Here's my "Universal senescence" essay. It can be found on the web - at: --> http://alife.co.uk/misc/universal_senescence/ <-- To offer a brief synopsis: I suggest that the tendency of many sorts of object to fall to bits represents a general rule of complex systems. This rule is distinct from the second law of thermodynamics, and - unlike the second law - can be applied to open systems. The aging of biological organisms represents a particular instance of this rule. I think the idea is a pretty obvious one - and I'd be suprised if it originated with me. Any references to prior work would be gratefully received. Universal senescence ==================== An increasing tendency to fall to bits -------------------------------------- A naive interpretation of the second law of thermodynamics describes it as an increasing tendency of things to fall to bits as time passes. This isn't what the second law /actually/ says - but the idea /does/ have a sort of intuitive appeal - since it /does/ seem that many common objects /do/ eventually fall to bits. Could it be that this tendency deserves to be described as a universal aspect of complex systems? Occasional disintegration ------------------------- Complex adaptive systems follow lawful behaviour just like other objects do - though in many cases the rules they follow may not yet be entirely clear. These laws are best regarded as /additional/ rules of thermodynamics designed to deal with complex adaptive systems. By far the most obvious rule is the statment of how such systems affect entropy - which I have previously attempted to describe [snip reference to my "bright light" essay]. Here I would like to propose that the phenomenon of senescence is a common feature of a range of complex adaptive systems - and can be characterised by the occasional disintegration of such systems. The suggested rule is different from the second law of thermodynamics. That also suggests that complex systems tend to fall to bits - but it can only be used to make that prediction in closed environments. The proposed rule does not have that restriction - the intention is that it can also be applied to self-organising systems in open environments. Subjects of senescence ---------------------- Probably the most familiar senescing objects are biological organisms. Senescence is common in biology, and - among more complex organisms - it is / nearly/ universal. However, other sorts of system also exhibit senescence. In particular, complex pieces of machinery also exhibit limited lifespans - and often have lifespan curves suggesting that progressive degradation followed by catastrophic collapse is occurring - the signature of senescence. To gives some concrete examples, I claim this is true of cars, houses, computers, stereos, clocks, motors, hyraulics and companies. Causes of senescence -------------------- Why do complex things tend to fall to bits? It appears that there are many reasons - and that different ones can apply to different sorts of system: - *Environmental damage* - complex systems are exposed to damage from their environment. Often no individual bit of damage it worth repairing - but the cumulative long-term effects of the damage is that the system degrades over time - and eventually stops functioning. - *High repair costs* - complex systems are often difficult to repair. They can need specialist knowledge to locate the problem and specialised tools to fix it. This can mean that some problems are more cheaply fixed with a new model. - *High cost of durable components* - one simple strategy aimed at preventing things from falling to bits is to build them out of strong, durable materials. Unfortunately, these are often expensive and difficult to machine. - *Planned senescense* - some things fall to bits simply because they were / designed/ to fall to bits. A broken piece of machinery often creates demand for a replacement. Sometimes, there is little incentive for manufacturers to build long-lived components - since doing so destroys their future market. - *Disposable soma* - reproductive and maintenance processes can compete for resources. Reproducing early has many advantages - and is consequently somatic tissue maintenance programs do not receive sufficient investment to support indefinite survival. - *Antagonistic pleiotropy* - this is the idea that genes that /delay/ the expression of other deleterious genes are favoured. More generally, it suggests that genes may be favoured if they have beneficial early effects but deleterious later effects. - *Cumulative parasite load* - systems accumulate parasites faster than they succeed in ridding themselves of them. The result is progressive loss of function - followed by catastrophic collapse. - *Obsolescence* - in a rapidly changing environment systems may be discarded because they are out of date. This effect is commonly seen in computer systems - but also arises among organisms who are in combat with parasites which evolve to adapt to common host genotypes - where older genotypes are more likely to encounter parasites that have evolved the capability of exploiting their resources. The role of complexity ---------------------- Complex systems are often more expensive to replace than corresponding simpler ones. This makes replacing them more expensive. However, they also have more different bits to go wrong. It is harder to identify the cause of problems - and it typically require an engineer with more spare parts and specialised knowledge to fix. The case of companies --------------------- The theory of "universal senescence" suggests that companies exhibit senescence. However - as far as I am aware - this theory has never been tested. It should not be too difficult to test - and the results may be of some interest. In theory, a number of mechanisms of senescence ought to apply to companies. In particular, companies: - ...are vulnerable to environmental damage; - ...can grow large, become unable to manoeuvre properly - and then crash; - can accumulate garbage in their components in the form of well-disguised dud employees or poorly-designed systems - in a way that makes the problem difficult to repair; - ...can reach a size where they become attractive to predators - and vulnerable to being swallowed up and destructively digested - in a merger with a larger company; - ...that have been around longer have increased chances of attracting parasites - either agents inside the company who do not have its best interests at heart or externally- run protection rackets - and the like. Companies are an interesting case - since most companies are still very young - and have not directly descended from other senescing companies. Thus - unlike most complex organisms with substantial genomes - they are not "built to senesce". However the theory suggests that they will - nontheless - exhibit senescence - and that the effect will /probably/ be big enough and visible enough to be evident from their lifespan curves. Unfortunately, companies /also/ exhibit the equivalent of "large infant mortality" - and the effect is a substantial one. This may act to obscure the effect of senescence over the lifespan of the majority of companies. This may make company senescence more difficult to detect. Modularity ---------- Can senescence be defended against using modularity? It seems that - by using a modular design and "unit tests" that failures in individual modules can be identified, isolated and repaired - without large-scale failures necessarily being involved. Modularity is - without doubt - a major weapon aganist senescence. However there are a few drawbacks: - Modularity is a design constraint that conflicts with efficiency. This is probably why (for example) we don't have twelve hearts - one heart simply works better; - Unit tests - and the time spent executing them - also represent something of a burden; Also, modularity doesn't /completely/ fix the problem. There is still the issue of connections between the modules. These themselves senesce - and may not be so easy to diagnose problems in. There are also the possibilty of unplanned-for failure scenarios within modules - failures that cause unit tests to mis-report, failures that knock out whole modules - and so on. Exceptions ---------- There are a few complex organisms that don't senesce. How do those fit into the idea of "universal senescence"? Not very well, it must be said. However, they are not very common - and the theory doesn't suggest that /all/ long- lived organisms must senesce - it merely provides reasons why most of them might. One way to ensure you have good repair mechanisms is to make sure finding a mate and reproducing is very, very difficult - so that it can take a very, very long time. Under such circumstances, selection will favour very long lifespans. I am happy to agree that selection is powerful enough to produce organisms with extremely long lifespans. However I am inclined to doubt whether that sort of selection will ever be acting very frequently. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
Tim Tyler wrote: > [snip} > Here I would like to propose that the phenomenon of > senescence is a common feature of a range of complex > adaptive systems - and can be characterised by the > occasional disintegration of such systems. > The earth's biosphere, a vast, complex adaptive system, has lasted for some 3.5 billion years without senescing. It fact, it has grown more complex as the life and ecosystems within it have evolved, and has been able to continually renew itself. Of course, it could be argued that one of its subcomponents -- the human one -- is malfunctioning like a cancer and may bring the rest of the biosphere to an end someday. [snip] [email protected]
Tim Tyler <[email protected]> wrote in message news:<[email protected]>... > Here's my "Universal senescence" essay. > > It can be found on the web - at: > > --> http://alife.co.uk/misc/universal_senescence/ <-- > > To offer a brief synopsis: > > I suggest that the tendency of many sorts of object to > fall to bits represents a general rule of complex systems. > [snip] Senescence is common in biology, and - among more > complex organisms - it is / nearly/ universal. > > However, other sorts of system also exhibit senescence. > [snip] Exceptions > ---------- > There are a few complex organisms that don't senesce. How > do those fit into the idea of "universal senescence"? > > Not very well, it must be said. However, they are not very > common - and the theory doesn't suggest that /all/ long- > lived organisms must senesce - it merely provides reasons > why most of them might. > > One way to ensure you have good repair mechanisms is to > make sure finding a mate and reproducing is very, very > difficult > - so that it can take a very, very long time. > > Under such circumstances, selection will favour very long > lifespans. > > I am happy to agree that selection is powerful enough to > produce organisms with extremely long lifespans. However I > am inclined to doubt whether that sort of selection will > ever be acting very frequently. The glaring exception to your rule of universal senescence of complex I think that this is one of those situations in which the explanation of the exception "proves the rule". Given your oft stated beliefs that incorporate this into your essay.
dkomo <[email protected]> wrote or quoted: > Tim Tyler wrote: > > Here I would like to propose that the phenomenon of > > senescence is a common feature of a range of complex > > adaptive systems - and can be characterised by the > > occasional disintegration of such systems. > > The earth's biosphere, a vast, complex adaptive system, > has lasted for some 3.5 billion years without senescing. > It fact, it has grown more complex as the life and > ecosystems within it have evolved, and has been able to > continually renew itself. [...] The version of the essay on my web page discusses the case of the earth's biosphere (under "Forces opposing senescence" and "The Earth"). My conclusions about how it fits into the theory are not easy to express concisely - but I suggest that the biosphere is still early on in its developmental process. In particular, it has not yet learned how to reproduce - and so is best regarded as not yet being reproductively mature. On http://alife.co.uk/misc/universal_senescence/ I suggest that the biosphere's apparent lack of a tendency for the probability of large-scale catastrophic failure to rise as time passes is likely is likely to come to an end when it ultimately faces competiton from its offspring after reproducing. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
Jim Menegay <[email protected]> wrote or quoted: > Tim Tyler <[email protected]> wrote: > > Here's my "Universal senescence" essay. > > > > It can be found on the web - at: > > > > --> http://alife.co.uk/misc/universal_senescence/ <-- > > > > To offer a brief synopsis: > > > > I suggest that the tendency of many sorts of object to > > fall to bits represents a general rule of complex > > systems. [...] > > Exceptions [...] > The glaring exception to your rule of universal senescence > of complex I'm sceptical ;-) > I think that this is one of those situations in which the > explanation of the exception "proves the rule". Given your > oft stated beliefs that > incorporate this into your essay. of an error-correcting mechanisms - if I were forced to choose between that theory and the "Red Queen" theory of Hamilton/Jaenike/Van then the Queen would get my vote. A possibility for the reason why I failed to mention the possibility of phylogeronty (species senescence) is that I had already written a previous essay expressing my approval of the idea: http://alife.co.uk/misc/species_senescence/ ...and did not want to repeat myself too much. Unfortunately, this essay can be criticised on the grounds that it is basically armchair speculation. Species senescence is a testable theory - but a reasonable empirical test would probably represent some work. Until this is done, hand-waving arguments about species attracting parasites as they age - and about how the "disposable soma" arguments about prioritising reproduction over longevity are likely to be a consequence of species- level selection (assuming that exists) are the sort of thing I can offer. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
Tim Tyler wrote: > > dkomo <[email protected]> wrote or quoted: > > Tim Tyler wrote: > > > > Here I would like to propose that the phenomenon of > > > senescence is a common feature of a range of complex > > > adaptive systems - and can be characterised by the > > > occasional disintegration of such systems. > > > > The earth's biosphere, a vast, complex adaptive system, > > has lasted for some 3.5 billion years without senescing. > > It fact, it has grown more complex as the life and > > ecosystems within it have evolved, and has been able to > > continually renew itself. [...] > > The version of the essay on my web page discusses the case > of the earth's biosphere (under "Forces opposing > senescence" and "The Earth"). > > My conclusions about how it fits into the theory are not > easy to express concisely - but I suggest that the > biosphere is still early on in its developmental > process. In particular, it has not yet learned how to > reproduce - and so is best regarded as not yet being > reproductively mature. > > On http://alife.co.uk/misc/universal_senescence/ I suggest > that the biosphere's apparent lack of a tendency for the > probability of large-scale catastrophic failure to rise as > time passes is likely is likely to come to an end when it > ultimately faces competiton from its offspring after > reproducing. Ok, I need some more time to read the essay out there, but in the meantime, since turnaround time on sbe is so long, let me put my next question regarding your idea of complex adaptive systems having inherent senesence: why don't bacteria senesence? Aren't they complex adaptive systems (simple relative to others perhaps, but complex enough to be alive)? In previous discussions about aging, I favored the idea that senesence is *programmed* into multicelluar eukaryotic life by evolution, and hence is not something that is necessarily an intrinsic property of life or complex adaptive systems in general. [email protected]
On 2004-03-10, Tim Tyler <[email protected]> wrote: > Here's my "Universal senescence" essay. > > It can be found on the web - at: > > --> http://alife.co.uk/misc/universal_senescence/ <-- > > To offer a brief synopsis: > > I suggest that the tendency of many sorts of object to > fall to bits represents a general rule of complex systems. > > This rule is distinct from the second law of > thermodynamics, and - unlike the second law - can be > applied to open systems. > > The aging of biological organisms represents a particular > instance of this rule. > > I think the idea is a pretty obvious one - and I'd be > suprised if it originated with me. Any references to prior > work would be gratefully received. > > Universal senescence [snip] Nice article, and I'm sympathetic to its general thesis. However, there are some challenging exceptions. For examples, some reptiles, e.g. tortoises, are very long- lived. If it be objected that these have a slow metabolism and therefore age very slowly, what about birds such as parrots? Churchill's parrot is still alive at the age of 103. And, very significantly, a centenarian parrot looks no different from a young one. Does the theory apply more to mammals than to birds or reptiles? AC -- Using Linux GNU/Debian - Windows-free zone http://www.acampbell.org.uk (book reviews and articles) Email: replace "www." with "[email protected]"
Anthony Campbell <[email protected]> wrote or quoted: > On 2004-03-10, Tim Tyler <[email protected]> wrote: > > Here's my "Universal senescence" essay. > > > > It can be found on the web - at: > > > > --> http://alife.co.uk/misc/universal_senescence/ <-- [snip] > Nice article, and I'm sympathetic to its general thesis. > However, there are some challenging exceptions. For > examples, some reptiles, e.g. tortoises, are very long- > lived. If it be objected that these have a slow metabolism > and therefore age very slowly, what about birds such as > parrots? Churchill's parrot is still alive at the age of > 103. And, very significantly, a centenarian parrot looks > no different from a young one. Does the theory apply > more to mammals than to birds or reptiles? The animals and plants which exhibit "negligible senescence" are mostly - I suspect - the product of selection for long lifespans - and good self-repair mechanisms. I suspect that the force driving such selection is most frequently difficulty in reproduction - caused by problems finding a mate, difficulty in dispersing seeds to other fertile areas - and so on. It does seem that such selection can prolong natural lifespans to a very large extent. Selection for long lifespans can be very effective - it seems - but the effect seems destined to be confined to rare species - or species in obscure habitits. Regarding how far such longevity can be taken: http://www.research.utas.edu.au/reports/1998/clone.htm ...is an article about the world's oldest known living thing. It weighs in at 43,600 years old. A vegetative growth pattern which allows an individual to spread over a wide area - combined with an effective defense against predation seems like it has been a fairly successful strategy for living for a long time in that case. It is interesting to note that the plant is sterile. Maybe by only appearing in one place on the planet, it manages to avoid the attention of most parasites and predators. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
dkomo <[email protected]> wrote or quoted: [http://alife.co.uk/misc/universal_senescence/] > Ok, I need some more time to read the essay out there, but > in the meantime, since turnaround time on sbe is so long, > let me put my next question regarding your idea of complex > adaptive systems having inherent senesence: why don't > bacteria senesence? Aren't they complex adaptive systems > (simple relative to others perhaps, but complex enough to > be alive)? The "simplicity" is significant in the case of bacteria. *Complex* systems are the ones which have the most difficulty building self-repair mechanisms - and the relative simplicity of bacteria means that they have fewer parts to go wrong - and that environmental damage stands a high chance of killing them outright - and a low chance of merely damaging one of their components. However, my answer to the question is to doubt the premise. It is commonly believed that many small micro-organisms don't senesce and die - but the view is mistaken. They /do/ senesce - albeit slowly. Follow an individual bacterium through multiple cell divisions (choosing at random when it divides) and after a while the bacterium you are looking at will die. Do this lots of times, plot the resulting lifespans on a graph - and bacteria will be seen to have infant mortality and senescence like most other organisms. Senescence will arise because not *all* mutations and environmental damage that can happen to a bacterium are neutral or fatal. Some are deleterious - and these will accumulate and ultimately kill their bearers - resulting in an increased probability of death as time passes. However, perhaps most bacteria will die of starvation, asphyxiation problems dividing or accidents before they have had much time to senesce. No doubt the next point will be about bacterial colonies. Even if individual bacteria age and die isn't the *colony* potentially-immortal - and lacking in senescence? This is much more reasonable - at least for planet-spanning bacterial populations - but I will not admit it ;-) Instead of recognising their indefinite longevity I have a prediction of doom for most of today's bacterial colonies. Though there are a few ocean-dwellers which may have lasted reasonably well from ancient times to the present day, I reckon - in the next billion years - they will all be effectively wiped out - and replaced by engineered creations - probably using different genetic substrates and phenotype- construction technology. Will we *ever* see the bacterial equivalent of a "wheel" - i.e. a fairly simple self-reproducing design that beats off all comers within its niche - and lasts indefinitely? It's a difficult question - and at the moment I'm not prepared to rule the possibility out - but I suspect we are talking about far-future events here. > In previous discussions about aging, I favored the idea > that senesence is *programmed* into multicelluar > eukaryotic life by evolution, and hence is not something > that is necessarily an intrinsic property of life or > complex adaptive systems in general. Senesence /is/ (to some extent) programmed into multicelluar life by evolution - but that doesn't mean it is not also an intrinsic property of complex adaptive systems. The latter effect is best seen as the underlying cause - and the adaptations which influence the aging rate in complex organisms are a response to it. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
in article [email protected], dkomo at [email protected] wrote on 3/11/04 10:10 PM: > Ok, I need some more time to read the essay out there, but > in the meantime, since turnaround time on sbe is so long, > let me put my next question regarding your idea of complex > adaptive systems having inherent senesence: why don't > bacteria senesence? Aren't they complex adaptive systems > (simple relative to others perhaps, but complex enough to > be alive)? I am very skeptical of the claim that bacteria don't senesce, because I share Tim's view that every kind of dynamical system in the universe must senesce. However, this also makes me very interested in any evidence that might exist supporting the claim that bacteria don't senesce. It would dramatically alter my views if I could be convinced that this was even possible. So, what is the evidence that bacteria don't senesce? Guy
Guy Hoelzer wrote: > in article [email protected], dkomo at > [email protected] wrote on 3/11/04 10:10 PM: > > >>Ok, I need some more time to read the essay out there, but >>in the meantime, since turnaround time on sbe is so long, >>let me put my next question regarding your idea of complex >>adaptive systems having inherent senesence: why don't >>bacteria senesence? Aren't they complex adaptive systems >>(simple relative to others perhaps, but complex enough to >>be alive)? > > > I am very skeptical of the claim that bacteria don't > senesce, because I share Tim's view that every kind of > dynamical system in the universe must senesce. However, > this also makes me very interested in any evidence that > might exist supporting the claim that bacteria don't > senesce. It would dramatically alter my views if I could > be convinced that this was even possible. So, what is the > evidence that bacteria don't senesce? > > Guy > > you may or may not find this interesting, was at pubmed at found this: "1: Exp Gerontol. 2001 Apr;36(4-6):675-85. Related Articles, Links Does bristlecone pine senesce? Lanner RM, Connor KF. Institute of Forest Genetics, USDA Forest Service, Placerville, CA 95667, USA. We evaluated hypotheses of senescence in old trees by comparing putative biomarkers of aging in Great Basin bristlecone pine (Pinus longaeva) ranging in age from 23 to 4713 years. To test a hypothesis that water and nutrient conduction is impaired in old trees we examined cambial products in the xylem and phloem. We found no statistically significant age-related changes in tracheid diameter, or in several other parameters of xylem and phloem related to cambial function. The hypothesis of continuously declining annual shoot growth increments was tested by comparing trees of varying ages in regard to stem unit production and elongation. No statistically significant age-related differences were found. The hypothesis that aging results from an accumulation of deleterious mutations was addressed by comparing pollen viability, seed weight, seed germinability, seedling biomass accumulation, and frequency of putative mutations, in trees of varying ages. None of these parameters had a statistically significant relationship to tree age. Thus, we found no evidence of mutational aging. It appears that the great longevity attained by some Great Basin bristlecone pines is unaccompanied by deterioration of meristem function in embryos, seedlings, or mature trees, an intuitively necessary manifestation of senescence. We conclude that the concept of senescence does not apply to these trees. Publication Types: * Review * Review, Tutorial PMID: 11295507 [PubMed - indexed for MEDLINE] 07> g -- Europe will never be like America. Europe is a product of history. America is a product of philosophy. -- Margaret Thatcher (1925 - )
Tim Tyler wrote: > > dkomo <[email protected]> wrote or quoted: > > [http://alife.co.uk/misc/universal_senescence/] > > > Ok, I need some more time to read the essay out there, > > but in the meantime, since turnaround time on sbe is so > > long, let me put my next question regarding your idea of > > complex adaptive systems having inherent senesence: why > > don't bacteria senesence? Aren't they complex adaptive > > systems (simple relative to others perhaps, but complex > > enough to be alive)? > > The "simplicity" is significant in the case of bacteria. > *Complex* systems are the ones which have the most > difficulty building self-repair mechanisms - and the > relative simplicity of bacteria means that they have fewer > parts to go wrong - and that environmental damage stands a > high chance of killing them outright - and a low chance of > merely damaging one of their components. > > However, my answer to the question is to doubt the > premise. It is commonly believed that many small micro- > organisms don't senesce and die - but the view is > mistaken. They /do/ senesce - albeit slowly. > > Follow an individual bacterium through multiple cell > divisions (choosing at random when it divides) and after a > while the bacterium you are looking at will die. I'm not sure this makes sense. When a bacterium fissions into two bacteria, how do you tell which one is the mother cell and which the daughter by observing the action from the outside with a microscope? Remember that during mitosis the DNA is replicated, then divided equally between the two cells. Properly, the mother cell is the one with the original DNA after mitosis. I don't think you can easily determine this unless that DNA is marked in some way. If you say, are you kidding? Just keep a careful eye on the original cell during division and you should be able to keep track of that cell during the entire mitosis. Yes, but because of the way the DNA is replicated and partitioned between the two cells, what you thought was the original cell could receive the replicated DNA instead of the original DNA. And it is in this replicated DNA that most mutations occur. Thus, it is useless to speak of a single bacterium's lifespan or whether it senesces or not. This is not an observable. You have to talk of the senescence of the bacterial colony as a whole. > Do this lots of times, plot the resulting lifespans on a > graph - and bacteria will be seen to have infant > mortality and senescence like most other organisms. > Many bacteria will die, but the colony will remain healthy and thriving unless threatened by external conditions. > Senescence will arise because not *all* mutations and > environmental damage that can happen to a bacterium are > neutral or fatal. Some are deleterious - and these will > accumulate and ultimately kill their bearers - resulting > in an increased probability of death as time passes. > Maybe. But it is only those mutated bacteria that become sickly or infertile or die. The ones without mutations will more than make up for these because of the incredible "fertility" of bacteria. Consider a single healthy bacterium. When it fissions, one daughter cell receives the original DNA, the other the relicated DNA. Mutations will mostly occur in the replicated DNA. If any of these are deleterious, that daughter cell's line will be threatened. However, the other daughter cell will go on and start a line of descendants numbering in the billions and trillions. In the fullness of time that deleterious mutation didn't matter in the least. > However, perhaps most bacteria will die of starvation, > asphyxiation problems dividing or accidents before they > have had much time to senesce. > Even if most do, the colony can still thrive because of the high reproductive rate. > No doubt the next point will be about bacterial colonies. > Even if individual bacteria age and die isn't the *colony* > potentially-immortal - and lacking in senescence? > Already made this point. > This is much more reasonable - at least for planet- > spanning bacterial populations - but I will not > admit it ;-) > > Instead of recognising their indefinite longevity I have a > prediction of doom for most of today's bacterial colonies. > > Though there are a few ocean-dwellers which may have > lasted reasonably well from ancient times to the present > day, I reckon - in the next billion years - they will all > be effectively wiped out - and replaced by engineered > creations - probably using different genetic substrates > and phenotype-construction technology. > > Will we *ever* see the bacterial equivalent of a "wheel" - > i.e. a fairly simple self-reproducing design that beats > off all comers within its niche - and lasts indefinitely? > It's a difficult question - and at the moment I'm not > prepared to rule the possibility out - but I suspect we > are talking about far-future events here. > > > In previous discussions about aging, I favored the idea > > that senesence is *programmed* into multicelluar > > eukaryotic life by evolution, and hence is not something > > that is necessarily an intrinsic property of life or > > complex adaptive systems in general. > > Senesence /is/ (to some extent) programmed into > multicelluar life by evolution - but that doesn't mean it > is not also an intrinsic property of complex adaptive > systems. > > The latter effect is best seen as the underlying cause - > and the adaptations which influence the aging rate in > complex organisms are a response to it. > -- > __________ > |im |yler http://timtyler.org/ [email protected] Remove > lock to reply. [email protected]
Guy Hoelzer wrote: > > in article [email protected], dkomo at > [email protected] wrote on 3/11/04 10:10 PM: > > > Ok, I need some more time to read the essay out there, > > but in the meantime, since turnaround time on sbe is so > > long, let me put my next question regarding your idea of > > complex adaptive systems having inherent senesence: why > > don't bacteria senesence? Aren't they complex adaptive > > systems (simple relative to others perhaps, but complex > > enough to be alive)? > > I am very skeptical of the claim that bacteria don't > senesce, because I share Tim's view that every kind of > dynamical system in the universe must senesce. However, > this also makes me very interested in any evidence that > might exist supporting the claim that bacteria don't > senesce. It would dramatically alter my views if I could > be convinced that this was even possible. So, what is the > evidence that bacteria don't senesce? > > Guy Let's start here: http://www.chelationtherapyonline.com/articles/p190.htm I did a google on "bacteria immortal". Most of the web pages I came up with repeat the assertion "bacteria are immortal." I didn't have time to view all the pages. If you're looking for counter-evidence, I believe one article mentioned that *some* bacteria appear to age. I repeat what I said in today's followup to Tim Tyler: it doesn't make sense to talk about the lifespan of a single bacterium. We need to talk about bacterial colonies when discussing senescence. Consider the following experiment. Culture a colony of bacteria under carefully controlled conditions of light, temperature, humidity and nutrients. In other others, give them suckers the best of tender loving care to make sure they don't die from external causes. Periodically cull the colony so that it doesn't suffer from overcrowding. Now, do you really believe that after X number of months, years or decades you'll come into the lab some day and find the colony dead from no other apparent cause than old age? Also, if you believe this, do you also believe that all those many batches of Hela cells around the world which have been reproducing happily for decades now will begin someday dying of old age? Yes, I know I've switched the playing field to eukaryotes here, but the principle is the same as with bacteria. [email protected]com
D:- I repeat what I said in today's followup to Tim Tyler: it doesn't make sense to talk about the lifespan of a single bacterium. We need to talk about bacterial colonies when discussing senescence. JE:- Your argument is classically group selective. If you only look at populations of assumed Darwinian selectee's (fertile forms) then everything alive becomes immortal except that such grouped immortal forms can change over time into a different species. Where does this get you? Now you have to explain how this evolution occurs. To do this you have to acknowledge the fitnesses of the individuals concerned. Immediately you do this, the non senescent group as one selectee disappears before your very eyes. You have to acknowledge that Darwinian forms must live, reproduce and die. If you delete any one of these, then none the others make any sense. Regards, John Edser Independent Researcher PO Box 266 Church Pt NSW 2105 Australia [email protected]
On Mon, 15 Mar 2004 00:48:02 +0000 (UTC), dkomo <[email protected]> wrote: >Tim Tyler wrote: >> >> dkomo <[email protected]> wrote or quoted: >> >> [http://alife.co.uk/misc/universal_senescence/] >> >> > Ok, I need some more time to read the essay out there, >> > but in the meantime, since turnaround time on sbe is so >> > long, let me put my next question regarding your idea >> > of complex adaptive systems having inherent senesence: >> > why don't bacteria senesence? Aren't they complex >> > adaptive systems (simple relative to others perhaps, >> > but complex enough to be alive)? >> >> The "simplicity" is significant in the case of bacteria. >> *Complex* systems are the ones which have the most >> difficulty building self-repair mechanisms - and the >> relative simplicity of bacteria means that they have >> fewer parts to go wrong - and that environmental damage >> stands a high chance of killing them outright - and a low >> chance of merely damaging one of their components. >> >> However, my answer to the question is to doubt the >> premise. It is commonly believed that many small micro- >> organisms don't senesce and die - but the view is >> mistaken. They /do/ senesce - albeit slowly. >> >> Follow an individual bacterium through multiple cell >> divisions (choosing at random when it divides) and after >> a while the bacterium you are looking at will die. > >I'm not sure this makes sense. When a bacterium fissions >into two bacteria, how do you tell which one is the mother >cell and which the daughter by observing the action from >the outside with a microscope? Remember that during mitosis >the DNA is replicated, then divided equally between the two >cells. Properly, the mother cell is the one with the >original DNA after mitosis. I don't think you can easily >determine this unless that DNA is marked in some way. > >If you say, are you kidding? Just keep a careful eye on the >original cell during division and you should be able to >keep track of that cell during the entire mitosis. Yes, but >because of the way the DNA is replicated and partitioned >between the two cells, what you thought was the original >cell could receive the replicated DNA instead of the >original DNA. And it is in this replicated DNA that most >mutations occur. > >Thus, it is useless to speak of a single bacterium's >lifespan or whether it senesces or not. This is not an >observable. You have to talk of the senescence of the >bacterial colony as a whole. > This is not the way that DNA works. The replication is semi- conservative. That is, the two strands separate and each serves as the template for the new second strand. As a result, there is no "original" DNA vs. the "replicated" DNA. Each of the two new DNA molecules contains an original strand and a replicated strand. Nor is it true that one strand contains the genes -- some are on one strand, others are on the opposite strand. Mutations are equally likely in either daughter. Also, when a bacterium replicates, there is no telomere to shorten since the DNA is ordinarily a circle and there are no ends. Therefore there is no DNA senescence. Cell structures are in constant turnover (there are no independent mitochondria or plastids or other complex organelles). So at the time of binary fission, the "life" of each daughter cell is considered to start from zero; the clock is reset and the cells are rejuvenated by fission. Even eukaryotes that reproduce telomeres are reconstituted by passing through the gamete/zygote stage which resets the aging clock.
dkomo <[email protected]> wrote in message news:<[email protected]>... > [snip] Now, do you really believe that after X number of > months, years or decades you'll come into the lab some day > and find the colony dead from no other apparent cause than > old age? > > Also, if you believe this, do you also believe that all > those many batches of Hela cells around the world which > have been reproducing happily for decades now will begin > someday dying of old age? Yes, I know I've switched the > playing field to eukaryotes here, but the principle is the > same as with bacteria. > > [email protected] Actually, HeLa may be an exception that helps to prove Tim's rule, at least for eukariotes. I believe I have read that Henrietta is now famous because her carcinoma is (or was) the only immortal human cell culture. Almost all other attempts at metazoan cell cultures senesce after a few dozen generations, and die out.
dkomo <[email protected]> wrote or quoted: > Tim Tyler wrote: > > dkomo <[email protected]> wrote or quoted: > > [http://alife.co.uk/misc/universal_senescence/] > > > > > Ok, I need some more time to read the essay out there, > > > but in the meantime, since turnaround time on sbe is > > > so long, let me put my next question regarding your > > > idea of complex adaptive systems having inherent > > > senesence: why don't bacteria senesence? Aren't they > > > complex adaptive systems (simple relative to others > > > perhaps, but complex enough to be alive)? > > > > The "simplicity" is significant in the case of bacteria. > > *Complex* systems are the ones which have the most > > difficulty building self-repair mechanisms - and the > > relative simplicity of bacteria means that they have > > fewer parts to go wrong - and that environmental damage > > stands a high chance of killing them outright - and a > > low chance of merely damaging one of their components. > > > > However, my answer to the question is to doubt the > > premise. It is commonly believed that many small micro- > > organisms don't senesce and die - but the view is > > mistaken. They /do/ senesce - albeit slowly. > > > > Follow an individual bacterium through multiple cell > > divisions (choosing at random when it divides) and after > > a while the bacterium you are looking at will die. > > I'm not sure this makes sense. When a bacterium fissions > into two bacteria, how do you tell which one is the mother > cell and which the daughter by observing the action from > the outside with a microscope? As I said, by choosing at random when it divides. > Remember that during mitosis the DNA is replicated, then > divided equally between the two cells. Properly, the > mother cell is the one with the original DNA after > mitosis. I don't think you can easily determine this > unless that DNA is marked in some way. You /could/ mark the DNA - if you were *really* keen. > Thus, it is useless to speak of a single bacterium's > lifespan or whether it senesces or not. This is not an > observable. [...] I don't agree. You can get a good idea of a bacterium's average lifespan by holding a bacterial colony in steady state (by limiting its nutrient supply) - and measuring the death rate - and the size of the colony. Another approach would be to limit the nutrient supply - to a degree that allowed maintenance of a few individuals - but did not allow reproduction. Tricky, perhaps - but not impossible. > Maybe. But it is only those mutated bacteria that become > sickly or infertile or die. The ones without mutations > will more than make up for these because of the incredible > "fertility" of bacteria. > > Consider a single healthy bacterium. When it fissions, one > daughter cell receives the original DNA, the other the > relicated DNA. Mutations will mostly occur in the > replicated DNA. If any of these are deleterious, that > daughter cell's line will be threatened. However, the > other daughter cell will go on and start a line of > descendants numbering in the billions and trillions. In > the fullness of time that deleterious mutation didn't > matter in the least. I admit on my page that the ability to run an evolutionary process can sometimes protect systems from senescence. However I also suggest that self-reproducing systems which face competiton from their offspring are likely to senesce nontheless. That is normally the case with bacterial colonies - and so I would expect them to senesce - i.e. for the probability of them catastrophically failing to increase over time. If you fail to distinguish between a colony and its (genetically different and quite likely physically separated) offspring then you may not be able to identify death - but it (or an analogous process) is happening nontheless - whole strains of bacteria are continually being completely wiped out and replaced by their descendants. The most common mechanism that allows descendants to be fitter is disease resistance. Most bacteria are preyed upon by bacteriophages - and disease resistance continually offers advantages to new strains - and penalises established ones. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
in article [email protected], dkomo at [email protected] wrote on 3/14/04 4:48 PM: > Guy Hoelzer wrote: >> >> in article [email protected], dkomo at >> [email protected] wrote on 3/11/04 10:10 PM: >> >>> Ok, I need some more time to read the essay out there, >>> but in the meantime, since turnaround time on sbe is so >>> long, let me put my next question regarding your idea of >>> complex adaptive systems having inherent senesence: why >>> don't bacteria senesence? Aren't they complex adaptive >>> systems (simple relative to others perhaps, but complex >>> enough to be alive)? >> >> I am very skeptical of the claim that bacteria don't >> senesce, because I share Tim's view that every kind of >> dynamical system in the universe must senesce. However, >> this also makes me very interested in any evidence that >> might exist supporting the claim that bacteria don't >> senesce. It would dramatically alter my views if I could >> be convinced that this was even possible. So, what is the >> evidence that bacteria don't senesce? >> >> Guy > > Let's start here: > > http://www.chelationtherapyonline.com/articles/p190.htm I found no evidence whatsoever at this web site supporting the claim that there is such a thing as a cell that does not senesce. The term "immortal cell" used on this web site refers to a claim that some cell lineages are able to support cellular reproduction for a very long time (perhaps forever). I don't see the relevance. > I did a google on "bacteria immortal". Most of the web > pages I came up with repeat the assertion "bacteria are > immortal." I didn't have time to view all the pages. Me either. And I don't see what good it does for anyone to repeat the claim that bacteria can be immortal in the absence of any evidence or theoretical support for the claim. I remain interested in potential evidence for immortality or (more to the point) the absence of senescence for any kind of organism. I become a little more confident that such a thing does not exist every time an advocate of the immortality view fails in to produce evidence when challenged. > If you're looking for counter-evidence, I believe one > article mentioned that *some* bacteria appear to age. Thanks. I find this sort of evidence about as interesting as further support for the phenomenon of gravity, but it might be illuminating for someone who believes that all bacteria are immortal. > I repeat what I said in today's followup to Tim Tyler: it > doesn't make sense to talk about the lifespan of a single > bacterium. We need to talk about bacterial colonies when > discussing senescence. I agree that it is generally worthwhile to track lineages rather than focusing on individuals, but that does not mean that bacteria don't have lifespans. The confusion over the distinction between cell division and death can be circumvented by studying death in cells that is not confounded by cell division. I predict that preventing any cell from dividing will eventually reveal their paths to senescence. > Consider the following experiment. Culture a colony of > bacteria under carefully controlled conditions of light, > temperature, humidity and nutrients. In other others, give > them suckers the best of tender loving care to make sure > they don't die from external causes. Periodically cull the > colony so that it doesn't suffer from overcrowding. OK. This is done in labs every day. > Now, do you really believe that after X number of months, > years or decades you'll come into the lab some day and > find the colony dead from no other apparent cause than > old age? I would predict that this would be inevitable if you could track the experiment for long enough. I think that more work on the theory side needs to be done so that we can predict the temporal scale of life history for any particular kind of system before we try to do the experiment. > Also, if you believe this, do you also believe that all > those many batches of Hela cells around the world which > have been reproducing happily for decades now will begin > someday dying of old age? Yes, I know I've switched the > playing field to eukaryotes here, but the principle is the > same as with bacteria. The switch makes no difference to me, because I am considering the issue of senescence from a completely general point of view. I don't know enough to answer your question with any confidence. While I am persuaded by the "Stan Salthe" view of universal life history paths, I also recognize that there are mechanisms which compromise the existences of systems while rejuvenating the system's life history stage. This is essentially how I think of biological reproduction, and it is IMHO the source of confusion over share the fundamental pattern of the DISINTEGRATION of an old, functional system(s) followed by the "prefab" integration of a new system. We are familiar with the notion in Biology that such a process leads to the re-setting of the organismal life-history clock. It may be that some of the lab tricks that have been developed to maintain cell lines, like the HELA cell lines, have similar effects. I am certainly not prepared to assume that all of the HELA cells in the world currently constitute a single, coherent system of any kind. Guy
"Guy Hoelzer" <[email protected]> wrote in message news:[email protected]... > in article [email protected], dkomo at [email protected] > wrote on 3/14/04 4:48 PM: > > > Guy Hoelzer wrote: > >> [snippage] > The switch makes no difference to me, because I am considering the issue of > senescence from a completely general point of view. I don't know enough to > answer your question with any confidence. While I am persuaded by the "Stan > Salthe" view of universal life history paths, I also recognize that there > are mechanisms which compromise the existences of systems while rejuvenating > the system's life history stage. This is essentially how I think of > biological reproduction, and it is IMHO the source of confusion over > share the fundamental pattern of the DISINTEGRATION of an old, functional > system(s) followed by the "prefab" integration of a new system. We are > familiar with the notion in Biology that such a process leads to the > re-setting of the organismal life-history clock. It may be that some of the > lab tricks that have been developed to maintain cell lines, like the HELA > cell lines, have similar effects. I am certainly not prepared to assume > that all of the HELA cells in the world currently constitute a single, > coherent system of any kind. > > Guy I like your phrasing as to disintegration and (re)integration. It seems to me that what we know about thermodynamics and non-linear dynamic systems (chaos thy) all works to result in the ultimite _disintegration_ of highly complex systems--the former, even if unlimited energy/resource input is presumed over all time, and the latter, if energy/resources are ultimately limited. All the common chaotic systems we know ultimately decay, including chemical clocks, atmospheric storms (Jupiter's Red Spot hasn't yet, but will, in time) cometary orbits (ditto for some), and even stars--should cells be different? ....tonyC
in article [email protected], Anthony Cerrato at [email protected] wrote on 3/19/04 8:27 PM: > "Guy Hoelzer" <[email protected]> wrote in message > news:[email protected]... >> in article [email protected], dkomo at > [email protected] >> wrote on 3/14/04 4:48 PM: >> >>> Guy Hoelzer wrote: >>>> > [snippage] > >> The switch makes no difference to me, because I am >> considering the issue of senescence from a completely >> general point of view. I don't know enough to answer your >> question with any confidence. While I am persuaded by the >> "Stan Salthe" view of universal life history paths, I >> also recognize that there are mechanisms which compromise >> the existences of systems while rejuvenating the system's >> life history stage. This is essentially how I think of >> biological reproduction, and it is IMHO the source of >> confusion over birth/death in >> fundamental pattern of the DISINTEGRATION of an old, >> functional system(s) followed by the "prefab" integration >> of a new system. We are familiar with the notion in >> Biology that such a process leads to the re-setting of >> the organismal life-history clock. It may be that some of >> the lab tricks that have been developed to maintain cell >> lines, like the HELA cell lines, have similar effects. I >> am certainly not prepared to assume that all of the HELA >> cells in the world currently constitute a single, >> coherent system of any kind. >> >> Guy > > I like your phrasing as to disintegration and > (re)integration. It seems to me that what we know about > thermodynamics and non-linear dynamic systems (chaos thy) > all works to result in the ultimite _disintegration_ of > highly complex systems--the former, even if unlimited > energy/resource input is presumed over all time, and the > latter, if energy/resources are ultimately limited. All > the common chaotic systems we know ultimately decay, > including chemical clocks, atmospheric storms (Jupiter's > Red Spot hasn't yet, but will, in time) cometary orbits > (ditto for some), and even stars--should cells be > different? Nope. That was the point I tried to make earlier. Cheers, Guy
