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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.
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.
The Kruger Dunning explains most post on
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."