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Aging Theories (cira)


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#1 caliban

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Posted 09 February 2003 - 03:29 AM


:: This Topic follows the CIRA Guidelines ::

This thread deals with the topic of how and why we age. Actually, I would much prefer to narrow it down to "why" we age, but for reasons that we shall investigate, this might not be practical.

To understand why we age is one of the biggest remaining mysteries in the biological sciences. Should someone come up with the answer, her name would certainly go down in history. Biologists are aware of that of course, and over the years there have been a huge number of theories on aging.

To understand why we age, two basic strands of theories exist:

(A) We age, because our systems break down over time (DAMAGE theories)
(B) We age, because there is an inbuilt mechanism that tells us to die (PROGRAM theories)

Not only for scientific but also for philosophical and religious reasons it would be extremely interesting to find clear evidence for (B). In fact, finding such evidence should make most readers her very happy indeed. However, such evidence is notoriously hard to produce. The famous "death hormone" has yet to be proven to exist. Some genes do affect lifespan dramatically, but it is more likely that their presence (life genes) or absence (death genes) actually impact on the effectiveness of repair.

This links us back to (A) and the huge number of damage theories (or rather damage observations) that have been advanced.
Some prominent ones include:
- free radical theory of aging: aging is the accumulating damage that free radicals cause
- somatic mutation theory: aging is the accumulating damage that occurs in the DNA during a lifetime
- wear and tear theory: rather than a cellular process the main cause of aging and death is the wear and tear that occurs in our vital organs over time
I personally would put my money largely on the free radical theory. There are other theories out there, usually describing the symptoms of aging. The "lipofuscin" theory is one of the oldest. The "crosslinkage theory" was popular in the eighties, the "de-methylization" theory is a younger candidate. More on these below, and all of them need to fit into the picture if we ever come up with a unified theory of aging.


We can see now, the question of "why" we age is hard to separate from the "how". There is another related question that for our purposes is extremely important:
How and why do we die?

The HOW part is rather difficult to answer. People do not die of old age. (It could even be argued that there is no conclosive definition of death). Old people leave life more easily than young people do, because their biological defence and maintenance does appear less rigorous. Statistics are telling. This of course leads back to the theories above.

The WHYpart is even more controversial.
Let us stick with a Darwinian theory of evolution for the present purposes: Does it make evolutionary sense to die? I contest that it does not, but let us come back to the question later.


Obviously, all these topics are linked.

For the present purpose, contributions are invited on the following eight (of course) points:

> (AA) Present a single DAMAGE - based theory
> (BB) Present a single theory leaning towards the PROGRAM theory
> (AC) Comment on or discuss a single DAMAGE based theory
> (BC) Comment on or discuss a single PROGRAM based theory
> (EE) Comment on theories about EVOLUTION and aging.
> (FF) Comment on the relationship between two or more theories
> (GG) Comment on aging theories in general
> (XX) Comment on the discussion in general or another point of interest

When you reply, please indicate in the first line the point that you would like to address by number and the theory/ies that you are addressing. (No need to stick with the colours, they are just for easy reference in this post)

Contributions and questions from everyone are very welcome!


Some literature:
Tom Kirkwood; The time of our lives, } one of the most prolific works, and one that we will surely come back to.
Robert Arking; The Biology of Aging, } a relatively comprehensive yet very readable overview of aging as a phenomenon
Robert Ricklefs / Caleb Finch ; The Biology of Ageing -A Natural History } another fairly good overview by established authorities
(These are the ones on my desk right now, I am sure there are better ones, feel free to recommend them under point (8).)
Thus as always: "aging theories" online, indexed by GOOGLE !
The subjects was also briefly adressed in numerous other places in this forum for example in "Scientific Reviews On Aging"

Edited by kperrott, 01 August 2003 - 03:29 AM.


#2 ocsrazor

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Posted 09 February 2003 - 06:02 AM

Hi Caliban,
(hi ocsrazor thanks for the swift and excellent contribution, I have taken the liberty to reformat your posts according to the guidelines above - caliban)




(BC) - Program based theory rejected by the aging research community
I should mention that the idea of "programmed aging" has been completely rejected by the aging research community for a few years now(~1994), because there is simply no evidence for it and because there is no selective pressure that would have produced such a system.



(EE) -Book by M.R. Rose
This was area of expertise for a few years, I have my own opinions on the subject, but I think the clearest presenatation of a global picture of aging has been presented by Mike Rose at UC irvine.
Evolutionary Biology of Aging, by M.R. Rose
http://www.amazon.co...il/-/0195095308



(AA) The Mitochondrial Free Radical Theory
For one of the key components of damage, Aubrey de Grey makes a strong case for the involvement of mitochondrial damage.

The Mitochondrial Free Radical Theory of Aging
by Aubrey D.N.J. de Grey
http://www.amazon.co...l/-/1587061554/



(FF) overview
For a very complete mechanistic view of the aging process Legendary Pharmaceuticals maintains an excellent information site:
http://www.legendary...senescence.html



(GG) chart of theories
Check out the big chart of senescence mechanisms, I used to have this on my office wall:
http://www.legendary...om/chartbg.html



(XX) maxlife conferencesLet me know if you have any specific questions, I'm getting a little rusty though. I stopped closely following the aging literature a while ago, because I'm so tightly focused on neuroengineering now. While I was involved in the field, I had the privilege of moderating two conferences where I got to observe some of the top aging researchers hash it out over what they thought were the key research targets.
http://www.maxlife.org/past_events.htm

Best,
Ocsrazor

Edited by caliban, 20 February 2003 - 12:14 AM.


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#3 ocsrazor

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Posted 09 February 2003 - 06:12 AM

(EE) deep space probe analogy

By the way,
My favorite simple explanation on why we age and die is the deep space probe analogy. (I forget who this is credited to, someone please remind me if they know) The analogy is that just like the space probes (Voyager, etc) we are designed (by evolution) with a rough operational lifetime in mind (in our case ~35-40 years) but NASA will keep squeezing as much working lifetime out of their systems as possible until components start to fail. Eventually a critical component fails and the probe is done for.

Best,
Ocsrazor

Edited by caliban, 20 February 2003 - 12:05 AM.


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#4 wannabe

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Posted 09 February 2003 - 07:44 AM

AA) Damage -- Dehydration via Cell Membrane Insult
This concept keeps me drinking water and eating right.
-- wannabe



Cell membrane functionality greatly determines hydration capacity. Hydration is the mechanism for nutrient uptake, and for the subsequent suspension-expulsion of metabolic waste.
Cells that are well hydrated are primed for anabolism, growth. Babies are well hydrated. Dehydrated cells move into the catabolic pathway, tissues are broken down, death. Our bodies lose water as we age.

Cell membranes are compromised in several ways, including:
1) Poor nutrition
Cell is not provided adequate quantity or quality of building materials.
EXAMPLE: A diet deficient in essential fats, and supplying instead heat damaged or hydrogenated fats results in cells producing a functionally compromised membrane.
2) Damage-- rancidity and carmelization
Free radicals from cellular metabolism and environment, and similarly, glycation from presence of glucose, damage the cell membrane, impairing functionality.

Edited by caliban, 20 February 2003 - 12:31 AM.


#5 ocsrazor

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Posted 09 February 2003 - 03:50 PM

AC) "Dehydration via Cell Membrane Insult"
wannabe - a couple of clarifications to your post on damage by dehydration

Dehydration and malnutrition have no direct connection to the funamental process of aging. Even if a person maintains perfect dietary and water intake habits, they are still going to age and die (just a little more slowly). Poor maintenance is certainly going to speed the aging process, but great maintenance cannot stop it. What we are after is a more fundamental cause for aging. So this is sort of off topic and belongs more in a post about health maintenance.

Loss of membrane integrity, means a dead cell, which does not affect overall fluid balance. So there is no solid connection between cell membrane damage and hydration, unless you destroy a huge number of cells at one time. Body fluid control problems with age are a side effect of a more general loss of neurologic and hormonal control of metabolism and are a global process. Good water intake will help lessen the effects of this loss of control, but it is not going to stop it.

Eating heat damaged or hydrogenated fats does not result in cell membranes with altered characteristics, they would never make it as far as the cell membrane before being broken down, but is bad for other more general nutrition reasons. The majority of the lipids in cell membranes are synthesized from basic components. You are right to say EFA intake is critical though, but this still is not the aging process, but just damage from poor nutrition.

So to sum up, adequate global hydration is necessary for maintenance of good health, but is not connected to membrane damage of cells, and none of this has any connection to the aging process except that membrane damage is part of a general pattern of damage to all cellular components being caused by oxidation (i.e. a side effect of a more general process of aging)

Best,
Ocsrazor

Edited by caliban, 20 February 2003 - 12:32 AM.


#6 wannabe

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Posted 09 February 2003 - 07:59 PM

AC) Damage -- "Dehydration via Cell Membrane Insult"

ocsrazor

Dehydration and malnutrition have no direct connection to the funamental process of aging.

We take supplemental antioxidants, nutrition, to stave off a broad range of age related problems, including telemere breakage that can speed senescence. It could be said we supplement to prevent subclinical malnutrition, which would include symptoms including telemere breakage, another post for this topic.

So this is sort of off topic and belongs more in a post about health maintenance

I see my contribution better falls under topic - (6) Comment on the relationship between two or more theories

Loss of membrane integrity, means a dead cell, which does not affect overall fluid balance.

I think you and other readers understand I was indicating a more gradual loss of integrity-- not total disintegration.

So there is no solid connection between cell membrane damage and hydration, unless you destroy a huge number of cells at one time.

I imagine a cell with a semi-permeable membrane that is damaged by oxidation or glycation could be compared to an animal that has an impaired ability to swallow and is chronically constipated. I think a closer look at the mechanics and disfunctions of water crossing the little "organs" of the cell coat would be revealing of how we dry up and lose the cells of organs and systems with age.

Edited by caliban, 20 February 2003 - 12:32 AM.


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#7 ocsrazor

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Posted 09 February 2003 - 10:12 PM

GG) What structures to observe?

In response to wannabe and as a general note for damage theories, the structures you want to look at as being involved in the aging process are those which cannot be repaired or are not renewed on a regular basis. DNA in particular, some slowly replaced proteins, slowly or non-replicating cell types (neurons in particular), and any other structure which is a "factory install" only (heart valves and muscle, lenses, etc). These are the critical components I was speaking of in the above deep space probe analogy.

Cell membranes are not a good candidate because their individual components (lipids & membrane proteins) are constantly turned over. A cell will turn over its entire membrane in a very short period of time and will speed up turnover in response to damage. So I wasn't kidding when I said that loss of membrane integrity means cell death, if they can't fix it, they die. There is no such thing as gradual membrane degradation unless something goes wrong with the machinery (DNA, proteins, etc) that produces the lipids that form the membrane, but this would probably kill a cell pretty quickly anyway. A limited form of this is what Aubrey de Grey is proposing in his theory of mitochondrial damage. He proposes that mDNA is damaged which leads to multiple components of mitochondria, membranes included, failing.

The only thing significant with membranes is that oxidized waste products from damaged lipids are a problem and are likely involved in processes such as atherosclerosis.

Telomeres are a valid topic for discussion here, but taking anti-oxidants is highly unlikely to do anything to slow their shortening, except in the general sense of preventing DNA damage as a whole. That said, their role is most likely limited to few cell types(the rapidly dividing ones), the most significant of which is the immune system. I buy the current line of thought that telomeres may be responsible for some of the immune deficits we see in the elderly, but I think their role may be limited to that and maybe some of the epithelial problems you see in very old humans.

Best, Ocsrazor

#8 wannabe

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Posted 10 February 2003 - 03:03 AM

AC) Damage -- "Dehydration via Cell Membrane Insult"

Ocsrazor, I found the reference I needed. My mistake-- I didn't distinguish cell membranes from collegen fibers wrapping them.
It was here I had read and transposed info from.
http://www.americana...T2/zindler.html

...many cells are surrounded by a wrapping of collagen, or else they must receive their nutrients from blood vessels which are wrapped with collagen fibers. In the young body, nutrients easily pass through these barriers into the cells, and wastes easily pass out of the cells into the blood. When the collagen is not excessively crosslinked, materials pass in and out of the cell as easily as Olympic runners leaping hurdles on a track. But as the collagen ages, the course becomes more and more tortuous. Runners have to pass through what comes to be more and more like a jungle-gym. They may get through to the finish-line, but they won’t win any races. The cells become more and more choked off from supply sources, and metabolism slows down. Fewer and fewer biochemical deadlines are met, and disorder increases. Regulatory processes become progressively imbalanced, and death ensues. If we could prevent just the cross-linking of collagen and elastin, a lot of derailed biochemical trains could be put back on their tracks, and we should be able to double our life-expectancy. "

again, full text is here-- http://www.americana...T2/zindler.html

L'chaim! (Hebrew toast, "To Life!")
-- wannabe

Edited by caliban, 20 February 2003 - 12:33 AM.


#9 ocsrazor

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Posted 10 February 2003 - 07:30 AM

AC) "Dehydration via Cell Membrane Insult"

Exactly, collagen and ellastin are the type of structures which do not get repaired fast enough as we age. I think the author is giving a little too much importance to just these specific structures, but they are indicative of the types of damage caused by the general process of oxidation and chemical crosslinking with age. I doubt you would get a doubling of lifespan if you prevented collagen and elastin crosslinking, but your skin and muscle tone would probably be much better, and hardening of the arteries and similar effects of aging may be prevented.



GG) Aging as combined degradation
I guess I should state my personal opinion that aging is a combination of a few different degradation processes that lead to multiple component failures. It is just a matter of what gets you first. In the oldest old, you see complete system failures, where everything just falls apart. It is interesting to look at human demographics of death to see what age cohort and to what disease people are succumbing as they age. This gives you an idea into what the different degradation processes might be (i.e. if you are going to die from cancer or heart disease it is usually going to be between ~ 50-70, but not later, at which point some other process becomes dominant.)

Edited by caliban, 20 February 2003 - 12:33 AM.


#10 ocsrazor

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Posted 12 February 2003 - 04:15 AM

BC) Further Refutation of the Programmed Aging Hypothesis

please see my posts in the following two threads:

http://www.imminst.o...t=ST&f=44&t=840

http://www.imminst.o...=44&t=681&st=12

Best,
Ocsrazor

#11 caliban

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Posted 14 February 2003 - 05:10 PM

BB) program theory - “longevity determinant gene hypothesis”

The anti-aging efforts of many early scientists and the dreams of many “immortalists” have been based on the “longevity determinant gene hypothesis” presented by Cutler in 1975. (*1) This thesis predicted the existence of a relatively few key regulatory factors governing aging rate of the entire organism.

! tbc !

#12 caliban

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Posted 14 February 2003 - 05:13 PM

BC) the GENE element in the “longevity determinant gene hypothesis”

It has yet to be determined whether Cutler was wrong in essence. I would think this unlikely.

Yet, the “genetic” base of the theory might be doubted.

There are definitely genes that influence aging. (*1)

But when we take a closer look at “WHY” that gene influences aging, we more often than not seem to face a genetic defect rather than a genetic modulator.

Hypothetical classification of longevity genes or their alternatives (*2).
1. Genes that cause aging (P53?).
2a. Genes that increase the risk of a specific illness early in life but do not appear to be related to aging (e.g. cystic fibrosis and CF gene).
2b. Genes that alter longevity because they increase the risk of a specific illness early in life whose features resemble, to some extent, some of the consequences of aging (e.g. Werners gene).
3. Genes that influence or cause age-related illnesses (e.g. Alzheimer’s disease and polipoprotein E _ -4).
4. Low-fitness genes that extend maximum life-span, probably by slowing down aging (as observed in lower organism mutations, e.g. daf genes).
5. Polymorphic genetic loci that influence the rate of aging (many quantitative trait loci with varying influences on aging and age-associated diseases).
6. Genes that influence differences in life-span among species (e.g. longevity enabling genes).


I would contend that such classifications while very useful on the one hand may also serve to obfuscate the issue. In truth, it is doubtful whether (1) exists in practice and as a category.
(4) is worded in an unfortunate manner: its focus is on the handling of ROS more than “Fitness”
(6) is a field where the water seems to be particularly muddy. In some instances and for some species extensive data exists, for other species there seems to be great uncertainty. Also, species specific AGE genes that operate in the matter suggested have yet to be proven to exist.




*1- a good list of them can be found at http://sageke.scienc...org/cgi/genesdb -but you or your institution need to have a subscription to SAGEKE (– not a bad investment by the way)
*2 Adapted from: Miller, RA. “A Position Paper on Longevity Genes” / Taken up in : Perls, Kunkel, Puca – “The Genetics of aging”


#13 caliban

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Posted 14 February 2003 - 05:16 PM

AA) Damage- The free radical theory of aging

The free radical theory of aging originally proposed by Harman et all 1955 (*1) assumes that there is a single basic cause of aging, modified by genetic and environmental factors. He postulated that free radical reactions are the reason for aging.

Indeed, as eg. Osiewacz et al.,1997(*2) showed, accumulation of damage by reactive oxygen species is critical in determining life span.

But the knowledge researchers have gained over the last decade makes it necessary to expand and modify the free radical theory of aging.



(*1) Harman: Harman D; Aging: a theory based on free radical and radiation chemistry; 1956; Journal of Gerontology; 11; 298-300.
(*2) Osiewacs: Osiewacz H.; Genetic regulation of aging; 1997; Journal of Molecular Medicine, 75; 715-727.

Edited by caliban, 20 February 2003 - 12:25 AM.


#14 ocsrazor

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Posted 14 February 2003 - 11:37 PM

BC) Longevity determinant gene theory really a "Program Hypothesis" ?

Hi Caliban,

I agree completely with everything you said in the last three posts with the one exception of classifying Cutler's 1975 paper as a programmed hypothesis. From reading his work and a conversation with him, I've always placed his ideas as strongly in the damage camp. The longevity determinant idea just gives you an estimate of how long certain systems are going to last when exposed to a particular level of wear and tear over many years. I have trouble seeing this as programmed, and see it more as that there are certain key systems whose loss is more important than others to an aging organism. I'm curious what would make you think of these ideas as part of a program hypothesis.

Best,
Ocsrazor

BTW - My specific use of the words hypothesis and theory is not accidental - as in the theory of evolution and the creationist hypothesis. Just a personal pet peeve about scientific word usage ;)

Edited by caliban, 20 February 2003 - 12:25 AM.


#15 ocsrazor

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Posted 17 February 2003 - 03:02 PM

FF) Damage Theory vs Program Hypothesis

Hi Kissinger,

There is NO (nada, zilch, nichts, etc.) scientific data for the program hypothesis, so if you are going to say you subscribe to it, could you please provide a rationale based on evidence.

This does make the problem of slowing aging more difficult because it is a process made up of several different failure mechanisms, each one of which contributes to the overall degradation of the organism. So aging will most likely never be "solved" in the sense of understanding it from the point of view of a single all-important cause, it will have to be engineered out, system by system. To get a true picture of the process as a whole you will have to understand all the sub-processes and how they interact with each other.

See the poster at: http://www.legendary...om/chartbg.html for a sense of what I mean.

Best,
Ocsrazor

#16 fueki

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Posted 17 February 2003 - 07:33 PM

BB) Program Theory- Telomeres
To Ocsrazor:
I think telomeres are evidence for Program (2) theory, so I acclaim Kissinger.

Edited by caliban, 20 February 2003 - 12:27 AM.


#17 ocsrazor

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Posted 17 February 2003 - 10:11 PM

FF) Further rebuke of the "Program" theory/hypothesis

Hi Gang,

Aging researchers have universally rejected the program hypothesis, because it is just not a valid point of view according to the data and gives no predictive value in trying to figure out the mechanisms of aging.

I'm going to repost my responses to the program idea from other posts here:

There is a developmental program for getting us to adulthood, but all the data suggests that after that it is just systems wearing out, there is no program anymore. Even telomeres, which only affect a limited number of cell types are just an example of a component with a limited lifetime going past its warranty. There just isn't any data for a prgrammed (or clocked) theory of aging, despite many years of looking for one. The strongest refutation of this idea was by Michael Rose, who is the foremost evolutionary thinker on aging, see his book for a complete explanation:

Evolutionary Biology of Aging, by M.R. Rose
http://www.amazon.co...il/-/0195095308

So the short answer to the question the original post asked is for development to adulthood, there is highly networked spatio-temporal system that uses certain key events for doing things such as starting production of certain hormones, or starting and stopping bone growth. There is no central clock, just a highly evolved interconnected system. For aging, there is no timing mechanism at all, because there was never any selective pressure to create it, we have only very recently been able to live beyond ~35-40 years, not enough time for evolution to act. We just have a system whose components become damaged by use and eventually lose the ability to repair themselves.


To summarize: There is a developmental program for sexual maturity, but there is NOT one for aging. The process winds us up and shoots us off in a certain trajectory, but how we fall from that trajectory is not controlled and is completely at the whims of our environment. There is no reason for an aging program to exist, because humans did not live long enough for the processes we call aging to come into play until very recently in the evolutionary time scale, so there was no selective pressure to create it. In addition, all the molecular and cellular evidence supports this line of thinking.

The observation that different animals have different life spans is very key to thinking about aging though. This clearly means that there is something different about the way they age. This means two things. One, they have different time scales for getting to sexual maturity. Two, that the mechanisms they use for defending against degradation are very different. This agrees more with the damage line of thinking, because the key difference seems to be in the time it takes for the defense systems to wear out in the face of constant damage.

Birds, bats, and tortoises are interesting because they all have extremely robust anti-oxidant defense systems which is probably tied to their developmental timescale. There is a particular evolutionary reason for the timescales at which organisms exist, but this should not be confused with aging. The overwhelming majority of organisms in the wild do not die of old age, they are out competed or killed just past sexual maturity, so there has been no evolutionary pressure to act on aging (i.e. aging is not a coordinated biological response)

Telomeres most likely play a very limited role in human aging, mostly in immune and other fast dividing cells and seem from current research to only affect the oldest old of humans. They are one of the last critical component failures. BUT, there is no indication at all that they are acting as an aging clock and do not seen to affect the majority of humans who die of another system failure long before their telomeres get them. The telomere aging clock is a myth that was propagated by the popular media and is not taken seriously by anyone in aging research (Even by Dr. Michael Fossel who contributed to the myth in his book "Reversing Human Aging" will now readily admit that this is complete B.S. if you ask him.)

OK, key points:
[>] There is a developmental program for sexual maturity, but many years of research have shown that post-adult aging is not under coordinated control
[>] Different species age differently because of the mechanisms they use to cope with degradation
[>] Telomeres are one of those mechanisms, but not the only one, and definitely not a central clock
[>] The point of view that aging is caused by a central program or clock is not helpful to aging research because:
[!] There is no evidence at all for coordination between systems in aging, there are simply many different possible failure modes (i.e. you die of whatever your weakest damage control system can no longer defend against)
[!] The idea of a program has not helped in the search for aging mechanisms, and has in the past hindered good ideas from coming to the fore.
[!] It is damaging to the general public's conception of aging because it isn't true, and the program idea provides ammunition for certain "moral" philosophers to say that human biological aging is predestined by divine will, fate, or some other such silliness

I hope this helps,
Ocsrazor

Edited by caliban, 20 February 2003 - 12:34 AM.


#18 Doubting Didymus

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Posted 18 February 2003 - 05:44 AM

EE) Evolution: "economic efficiency"

Hullo everybody. I would just like to make a few points in regards to some of ocsrazors startements.

Ocsrazor rightly says: "there is no selection pressure that favours ageing". While this is true, it is misleading to think that selection pressures have no part in this picture. Generally, people think of selection pressures as a positive thing, pushing a species toward some novel adaptation. Just as often, however, selection pressures act like barriers, actually preventing evolution in certain dimentions, even where certian perspectives would suggest such evolution would be a benefit.

One such case is ageing. Here, the question may not be: what pressure is causing aging, but an inverted query: what is stopping a species from evolving adaptations that prevent ageing and extend life? It is easy to see why it would be a selective bonus to live longer. For one thing, you have a greater opportunity to spread your genes. Secondly, it is thought by some in the evolutionary sciences (I stress: some) that the practice of grandparenting constitutes a selective pressure and may even have played a part in pushing human lifespans past reproductive age, an uncommon trait among animals. (one more time: not a consensus issue!)

What, then, prevents humans and other animals from evolving 'protection from ageing'? One answer that keeps popping up is to do with a kind of darwinistic economic efficiency. In short: a selective pressure may exist in favour of clearing a generation away in time for the generations that come after it. It is important to note that this pressure would not need to be positive in any way. It would not predict the prescence of 'programmed death clocks' which we do not, in fact, find. But it does not have to. Organisms will always eventually wear out and die in the abscence of any built in protection. This pressure would simply function against evolution toward greater lifespans. The spans we see would be a neat balancing act between a selection pressure in favour of increasing ageing, and a selection pressure against the same.

So while there is no selection pressure positively for ageing, it is wrong to think that selection pressures play no part in determining our useby dates. Just like everything in biology, ageing is irreversibly tied to evolution.

Edited by caliban, 20 February 2003 - 12:38 AM.


#19 ocsrazor

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Posted 18 February 2003 - 07:15 AM

EE) Evolution - Comments on "economic efficiency" (Didymus)

Response to Didymus' Comments
Speaking as a professional biologist, the term selection pressure has neither a positive nor a negative connotation. The literature on this subject clearly shows there is no selective pressure against increasing lifespan in humans and there probably is a slight upward pressure for increased lifespan, but there has not been enough time for evolution to act for there to be a noticeable difference. Modern culture has completely thrown out all the rules though, so there is no longer any selection pressure for humans in the classical sense.

It is not that anything is stopping the increase of lifespans it is just that there is often a great advantage to rapidly get to breeding age, which is tied to shorter lifespans. This fast trajectory is favored in species under strong selective pressure such as those facing predation, because it is more advantageous for them to produce lots of offspring rather than to spend more time nuturing their young. Our primate ancestors slowly climbed out of this hole, switched to the nurturing strategy, and gradually saw an increase in lifespan as their intelligence reduced selective pressure. The effect seems to be that if you have a species with a lack of pressure from environmental challenges then evolution will select for increasing lifespan (i.e. you get better defense mechanisms) This has been observed in other species with low selective pressure such as some birds and bats who have a lack of natural predators.

Evolution did not push humans to living beyond reproductive age, technology and culture did. Stone age humans did not live much past thirty.

The ideas you mention about grandparenting and about there being pressure for us to die to get out of the way are part of a line of reasoning called the group selection hypothesis which is not considered to be valid by any serious researchers in evolution now. Another no data hypothesis, there just isn't any evidence for it, and a ton against it. The Rose book and his and others many years of collected research put that one to bed around 1994. In short there is no mechanism by which these type of activities can affect succeeding generations. If you need additional reference material to be convinced please let me know.

Just a general note too: I want to apologize if I come off too combative in my replies. Alot of the things we are discussing are common misconceptions among the general public and I just want to make sure that many of the incorrrect ideas that are floating around out there get cleared up. This is an area I have a great passion for and that I spent a few years becoming expert in, so if I jump on your post, please don't take it the wrong way [blush]

Best
Ocsrazor

Edited by caliban, 20 February 2003 - 12:40 AM.


#20 Doubting Didymus

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Posted 19 February 2003 - 12:43 AM

EE) Evolution (response)

Comments on evolution and aging

Response to Didymus' Comments
(...) the term selection pressure has neither a positive nor a negative connotation.  (...) Modern culture has completely thrown out all the rules though, so there is no longer any selection pressure for humans in the classical sense.


There are always selection pressures. Modern culture has removed some of the more superficial selection pressures, but otherwise we are evolving today as much as we ever were. My use of 'positive' and 'negative' selection pressures refers only to selection for, as opposed to selection against, traits. Obviously selection pressures can not be positive or negative in and of themselves. You say that the literature clearly shows that there is no selection pressure against increasing lifespans. I take issue with this. For one thing, you yourself state:

It is not that anything is stopping the increase of lifespans it is just that there is often a great advantage to rapidly get to breeding age, which is tied to shorter lifespans.  


This is exactly what I mean by a selection pressure against increased lifespans. Selection favouring trait a over trait b is no different from selection pressure directly against trait b. Again, there is no selection pressure causing us to die early, but it is quite likely that there are selection pressures against evolving greatly extended lifespans. Your quote just an inch above these words qualifies as one such pressure.

This fast trajectory is favored in species under strong selective pressure such as those facing predation, (...)


Again, this is precisely my point. animals tend to evolve greater lifespans whenever they are 'allowed' to (naughty Didymus, no anthropomorphising!). As you point out, it is largely tied to reproductive age and life expectancy. A species that can not expect to live very long will evolve a tendancy to grow quickly to reproductive age, get all your breeding out of the way as fast as possible, and die. Species that have fewer predators, nurture their young, and posess various other characteristics, evolve long lifespans in the form of defensive mechanisms, a great selective advantage for a variety of reasons. Evolution is not always as slow as people think, and we've been nurturing our young for a very long time. Why have we not evolved the lifespan of a large ocean tortoise? You claim that the reason is simply a matter of time. I am not convinced. The entire human genome can be theoretically overwritten in the space of three years. Following is a quote from a fellow moderator at the infidelboards evolution forum.

Originally posted by rufusatticus, Professional population geneticist
For humans the errors in DNA replication produce 1 point mutation on average every three cell divisions. From zygote to zygote this produces an accumulation of on average 100 point mutations in an offspring compared to its parents. With ~120 million children born every year, that amount to 1.2 billion expected point mutations a year. With the human genome being only 3 gigabases in size, that means that it take on average arround three years to have a mutation at every point in the human chromosome in at least one person in the world.


Note that this would be mostly neutral changes, plus a good deal of detrimental change as well. Another good deal of these mutations would be positive, and natural selection can see to it that only these positive mutations are kept.

There is even evidence that longer age has genetic influences present today. See this article in the AJHG: Here.

To quote:

Jeanne Calment, who died recently in her 123d year, being the oldest human being alive on earth, epitomized our quest for longevity... a survey of Jeanne Calment's ancestry revealed a striking aggregation of the longevity trait: 24% of her 55 immediate ancestors have lived to age >80 years, as compared to merely 2% of an adequately paired control group (Robine and Allard 1998).


It is for reasons like this that I am skeptical that 'not enough time' is the only reason humans lack sophisticated age extention mechanisms. I think we have had bucketloads of time, and even have the neccesary mutations present in the population.

The ideas you mention (...) are part of a line of reasoning called the group selection hypothesis which is not considered to be valid by any serious researchers in evolution now.  (...)


I am fully aware of the failing of group selection. The examples I tentatively cited (I have my own reservations about many things), are nothing to do with group selection at all. They are standard evolution by natural selection for traits in individuals.

Just a general note too: I want to apologize if I come off too combative in my replies.  (...)


No problems. I think we agree on much more than we disagree on.



Kindly refrain from quoting extensive sections from previous posts in this thread. - Thanks, caliban

Edited by caliban, 20 February 2003 - 12:49 AM.


#21 ocsrazor

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Posted 19 February 2003 - 05:57 AM

EE) More Comments on Evolution and Aging
OK Didymus, lets see if I can clear some of this up.

My comment about modern culture throwing out selection pressure in the classical sense didn't mean that there isn't any pressure at all, but that it is something all together different from purely biological evolution. It is cultural and technological selection layered on top of biological selection which has added a whole new type of complexity and which is just now starting to be examined - extremely interesting stuff! (another thread entirely) The mechanisms there are just starting to be worked out though and they apparently have emergent properties which in some ways are very different from the biological paradigm, that is what I meant by the rules are different now.

The key idea about pressure for increased lifespan is that the pressure isn't on aging itself, but it is on the reproductive period of a species. There definitely is selection for longer time of fertility in species with low environmental stress, but long life after the reproductive period is most likely just a nice side effect (i.e. increased defense mechanisms which continue to function even past their evolutionary usefulness). Evolution just doesn't care about us once we have left successful offspring, and there doesn't seem to be any strong reason to get rid of us either. The pressure against longer lifespans (and for fast breeding times) in humans really is just about nonexistent.

No argument here about evolution already acting to increase our lifespans (as a side effect of increasing the reproductive period and length of childhood) up to the last ice age. There is a significant difference between our lifespan and that of our closest primate ancestors. Given more time under classical selection pressure I think we would have been the record holders for lifespan - it is just that now we are going to do it faster with technology - so the old rules no longer apply.

The tortoise is actually a really interesting case of at least two different effects increasing its lifespan. One, is a lack of predation, which we share. Two though, is that tortoises never stop growing. They continue to get larger throughout their lifetimes and so they continue to have large amounts of cell division going on throughout their lifespan. This seems to have the interesting effect of preventing accumulation of damage. This is actually seen in a number of long lived primitive species (reptiles on down). This is one of the reasons my money is on stem cell replacement as one of the key treatments for human aging - to replace cells that stop dividing with age and accumulate damage. (There is a key issue here about aging and regeneration that I might want to start another post in this thread on)

Why we haven't done it (evolved extremely long lifespans) really is a matter of time. Its not that the mutations necessary for long life aren't out there, I'm sure they are in part of the population. It is that we breed so slowly and that we don't tend to have a number of breeding partners or a large number of offspring. So it just takes a loooong time for us to spread this type of beneficial mutation through a large amount of the population. No problem with the numbers in the population geneticists quote, but they don't indicate that human evolution is going to be very fast, just that there is a chance that in each generation a few members of our species might hit on the right combination of mutations. But there is no indication this is going to be spread quickly.

I'm familiar with the AJHG article, read it about two years ago. No question that if you have ancestors who are long lived you are likely to be too, but the authors also point out how rare this is among the general population. The reason for this is probably that when we go to select a mate we usually don't include asking how old their grandparents are (or were) as a factor (but this probably was a factor ice-age and before when lifespans were much shorter and cut into the reproductive period). If we did select for grandparent age (i.e. our desire for longevity becomes the selection pressure), you betcha we would probably get extended lifespans in a majority of the population in about 20 generations. So long life probably isn't strongly selected for, but there is no reason to think that it is selected against, hence the slow upward drift.

The final point on the grandparenting and pressure to die ideas - I have always heard these brought up in the context of group selection. I can't see any mechanism by which natural selection could act on an individual to produce these kinds of effects. If you could provide some evidence for this line of thought Didymus it would be easier to address these issues. I could possibly see some very recent (~5000 yr) cultural influence in this direction, but not biological, and even this is a stretch.

Best Stuff,
Ocsrazor

Edited by caliban, 20 February 2003 - 12:50 AM.


#22 Doubting Didymus

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Posted 19 February 2003 - 11:53 PM

EE) Evolution

My comment about modern culture throwing out selection pressure in the classical sense didn't mean that there isn't any pressure at all, (...)


Ah, my apologies. I thought you were repeating the common misconception that humans have somehow stopped their biological evolution, just because we don't die from quite as many ailments. I assume that your references to cultural and technological evolution refer to memetics? If not, then you are using 'evolution' in a way that doesn't gel with me.

Evolution just doesn't care about us once we have left successful offspring, and there doesn't seem to be any strong reason to get rid of us either.  The pressure against longer lifespans (and for fast breeding times) in humans really is just about nonexistent.


This is not entirely true. Evolution 'cares' a great deal about any factors that affect a population. This would certainly include the previous generation. Selection would favour any traits of an ageing generation that benefits the next generations, particularly in the case of descendants.

(...) Given more time under classical selection pressure I think we would have been the record holders for lifespan (...)


I'm not sure I agree. I am not convinced that there are no selection pressures that would act to counterbalance the pressure toward long life. We will get to this a little later.

(...) tortoises never stop growing. (...) This seems to have the interesting effect of preventing accumulation of damage. (...) 


Why do you suppose humans have not been able to evolve cellular defenses such as these? Your previous example of a selection pressure for short sharp fertility periods is one candidate. Remember that in the eyes of evolution, a selection pressure that favours one trait over another, mutually opposed trait is exactly the same as a selection pressure directly against that trait.

Why we haven't done it (evolved extremely long lifespans) really is a matter of time. (...) No problem with the numbers in the population geneticists quote, but they don't indicate that human evolution is going to be very fast, just that there is a chance that in each generation a few members of our species might hit on the right combination of mutations.  But there is no indication this is going to be spread quickly.


The point of that quote is that evolution can work very fast indeed, if only a selective advantage is strong enough. The difference in our respective positions is that you see few or no selection pressure at all working on our age, while I see many selection pressures balancing against each other. Each of these positions is an explaination of the same phenomena. My point of contention is that, for the abscence of a selection pressure against long life to be plausible, I must also accept that there is either no selection pressure in favour of long age, or a very weak one. Naturally I do not regect it outright, but I as skeptical about it, as selection pressures are usually as common as dirt.

(...)  So long life probably isn't strongly selected for, but there is no reason to think that it is selected against, hence the slow upward drift.


Too simplistic. Selection pressure for long life could take many varied forms, other than simple mate selection on the basis of parental age. Selection could act on factors that strongly benefit the young individual, but also benefit the old. These are the 'defensive mechanisms' you often refer to. It is quite likely that cellular defense, immune system, and other health promoting mutations would also have the effect of increasing age. These would be selected for during the early years of reproductive age, but naturally would also increase lifespan as a spandrel. In my opinion, selective pressures should strongly favour individuals with the equipment to live a long time, which is why I seek an explaination for why this does not occur.

(...) pressure to die ideas - I have always heard these brought up in the context of group selection.  I can't see any mechanism by which natural selection could act on an individual to produce these kinds of effects.  (...)


You can't see any biological selection influence? Natural selection does not act for the benefit of the individual, but for the benefit of smaller selective units. Laurent Keller, in Levels of Selection in Evolution does a great job of outlining the properties that must define such a unit, if it is to be selected apon in a population. There are three primary properties: Heritability, being the capability of high fidelity self replication. Mutability, the capacity to alter naturally, and differential replication efficacy, the capacity for some forms of the unit to be better at replicating than others. It is the well known work of Richard Dawkins that has estabished the gene as this selective unit, and Keller is urgent in his desire to get readers to accept this, and move on to how different selective levels may influence gene populations.

Given that the true selective unit is the gene and not the individual, it becomes easier to see how selection can produce the effects in question. Genes that influence grandparenting that benifets a descendant, or that increase the period that that grandparenting continues for, are likely to be benifiting copies of themselves, and those genes will increase in frequency. Similarly, genes that influence a long aged period could be selected against, particularly those that tend to extend life a long way beyond reproductive age. Individuals that take up resources but do not reproduce are a negative influence on the prospects of subsequent generations, which would also carry those genes. Populations of genes would be favoured that do not allow for a generation to take a free ride on its descendant generations.

I should clarify that I do not particularly champion either of these ideas, but I do suspect that selective pressures like these are constantly wrestling back and forth over many or most biological atributes. This is why I suspect selection, and not simply a lack of time, is a large factor in explaining the lifespans of humans and other animals.

Edited by caliban, 20 February 2003 - 12:58 AM.


#23 ocsrazor

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Posted 20 February 2003 - 01:28 AM

EE) Comments on Evolution and Aging III

Quotes from Didymus:

I thought you were repeating the common misconception that humans have somehow stopped their biological evolution, just because we don't die from quite as many ailments. I assume that your references to cultural and technological evolution refer to memetics? If not, then you are using 'evolution' in a way that doesn't gel with me.


I defintiely don't think we have stopped evolving, just that the external environmental pressures have been to a large extent replaced with human created (cultural and technological) pressures. Memetics would be the method of transmission of the pressure for the cultural influences, and for the technology it is another story entirely which is off topic.

--A thread has been started entitled Forces Beyond Biological Evolution in the Singularity section to continue this discussion. It includes a post by Lazarus Long that was previously posted here--

Evolution 'cares' a great deal about any factors that affect a population. This would certainly include the previous generation. Selection would favour any traits of an ageing generation that benefits the next generations, particularly in the case of descendants.


I agree with this completely, and there have been a number of studies showing the effect of population density on lifespan in small animals, with the result being that a slightly scarce resource increases lifespan (the CR effect) and extreme pressure reduces lifespan (faster breeding times). I meant that for humans in particular there doesn't seem to be any strong environmental pressure from having the older generation around. This is getting into a gray area where culture takes over and becomes the dominant force though. More on this below.

On the issue of the tortoise, the reason why didn't develop mechanisms for longevity like some more primitive species is because these species never stop growing. As mammals we have a fixed adult size and a more controlled metabolism which has its own advantages. But this is not to say we haven't evolved any defenses against aging, we have a stronger antioxidant defense system than just about any other mammal. It is just that the path taken by the tortoise is not a viable option for our body structure.

The difference in our respective positions is that you see few or no selection pressure at all working on our age, while I see many selection pressures balancing against each other. Each of these positions is an explaination of the same phenomena. My point of contention is that, for the abscence of a selection pressure against long life to be plausible, I must also accept that there is either no selection pressure in favour of long age, or a very weak one. Naturally I do not regect it outright, but I as skeptical about it, as selection pressures are usually as common as dirt.


I think the differrence in our positions is that I see the selective pressure focused on genes that are important for reproduction, which may in fact be the pressure against longer lifespans you are searching for. This general line of thought is called antagonistic pleiotropy and has shown that positive changes to genes that are important in the reproductive period may in fact be detrimental later, and if the species has a choice between making a gene better for more successful reproduction or for more successful aging, reproduction is going to be selected for every time. It is only when a change benefits both reproduction and aging that you get an extension in lifespan. More of these opportunities seem to emerge with a reduction of environmental pressure.

Thank you for mentioning the Keller book, here is the Amazon link for anyone else who might be interested
Levels of Selection in Evolution
I have switched fields to neuroscience and engineering so I have not had time to keep up with reading in aging or evolution, but I am interested in applying ideas about selection to network behavior in the brain. I am also very interested in looking at how selection rules scale in different size systems, so this may be something I'll need to read.

I am highly suspicious though, of evolutionary psychologists and sociologists who often tend to operate with little or no data. One line from the reviews particularly caught my attention that said that selection rules are probably not different in different size systems. My instincts from looking at complex systems would tell me this is fishy, but I'll have to read the book to get a complete picture.

Probably the main reason that I am skeptical about the grandparenting and pressure to die issues is that you just don't usually see these effects in nature. Relatively older animals are a rarity in nature and complex social interaction between generations is extremely rare. Scarce resources are an issue, but it is broader than just the elder generations, in that you can get the same types of effects by having lots of young competitors as you can by having multiple generations. For humans I guess I would tend to place these in the cultural forces category and say that the feedback effects on genetics are not sufficiently known yet.

In addition, I strongly believe time is a factor and that we haven't really had these issues around for very long on the evolutionary scale. As an example of what I mean check out this paper A Speed Limit for Evolution

Best Stuff,
Ocsrazor

P.S. I'm considering splitting this topic off into a new thread: Evolution of Aging

#24 caliban

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Posted 20 February 2003 - 11:01 AM

XX) housekeeping- new moderator for this thread: ocsrazor

I will be away for two weeks.
Ocsrazor has kindly agreed to navigate the topic for me during that time.
As we are reminded ;)) - he is an expert in the field and the topic will be in the very best hands.
Thanks ocsrazor!
Apologies for not having the time to fully contribute. When I come back, I will write an abstract overview and summary of the discussion since the topic was started. Looking forward!

#25 Bruce Klein

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Posted 24 February 2003 - 09:08 AM

I'm considering splitting this topic off into a new thread: Evolution of Aging

Sounds like a winner.. thanks for taking over on this one. Seeya soon Caliban.

Suggested Reference Source :: Ben Best's Mechanisms of Aging
http://www.benbest.c...tml#conclusions

#26 kevin

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Posted 28 February 2003 - 07:09 AM

(FF) Comment on the relationship between two or more theories

It has been mentioned that there is a program for sexual maturity. I would like to add to this that the possibility of the active program for aging is itself the program for sexual maturity. This idea has been given some credibility in studies performed by the noted aging expert Cynthia Kenyon. Here is a link to a now relatively old, (Jan 17, 2002), press release regarding the possibility of the existence of a hormone, acted upon by the stem cells of our reproductive system, which influences lifespan. I don't believe there is a master clock governing the rate at which we age but I do believe that our bodies stop repairing themselves as effectively after we have reached sexual maturity. Perhaps sex is the answer after all.... lol

http://www.eurekaler...--scf011502.php

Edited by ocsrazor, 28 February 2003 - 02:38 PM.


#27 ocsrazor

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Posted 28 February 2003 - 03:07 PM

(FF) Comment on the relationship between two or more theories


Welcome to the discussion Kevin,

I wanted to get you to clarify your statement about an active program for aging. Active indicates controlled, a couple of sentences later you state there is no master clock for aging. These two statements would seen to be contradictory.

General comments on the paper you mentioned. This paper really doesn't argue for an aging program, but it does show the tight linkage between reproduction and aging, and also highlights that the trajectory of aging can still be hormonally modulated as an adult (in worms at least). This fits in well with many of the ideas from caloric restriction research which show that the life extending mechanism of CR is probably hormonally modulated. Aging is the unraveling of the program for sexual maturity, but the mechanisms that were active in a young organism are still at work, desperately trying to hold things together.

There is a very tight linkage between the appearance of sex and death in the evolutionary tree. Sex focuses selection pressures on the germline, rather than on the organism as a whole - the disposable soma idea.

Best,
Ocsrazor

PS. Excellent paper Kevin! This was after I left the aging field, so the the first time I had seen it.

#28 kevin

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Posted 01 March 2003 - 06:28 AM

(FF) Comment on the relationship between two or more theories

OcsRazor,

I'm glad the paper was a worthwhile read as I am sure I do not have the background to judge it's merit. Paper reading is a skill I have only recently begun to try to develop and my abilities are still very much lacking in that area. However, to attempt to clarify the contradictory statements in my previous post, perhaps the word 'active' was misused. I believe that although the hormonal signals sent out by the germline stem cells which appear to shorten lifespan, may be thought of as an 'active' control on aging, and that the possiblity exists that it's influence, without the counterbalancing signals of the somatic tissue, may affect aging, it is more likely that the hormone's effect is only an influential one, rather than a strict control, as their removal only extends life rather than perpetuates it. If the hormone the germ line stem cells produces was the 'master clock', you would expect their removal during infancy would stem the onset of aging totally extend of just extending lifespan.

I find that rather than believing in a 'master clock/control' that I concur with many of the ideas I found on Ben Best's website where he discusses the basic mechanisms of aging as he sees them and how he believes, as do many others, that aging is a result of the effects of many factors.
(great link in BJ's post.. thanks.. I even printed some of it for my parents.. )

To reiterate... I have a long way to go when it comes to learning about aging, philosophy and many subjects I find spoken about on this website with more knowledge than I possess. It's great that I'm going to have a few millenia to work on my gaps, I'm a slow learner....

Edited by ocsrazor, 03 March 2003 - 03:57 PM.


#29 fueki

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Posted 01 March 2003 - 02:04 PM

(BC) Comment on or discuss a single PROGRAM based theory

To kperrott, ocsrazor:
Don't you think, telomeres are major biological clock of aging [?]
[!]
PS. ocsrazor, do you use yahoo messenger sometimes?

Edited by ocsrazor, 03 March 2003 - 04:00 PM.


Click HERE to rent this BIOSCIENCE adspot to support LongeCity (this will replace the google ad above).

#30 ocsrazor

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Posted 01 March 2003 - 05:07 PM

(XX) Comment on the discussion in general or another point of interest

Kevin,
I have only skimmed Ben's stuff, but what I have read looks terrific. On the paper reading, it's definitely a learned skill. The only way to get good at it is to read lots of papers and learn the technical jargon for the particular field you are looking at.

I.P.,
In an earlier post in this thread I covered telomeres:

Telomeres most likely play a very limited role in human aging, mostly in immune and other fast dividing cells and seem from current research to only affect the oldest old of humans. They are one of the last critical component failures. BUT, there is no indication at all that they are acting as an aging clock and do not seen to affect the majority of humans who die of another system failure long before their telomeres get them. The telomere aging clock is a myth that was propagated by the popular media and is not taken seriously by anyone in aging research (Even by Dr. Michael Fossel who contributed to the myth in his book "Reversing Human Aging" will now readily admit that this is complete B.S. if you ask him.)


There is more on pages 1 & 2 of this thread.

Best,
Ocsrazor




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