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Why We Fall Apart
DM_NeoFLeX writes "An article in the September 2004 IEEE spectrum raises some interesting ideas comparing aging in organic organisms to aging in Electronic/Electrical systems. From the article: "The [reliability theory] is so general it can be applied to understanding aging in living organisms...In the ways that we age and die, we are not so different from the machines we build.""
According to the article the fountain of use is temporarily unavailable.
shucks.
I'll post the article for anyone else having problems with the site:
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Cryptic, i'll give you that, but I expect they will find out the question to the answer soon enough.
#hostfile 0.0.0.0 primidi.com 0.0.0.0 www.primidi.com 0.0.0.0 radio.weblogs.com
that human aging can be modeled according to reliability theory that applies for machinery. The difference is, while machines start off 'perfect' (You don't buy a multi cpu system with 2 cpus dead on arrival) the human body 'ships' as a redundant system with many failures already in place.
Engineering's reliability theory explains human aging
By Leonid Gavrilov & Natalia Gavrilova
CHILDHOOD IS A SPECIAL TIME INDEED. If only we could maintain our body functions as they are at age 10, we could expect to live about 5000 years on average. Unfortunately, from age 11 on, it's all downhill!
The problem is that our bodies deteriorate with age. For most of our lives, the risk of death is increasing exponentially, doubling every eight years. So, why do we fall apart, and what can we do about it?
Many scientists now believe that, for the first time in human history, we have developed a sophisticated enough understanding of the nature of human aging to begin seriously planning ways to defeat it. These scientists are working from a simple but compelling notion: the body, far from being a perfect creation, is a failure-prone, defect-ridden machine formed through the stochastic process of biological evolution. In this view, we can be further improved through genetic engineering and be better maintained through preventive, regenerative, and antiaging medicine and by repairing and replacing worn-out body parts. In short, the rate at which we fall apart could be decreased, maybe even to a negligible level.
The quest to understand and control aging has led us, two biologists, to draw inspiration from what might seem an unlikely source: reliability engineering. The engineering approach to understanding aging is based on ideas, methods, and models borrowed from reliability theory. Developed in the late 1950s to describe the failure and aging of complex electrical and electronic equipment, reliability theory has been greatly improved over the past several decades. It allows researchers to predict how a system with a specified architecture and level of reliability of its constituent parts will fail over time.
The theory is so general in scope that it can be applied to understanding aging in living organisms as well. In the ways that we age and die, we are not so different from the machines we build. The difference, we have found, is minimized if we think of ourselves in this unflattering way: we are like machines made up of redundant components, many of which are defective right from the start.
THE RELIABILITY ENGINEERING APPROACH to human aging provides a common scientific language and general framework for scientists working in different areas of aging research. It helps them knock down the barriers that specialists have constructed and allows them to understand each other better.
Most important, it helps define more clearly what aging is. In reliability theory, aging is defined through the increased risk of failure [see "Terms To Know"]. More precisely, something ages if it is more likely to fall apart tomorrow than today. If the risk of failure does not increase as time passes, then there is no aging in terms of reliability theory.
By looking closely at human aging data, we can find a striking similarity between how living organisms and technical devices age and fail. In both cases, the failure rate follows a curve shaped roughly like a bathtub [see graph, "Stages of Life"]. The curve consists of three stages, which we call the working-in or infant-mortality, normal-working, and aging periods. Engineers do not often see all three stages in a single product--infant mortality is a somewhat avoidable warranty disaster and most electronics become obsolete well before they would start to age--but the bathtub curve is still illustrative of the way things fail in general.
At the start of a machine's life, the working-in period, failure rates are high; they then decrease with age. During this period, defective components fail. For example, the risk of a new microprocessor failing is often higher at the very start, because of defects in the silicon or because small variations in the fabrication process lead to circuits that give out under the initial stress of operation. The same working-in period exists early in life for most living organisms, includ
Why we fall apart is simple.
Sex.
If we reproduced by mitosis, we'd be effectively immortal, even better, we'd get up to 2^n chances to survive in the nth generation of offspring.
Given our specific method of sexual reproduction, you have basically one life to live. Anything that breaks down, any bad mutations (cancer), and that's it. Plus, you have to die to make room for your offspring, which I guess happens with protists and such bacteria as reproduce mainly asexually, but the offspring who you are making room for are arguably you.
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A general theory of ageing can sound good, but can it be applied?
If it could, then the first place where even a partial application should show some effects and some value would be in medicine.
I don't see any signs of applicability there, and it looks as if there is a good reason for that. As the article admits, biological bodies are made up of a vast number of bits and pieces all doing their specific thing. When each goes wrong it produces effects which can only be countered, if at all, by doing something specific to engage with the bit that has gone wrong.
General theory may not be able to provide any general help when there appears to be no general problem, only a lot of specific ones.
-wb-
Scientific American had a most excelent article on this years ago, it's still there...if you subscribe.
Nothing in the world is more dangerous than sincere ignorance and conscientious stupidity.
The article brings up some interesting points, but it brushes with a much to large a brush. Forinstance, for many functions cells are supposed to die to get a working system, unlike where the article suggets these deaths are a symptom of preliminary failure. Which is thus not the case.
The interesting part is more how the failure rate can be predicted by a kind of standard failure rate curve, as well as noting that humans start off with flaws from the start. With large redundancy to catch errors.
However, this doesn't really help much for solving aging though I believe, while it's certaintly nice to show it all falls within a certain class of failures. It doesn't tell you how to reduce it, thus for people looking for longer lifespans, move to the places with the real action and engineering.
Quickshot
I'm not sure if the texts are available to everyone else (I'm reading from a university with a site-license, I think), but here are two good articles published in Nature some time ago. Why do we age? (Thomas B. L. Kirkwood, Steven N. Austad)
Abstract Full Text
Oxidants, oxidative stress and the biology of ageing (Toren Finkel, Nikki J. Holbrook)
Abstract Full text
reason defies logic
Actually sex evolved because of one inherent problem in mitosis - accumulated errors. Any individual cell that relies on duplicating its genome each generation also duplicates mutations which eventually accumulate. The odds of another spontaneous mutation correcting the error is virtually nil. However, the odds of two cells having exactly the same errors is also very low. Thus cells that are able to cut and paste from each others genome (have sex) are able to repair themselves and have a selective advantage over those that don't.
This, not diversity (as many people think) is the driving force for origin of sexual reproduction. The evolutionary biologist John Maynard Smith explains this in much more detail in his book "The evolution of sex" which can be googled for synopses.
To get back on topic, he also has published quite a few good papers on the evolutionary basis of ageing which can be summed up as follows. Even the most fit organism will eventually die by some unlucky event such as being hit by lightning or eaten by a lion. If you can increase your fitness in the short term even at the price of shortening your life you can do better overall. For example suppose that large breasts, while causing back problems later in life also increase the odds of finding a mate. If the odds of being eaten by a lion make it unlikely that any female will live past 40 then it becomes advantageous to have big breasts even if it shortens your potential lifespan.
Of course none of this tells us how to lengthen our lives or anything about the mechanism of ageing but it does tell us how it was selected for.
You don't buy a multi cpu system with 2 cpus dead on arrival
I suspect IBM's eFuse is at least partially a way to improve yields. If we don't need 'perfect' electronics they might get cheaper. Linux can work around bad RAM chips, too.
My God, it's Full of Source!
OUTSIDE_IP=$(dig +short my.ip @outsideip.net)
The article says we have a lot of defective components (brain cells) from the get-go. Being extra careful in very early development (taking folic acid) can prevent a lot of those defective components (folic acid in the first month of pregnancy reduces the chance of neural tube defects).
Autism is marked excess brain cells and low blood flow in the connections between brain cells. Perhaps the excess brain cells just take up too much room, so the connections are either cramped or not there.
Evolution takes into account that a large portion of our initial brain cells won't work. Perhaps folic acid makes too many work, leading to too many brain cells, not enough connections, and autism? Folic acid was recommended to pregnant women in 1992 and made an additive to wheat in 1998. Autism rose exponentially then. It was rising exponentially for a decade before that, too, though. Autism now affects 1 in 150 children (detectable at age 2), while neural tube defects affect 1 in 5000 (detectable when 3 months pregnant) (they were 32% more common before folic acid was added to wheat).
So, a theory. Fodder for future research. If this theory happens to be true, supplementing wheat with folic acid should be stopped.