65 in 1940, and another who lives a bit past 65 in 1990. People whose life expectencies have increased from below 65 to just above 65 will reduce "average life expectancy of people at age 65" just by their living past 65. Their negative life expectancy past 65 in 1940 was not counted, but there marginally positive life expectancy past 65 in 1990 is.
That was a sarcastic comment.
Strange women lying in ponds distributing swords is no basis for a system of government.
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.
Remember "Bring 'em on"? *sigh
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.
This is also called sibling altruism and consistent with selfish gene theory.
Life is complex...
Ain't it though? I'd like to point out that the relatively simple mechanism of evolution gives rise to that wonderful complexity.
There is no trap so deadly as the trap you set for yourself
-Raymond Chandler, The Long Goodbye
clotho wove the string, lachesis measured the string, atropos cut the string.