84 replies to this topic

[Brett Black]

Think about it. Simple life often grows indefinitely. The offspring would have to outgrow the parent to beat him in sexual competition. And the parent has a serious size/experience advantage. The offspring might be growing faster, meaning he(his DNA) really is more evolved, but it will not reach the size of the parent for another 10 years or maybe 100 years. The chances of it dieing from accident or getting killed are the same as the parent if not worse being smaller. So think about it, how would the "race" exactly pan out without an ageing/weakening penalty. Would it provide more evolution or would it infact disable "small scale" evolution in favour of hopeful "huge scale" steps(offsprings that maul their parents)? How does current theory of evolution see most of evolution? Small steps or huge steps?

Aging does not pose a (straightforward) fitness "test." In other words, an organism that dies due to the effects of aging is not dying due to a lack of fitness for the environment in which it lives. So death from aging would seem quite arbitrary, with no relation to fitness, and thus confer no obvious fitness advantage to the species. But, of course, successful evolution is all about selecting adaptions that promote fitness.

Thus, the examples you give of a chronologically younger animal becoming dominant over a chronologically older animal, merely because the older animal has been weakened by intrinsic aging, are not (necessarily) examples of a fitter animal taking the place of a less fit animal.

The offspring might be growing faster, meaning he(his DNA) really is more evolved

What does this mean? It sounds like a basic misunderstanding of evolution.

---

Another thing:

A fundamental constraint on the genetic diversity within a species, is the number of individuals that exist of that species. Therefore, programmed aging and death would, ultimately speaking, act as a barrier to genetic diversity and thereby potentially reduce the chances of successful adaption and survival in changing envionments.

Edited by Brett Black, 01 April 2014 - 03:52 AM.

[addx]

Think about it. Simple life often grows indefinitely. The offspring would have to outgrow the parent to beat him in sexual competition. And the parent has a serious size/experience advantage. The offspring might be growing faster, meaning he(his DNA) really is more evolved, but it will not reach the size of the parent for another 10 years or maybe 100 years. The chances of it dieing from accident or getting killed are the same as the parent if not worse being smaller. So think about it, how would the "race" exactly pan out without an ageing/weakening penalty. Would it provide more evolution or would it infact disable "small scale" evolution in favour of hopeful "huge scale" steps(offsprings that maul their parents)? How does current theory of evolution see most of evolution? Small steps or huge steps?

Aging does not pose a (straightforward) fitness "test." In other words, an organism that dies due to the effects of aging is not dying due to a lack of fitness for the environment in which it lives. So death from aging would seem quite arbitrary, with no relation to fitness, and thus confer no obvious fitness advantage to the species. But, of course, successful evolution is all about selecting adaptions that promote fitness.

Thus, the examples you give of a chronologically younger animal becoming dominant over a chronologically older animal, merely because the older animal has been weakened by intrinsic aging, are not (necessarily) examples of a fitter animal taking the place of a less fit animal.

The offspring might be growing faster, meaning he(his DNA) really is more evolved

What does this mean? It sounds like a basic misunderstanding of evolution.

Yes it does, its only a question of which of us misunderstands it.

Another thing:

A fundamental constraint on the genetic diversity within a species, is the number of individuals that exist of that species. Therefore, programmed aging and death would, ultimately speaking, act as a barrier to genetic diversity and thereby potentially reduce the chances of successful adaption and survival in changing envionments.

And this is also quite near the source of misunderstanding.

To remove the misunderstanding one should perform an experiment.

Sexual selection, especially of simple life is based on the ability to outcompete the other contender. Tools(muscles etc) used for thriving(acquiring nutrients) and extinction avoidance(defense, survival) are mainly used to manifest this competition as well and are thus bettered by the selection process proving the mechanism to be worthwhile. Tools used for thriving are usually "grown" by succesfull thriving(food increases size of muscles or even the entire body in simpler life) and this results in the older, bigger, stronger animals reproducing more at the expense of younger, smaller, weaker animals. Simpler life as said, often grows indefinitely.

Now, the offspring might infact have superior genes which is demonstrated by his ability to "thrive"(acquire food and grow) better, but in order to reach the size of his parent he has some catching up to do. It might take a year or two of his accelerated thriving for him to be able to outcompete his parent in sexual competition. During that time his parent is still eating food and spreading his inferior genes on more future food wasters while infact the population would benefit if the faster growing offspring started spreading his genes sooner, BEFORE the superiority of his genes is demonstrated by the best achieved state(in size and strength) among competition. If the the older population is increasingly penalized by sheer time they spent alive - this becomes possible.

The offspring also has the penalty of competition for the same nutrients with the bigger parent which also reduces his chance of growing of spreading his superior genes. If the parent doesnt age the offspring has much trouble acquiring his position in spite of his superior genes. They have to be REALLY superior for him to "break through" all that's standing against him. So, ageing makes a lot of sense.

Anyway, the maths can be calculated and it can be shown that there is a threshold at which point it pays off to recycle/penalize/age generations for faster spreading of superior genes especially given a limited life source supply(food). The speed of recycling is also important for interspecies evolution competition(competeing for the same food) and the balance of the foodchain. Increasing recycling through aging reduces population growth speed or spread speed, but there's no reasoning to why spread speed(evolving in number of "units") would be more important than evolving itself(evolving the quality of "units) as it is obvious that a balance is neccessary. Ageing provides that balance since almost the dawn of life.

So this should not be a question of beleif since it can be simulated and calculated. And I still can't beleive only one person voted yes for a purposeful mechanism. Geez.

[Vardarac]

I think the response has mainly to do with the fact that the ability to age, whether selected for or not, most easily manifests itself as a series of insults and breakdowns to the organism rather than as a sophisticated, concerted, programmed system of death.

Liken this idea to the difference between necrosis and apoptosis. One is the death and breakdown of the cell due to the inability to continue homeostasis, which may result in the release of damaging substances to the rest of the body, while the other consists of a sequence of induced, controlled reactions that breaks down the cell while causing minimal damage to the rest of the body.

In other words, it is easier to allow an organism to simply blunder into death without needing to orchestrate it.

Edited by Vardarac, 01 April 2014 - 08:53 AM.

[addx]

I think the response has mainly to do with the fact that the ability to age, whether selected for or not, most easily manifests itself as a series of insults and breakdowns to the organism rather than as a sophisticated, concerted, programmed system of death.

Liken this idea to the difference between necrosis and apoptosis. One is the death and breakdown of the cell due to the inability to continue homeostasis, which may result in the release of damaging substances to the rest of the body, while the other consists of a sequence of controlled reactions that breaks down the cell while causing minimal damage to the rest of the body.

In other words, it is easier to allow an organism to simply blunder into death without needing to orchestrate it.

An organism is a sack of cells. That grows from one single cell dividing. Which has conserved most of its original eukaryotic functioning in some form meaning instincts to divide, sustain, thrive and execute various survival tactics as a single cell.

Now as the cells form the body by containing themselves in a sack they differentiate to create different bodily functions. When evolving into a sack of cells the cells slowly lost their "amoeban immortality and independence" and were increasingly controlled by each other(each others product/function in a symbiotic way) infact directly or indirectly.
Increasingly controlled means their metabolism is increased or decreased depending on more central/coordinated states/conditions/decisions to provide the effect that the cell differentiated to produce. The cell once being a single cell life form normally used its metabolism to sustain itself and replicate and defend and repair by acquiring and processing certain nutrients. Such nutrients are now provided on an as needed and as available basis by central mechanisms. As needed means when the central body needs the function of the cell. Mechanisms for repair, defense and replication are "hijjacked"(but infact the cell evolved for this hijjacking by evolving receptors etc) by the central system(infact by other tissues that differentiated to do this).

In this way, the central system can "abuse" the cells in the sack for a "higher purpose"("squeezing" the muscle cells to provide movement, squeezing the pancreas cells to provide insulin, whatever) of the central organism. In this way, the sack of cells can absorb more nutrients and spread further and conquer more obstacles to spreading than when each cell was individual.

The controlling central system requiring the cells to provide their function while not providing enough nutrients for repair mechanism, not allowing rest time for repair mechanism, not triggering repair mechanism of cells causes them to degrade in function and eventually die. The degrading tissues manifest as ageing. Central systems cause a "lifetime" cycle of providing more "growth" to final form after which growth is more and more inhibited or limited to tissues being heavily used(muscles) and ageing begins through cummulative effects of sacrifice and maybe other factors as well. Interestingly tissue growth and degradation process seem to be manifested mainly through opioids as is sacrifice for nutrients or other strategies of enduring. Gee wiz. Isn't that a coincidence.

Sacrifice of cells happens during a period in which the organism fails to absorb nutrients and detects central lack of nutrients, abuses its tissues to provide more action for finding nutrients and even the fails. The tissues are left "raped" and "hungry". In this way the central stress of the organism causes tissue-wide ageing which eventually causes death stemming from some tissue completely losing ability to sustain the central organism.
This system is therefore balanced with stress making less able DNA configurations(resulting in an inability to feed/repeair their lower level tiers - cells,tissue) die sooner providing natural selection to "sublimate" toward the central tier/upper tier/higher tier - the controling brain. So the cells evolve the brain by killing the entire organism it if the brain fails to serve. Isn't that nice? It's just another way to look at it, but a better way to look at it.

For example, it has been shown to me on this forum that the muscle stem cells removed from old rats were revived to function as stem cells of young rats by pharmacologically manipulating stress pathways of the isolated stem cells before inserting back into body, namely p38 map kinase IIRC. So, the cells have immortality in them as do bacteria. But they make their central controller(nervous system, newly evolved tier) die because it fails to feed them(in simple terms). You see, evolution is completely misunderstood. It's so wrongly explained that it makes me cry.

Edited by addx, 01 April 2014 - 01:01 PM.

[addx]

The central controller can only evolve behavior methodes through evolution properly if the organism has a final/mature form. This way the central controller is given time to prove behavior success with the final form(mature form). If it is successful during this time it will spread more. Causing evolution of behavior to take precedence over evolution of form. Ageing itself enabled this. And it also enabled a mechanism for governing speed of evolution vs. speed of population growth.

Evolution later even went further to focus on evolution of behavior by creating the mammalian PFC system of "changing" behavior through experience evolving yet another behavior refining tier that also piggybacked onto existing tiers by opioidergic connections. Behavior is "invented" or "extincted" based on experience causing ability to change behavior without reconfiguring DNA.

So, it seems to me that science first needs to actually elucidate HOW evolution was guided and I can't see gene mathematics explaining anything I'm trying to put forth here.

Edited by addx, 01 April 2014 - 01:27 PM.

[Vardarac]

Correct me if I'm wrong. Is this basically what you are saying?

1. CNS dysregulation causes cellular dysregulation and therefore pathology. Both types of degradation are mutually and self-reinforcing.
2. This is selected for as a form of population-beneficial phenoptosis and is not the result of an evolutionary trade-off of long-term fitness for short-term fitness.

Two things confuse me about your contention.

1. Why would the selection of organisms that do not have the ability to perfectly regulate for the long term suggest that aging per se is itself a concerted mechanism as opposed to a series of mistakes that may provide a population-level evolutionary advantage?
2. Why does this matter? (Note that I strictly mean the evolutionary origin or purpose of aging, not the CNS theory of aging as you have put it - That's for another thread, methinks)

Edited by Vardarac, 01 April 2014 - 01:28 PM.

[addx]

Correct me if I'm wrong. Is this basically what you are saying?

1. CNS dysregulation causes cellular dysregulation and therefore pathology. Both types of degradation are mutually and self-reinforcing.
2. This is selected for as a form of population-beneficial phenoptosis and is not the result of an evolutionary trade-off of long-term fitness for short-term fitness.

Two things confuse me about your contention.

1. Why would the selection of organisms that do not have the ability to perfectly regulate for the long term suggest that aging is itself a concerted mechanism as opposed to a series of mistakes that may provide a population-level evolutionary advantage?
2. Why does this matter?

The bold question is right on. It can still be seen as a series of compromises evolution made in order to enable multicellular life. I don't really have much problem with that except it seems that evolution kept making smart compromises into a very focused direction so I have an issue regarding them as mistakes. I'll explain the focused direction:

I have explained that ageing provides better(more preemptive, higher order) selection after a certain treshold even for single cell life.

I have explained that the control of ageing is important in interspecies competition and keeping the foodchain more stable.

One more thing that needs explaining is perhaps this "essential focus" that was caused by this series of "mistakes".

The evolution of behavior(and therefore diversity) of multicellular life would be greatly impaired without ageing. Evolution of mammals would never occur without ageing. This is because ageing favours survival through behavior rather than survival through form. This "forces" more evolution of behavior rather than evolution of form. If an organism reaches final form through maturing than only evolution of behavior can allow it to thrive further.

Ageing caused eons of increased behavior selection and finally forces the evolution of the CNS, learning, consciousness, awareness.

Final form is the result of maturing after which ageing begings. The body has all the mechanisms to keep the body immortal and selfrepair indefinitely but it inhibits them! This actually has to be a mechanism. While stress pathways do cause accumulated "senescence" there is a reason, a mechanism why the body doesn't repair them as thorougly as it would during maturing phase.

After ageing developed the behavior of the form rather than the final form itself became more important for sexual selection and this increased the evolution of behavior patterns and it also caused a selection preference for thriving ability rather than extinction avoidance.

Since then the thriving ability and extinction avoidance became more and more served by the same tools, muscles, skeletal structure causing an increased level of alignment of between evolving thriving and extinction avoidance form. But one must never lose sight of the fact that the thriving ability is evolved by an interaction with a life source and extinction avoidance is evolved by interaction with a death source(often on the way to the life source, heh) providing evolution of more distinct behavior patterns for thriving and extinction avoidance even though they mostly use the same tools.

Meaning each lifeform is evolved by two or more factors which are usually also life forms further up or down the food chain with their own evolution speeds. They evolve each other and the entire food chain and this is where speed of evolution starts to matter and ageing along with reproduction becomes a greates tool at avoiding extinction at the species level.

Why does it matter? Because the mechanisms for ageing are the same mechanism that "allow" disease, degeneration and so on. Such diseases are generally even called "ageing". Once the life form reaches maturity suddenly growth and repair becomes limited and inhibited to several tissues like muscles. If the mechanisms for this are elucidated such disease can be helped. In the process we will infact enable immortality.

Currently

we have gerontologists looking for errors in DNA and telomerase lengthening.
we have psychologists and neurologists being mostly clueless about how the brain works yet is is obvious when one realizes how it evolved and what "forces" guided this.
we have biologists spewing crap about group selection not knowing the first thing about integration and evolving systems
we have doctors thinking that masking symptoms is treating disease. that cholesterol is an enemy of the body and so on.
...

All that isn't going anywhere...

So, that's kinda the purpose.

Edited by addx, 01 April 2014 - 03:33 PM.

[Vardarac]

The body has all the mechanisms to keep the body immortal and selfrepair indefinitely but it inhibits them!

I can't speak for the others, but this is where you're losing me. Several forms of accumulated damage and their attendant effects will inevitably happen regardless of the effectiveness of the body's repair mechanisms; this follows from chemistry and is an axiom of molecular genetics.

I think you must also provide evidence that these mechanisms are inhibited rather than passively losing effectiveness over time.

This is not to dismiss your CNS hypothesis. What I am saying is that I think it is premature to dismiss the other hypotheses of aging and the attendant evidence. Yes, I understand that you are saying that if the CNS continues to send bad signals, and that this results in accelerated aging, then replacement without CNS correction will be ineffective.

But, even if your CNS hypothesis is correct, it would still follow from other evidence that old cells and organs may need to be replaced.

This actually has to be a mechanism. While stress pathways do cause accumulated "senescence" there is a reason, a mechanism why the body doesn't repair them as it would during maturing phase.

To use another analogy, a refrigerator with planned obsolescence can simply fall apart; it doesn't have to undergo controlled demolition or kick in a "clog coils" procedure after an approximate range of service time. The "mechanism" could be a series of passive errors, built-in, acquired, or both; it doesn't have to be the brain literally telling the body not to repair itself.

Edited by Vardarac, 01 April 2014 - 04:01 PM.

[addx]

Seriously, I'm very grateful for you reading my spewings and not just reading but actually giving them a chance.

So seriously, thanks!

The body has all the mechanisms to keep the body immortal and selfrepair indefinitely but it inhibits them!

I can't speak for the others, but this is where you're losing me. Several forms of accumulated damage and their attendant effects will inevitably happen regardless of the effectiveness of the body's repair mechanisms; this follows from chemistry and is an axiom of molecular genetics.

I don't deny irreparable damage can happen, but it is not really the cause of ageing or is just a small portion of it.

Do you beleive you lose hair because of accumulated unrepairable damage? It seems to be quite a pattern that it is even named so, male-pattern baldness.

This is not to dismiss your CNS hypothesis. What I am saying is that I think it is premature to dismiss the other hypotheses of aging and the attendant evidence. Yes, I understand that you are saying that if the CNS continues to send bad signals, and that this results in accelerated aging, then replacement without CNS correction will be ineffective.

But, even if your CNS hypothesis is correct, it would still follow from other evidence that old cells and organs may need to be replaced.

This actually has to be a mechanism. While stress pathways do cause accumulated "senescence" there is a reason, a mechanism why the body doesn't repair them as it would during maturing phase.

To use another analogy, a refrigerator with planned obsolescence can simply fall apart; it doesn't have to undergo controlled demolition or deliberately clog its own coils. The "mechanism" could be a series of passive errors, built-in, acquired, or both; it doesn't have to be the brain literally telling the body not to repair itself.

But the refrigerator did not evolve from an immortal amoeba that could repair itself indefinitely.


Check it out for yourself. Check out the functions of mu-opioid and kappa opioid receptors on the cellular level and then psychological. Then check out age-wise how the balance proceeds through life, check out sliced old rats or whatever. Mu opioid receptors enable subsequent growth of cells in exchange for sacrifice(for the CNS higher idea) if other factors align(growth hormone, insuline factors etc). Kappa opioids do the same thing - but they work differently, they alow just the sacrifice and mostly degrade the cell also depending on factors.

As all organisms age tendency to increase kappa opioid functioning appears. Mu opioids provide the growth spurt of the body and the learning spurt of the mind during maturation. Kappa opioids take over after that. Basicly on all levels one after the other, the last level being the last evolved. They do combine with some other factors to provide this, I wish I had elucidated which but it's hard to make sense out of stuff science doesnt purposefully investigate.

Edited by addx, 01 April 2014 - 04:21 PM.

[addx]

I have a favour to ask as well.

I have not really read any books on any of the topics involved in this thread. I have no education in that direction nor anything. All I have thousands of pubmed studies read and some basics from school and things I picked up. I am eternally interested in how things work, an extreme INTP personality resulting in me producing video games with gravity, collision, bouncing, AI, etc at the age of 11-12. I naturally observe, understand, simulate and evolve systems in my head and learning programming via trial and error without any help of a manual or tutorial internet or a teacher at that age resulted in something similar to learning a second language by living in 2 countries at young age. Programming for me is like speaking and it seems my brain "simulates-cycles" systems to their final equilibrium(if exists) instantly with great accuracy or so my experience has shown. I have issues explaining my thinking into words to other people. As can be seen here. This naturally results from words and language infact being a way to defer intrinsic meaning rather than to refer to concrete external things.

I am wondering how many of evolution concepts introduced just in this thread have been described before in any theories or literature?

From comparing to what seems known to me from external sources it seems evolution was never worked out by anyone in the way I am attempting.

Evolution seems mostly considered a random trial and error process proceed through natural selection.

It seems to me that noone yet considered evolution speeds and their influence on how things panned out, food chain competition, life source, death source etc and so has noone has been able to resolve how evolution "guides" itself and evolves lifeforms that have intrinsic ways of being more selective of beneficial mutation. Ageing for example, regardless of the fact if we consider it accidental or not, has a profound influence on evolution that I have not seen elucidated.

From the perspective of all the common sense mechanisms that explain even things like the evolution of the structures of psyche and how it was selected for seem fundamental to theory of evolution.
Gene theory seems as important as quantum theory, a mere tool next what I think should explain evolution.

Im writing some material separately on this all and I am baffled by the mechanisms and consistencies I am able to uncover.
Im just working it out logically how evolution would "evolve" and then it show that it actually did happen like that.
Higher order mechanisms that direct certain features divided basically between "thriving" and "extinction avoidance" etc. Sexual reproduction is a higher order evolution mechanism providing selection before death proves it, meaning it attempts to predict-simulate future based on a prediction made from a derivation of "state".
The last evolving structure of the nervous system is infact vmPFC of humans and great apes enabling mind simulation of future and emotional(behaviour stimulating) response to the simulation-future projection of behavior.
Im writing mostly because I think I have some very interesting concepts that I have never seen mentioned and regardless of the fact that I don't read books, I should have seen it somewhere because. Most of all I need to form these thoughts in my head into coherent words that my conscious self can understand and others with it to finally get it out of me. It sounds insane but is it?

Anyway, some advice regarding this would be greatly appreciated

Edited by addx, 01 April 2014 - 07:16 PM.

[addx]

Ha, I found it,

http://en.wikipedia...._systems_theory

http://en.wikipedia....pmental_biology

etc.

It doesn't seem from wiki they made much sense of things though?


And there is no words to describe the disgust I feel toward the following crap spewed out by Dawkins pasted from wiki

"
In his book River out of Eden, Dawkins coins the phrase God's utility function to explain his view on genes as units of selection. He uses this phrase as a synonym of the "meaning of life" or the "purpose of life". By rephrasing the word purpose in terms of what economists call a utility function, meaning "that which is maximized", Dawkins attempts to reverse-engineer the purpose in the mind of the Divine Engineer of Nature, or the Utility Function of God. Finally, Dawkins argues that it is a mistake to assume that an ecosystem or a species as a whole exists for a purpose. He writes that it is incorrect to suppose that individual organisms lead a meaningful life either; in nature, only genes have a utility function – to perpetuate their own existence with indifference to great sufferings inflicted upon the organisms they build, exploit and discard.
"

You can see why when you read my reasoning in this thread.

Edited by addx, 01 April 2014 - 09:16 PM.

[addx]

Ageing + sexual reproduction = timeframe for reproduction = higher level of selection. This mechanism infact evolved new tiers of selection by selecting for abilities, creating harems etc.

Ageing appeared with simulatenously with sexual reproduction in eukaryotes.

The variety-stability of genome aspect is of less evolutionary importance infact, I believe yeast infact reproduce all their genes.

A nice schema of ageing evolving through evolution.

http://mathforum.org...sh/Programd.pdf

As new tiers evolved to provide more selection, faster evolution, follow my tiers and that pdf, I just found it btw

[xEva]

addx, I noticed you have several misconceptions.

1. you wrote "immortal amoeba that could repair itself indefinitely". Not so. Unicellular organisms also age. When a cell divides, the resulting daughter cells are not exactly the same. One gets most of old organelles and lysosomes stuffed with junk like lipofuscin, and is considered an aged "parent". The other cell gets a better deal. When environment is good, an aged cell will divide multiple times, each time diluting its "aged" content. Still, the cell line that consistently gets the short end of the deal is considered "old" and less fit, more likely to die when environment changes to the worse.

2. then you assume that an offspring must necessarily have superior to its parents genome. Why? As I understand it, the driving force of evolution is adaptation to the ever-changing environment. Usually a younger organism is "more flexible", which gives it better chances to survive when things change drastically than a "fixed in its ways" parent.

3. then you seem to imply that the brain "serves" the organism. I believe it's the other way around. The body is the interface for the "brain" acting out in its environment. This is especially true of humans. People tend to forget that it is only 3 lbs in between the ears that are truly alive. The rest is the interface and support crew.

There were other misconceptions, most were addressed by other guys. I thought of these 3 now. Basically, since you position yourself as a budding genius, without proper education, I'm sorry to say, you will not be able to make a contribution. At the very least you should read what others have written. Otherwise you come across as lacking some basics, including basic understanding. But with proper education -- hey who knows what you could achieve.

[addx]

addx, I noticed you have several misconceptions.

1. you wrote "immortal amoeba that could repair itself indefinitely". Not so. Unicellular organisms also age. When a cell divides, the resulting daughter cells are not exactly the same. One gets most of old organelles and lysosomes stuffed with junk like lipofuscin, and is considered an aged "parent". The other cell gets a better deal. When environment is good, an aged cell will divide multiple times, each time diluting its "aged" content. Still, the cell line that consistently gets the short end of the deal is considered "old" and less fit, more likely to die when environment changes to the worse.

It doesn't seem like you're really proving me wrong. You just said that the amoeba can prolong its life indefinitely in good conditions. If we could do that I guess this forum wouldn't exist, would it.

Also, animal life really didnt evolve from todays amoebas as they have like 5-10 times more base pairs in DNA than humans.

Point of that line was that there's no reason why a single cell life form that evolved mechanisms to repair itself couldnt repair itself indefinitely given there's no new condition of the environment that the lifeform is "not ready for" which could simply be a chemical that causes it to deteriorate.

Humans or even pretty much any complex life inevitably dies of old age in any conditions and the lifespans achieved in captivity are pretty converged around the average lifespan of the population.

"Senescence" liking scientists like to explain this fact by developing theories based on accumulation of "senescence" providing accelerated rate of organ failure causing this convergence. It even nicely explains for the randomness of organ failure. Or so it seems. I can't even read that sentence without my logic circuits screaming at it.

2. then you assume that an offspring must necessarily have superior to its parents genome. Why? As I understand it, the driving force of evolution is adaptation to the ever-changing environment. Usually a younger organism is "more flexible", which gives it better chances to survive when things change drastically than a "fixed in its ways" parent.

Where do I assume that? I never said that.

But yes, ageing being a mechanism means that a "lifeform" or genotype depends upon its current mature generation producing enough offsprings to generate a sufficient number of advanced offsprings or at least same ones. Increasing sexual selection evolution causes that only the advanced offsprings reproduce once they replace the generation that spawned them.

If you evolve a mechanism to pick the best specimen out of a generation to reproduce (which reptiles for example obviously do) why not make use of it? If you combine ageing with such a mechanism you increase the speed of evolution if an advanced specimen can be found in the young population. The old big reptile dieing to be replaced by the best of the young ensures that the young will start spreading its even better genes sooner. If a better specimen can't be found in the young population before the old big reptile dies of old age weakness the species will degenerate.

3. then you seem to imply that the brain "serves" the organism. I believe it's the other way around. The body is the interface for the "brain" acting out in its environment. This is especially true of humans. People tend to forget that it is only 3 lbs in between the ears that are truly alive. The rest is the interface and support crew.

It's just a matter of perspective, not a misconception.

The increasing nervous system layers were evolved by the body(evolved by the single cell dividing and differentiating) so the body(sack of cells) would be better controlled(in ways of acquiring nutrients and reproducing and surviving).

If you really want to choose a "true" perspective, the chronological one is infact correct. Don't let my uneducated ass stop you from logic thought.

There were other misconceptions, most were addressed by other guys. I thought of these 3 now. Basically, since you position yourself as a budding genius, without proper education, I'm sorry to say, you will not be able to make a contribution. At the very least you should read what others have written. Otherwise you come across as lacking some basics, including basic understanding. But with proper education -- hey who knows what you could achieve.

I didn't ask you for advice, I asked vardarac and purposefully so, because he tried and succeed in understanding my concepts so it's not about me anymore.

You on the other hand, judgeing by the misconceptions you thought were invalidating, are not here to be constructive.

I'm not a budding genius. I'm 32 years old working as a the lead software architect for credit card enterprise solution software. I'm probably among top 5 salaries in IT in my country and I have been that since the age of 25. With no education. I'm not about to start college and for this I'd need expertise in biology, neurology, psychology, evolutionary biology etc. It would take a life time. I just have this thing in my head and don't know what to do with it.

Now if educated poeple werent so threatened by an uneducated person having some bright ideas something could be achieved. But it makes them a tool of the uneducated person and they don't like it.

Edited by addx, 02 April 2014 - 07:29 AM.

[addx]

But yes, ageing being a mechanism means that a "lifeform" or genotype depends upon its current mature generation producing enough offsprings to generate a sufficient number of advanced offsprings or at least same ones. Increasing sexual selection evolution causes that only the advanced offsprings reproduce once they replace the generation that spawned them.

If you evolve a mechanism to pick the best specimen out of a generation to reproduce (which reptiles for example obviously do) why not make use of it? If you combine ageing with such a mechanism you increase the speed of evolution if an advanced specimen can be found in the young population. The old big reptile dieing to be replaced by the best of the young ensures that the young will start spreading its even better genes sooner. If a better specimen can't be found in the young population before the old big reptile dies of old age weakness the species will degenerate.

Just to note. The degeneration of low population complex species is explained(by simply saying it is so because it can be seen/observed to happen at the same time) to be a consequence of reduced variety in the gene pool.

Stemming from my explanation the situation is a consequence of high evolution speed(meaning increased recycling through ageing) vs. population size (decreased ageing) resulting in species evolution failure and extinction.

The reducing gene pool actually provides a deperate attempt at a bigger mutation that would surpass the extinction threat to the species resulting from taking too high evolution speed risks.

The species might be "taking the risk" because another species is extincting them, directly(eating them) or indirectly(competeing for the same life source), causing increased ageing(from increased perception of stress from whatever is extincting them) for increased selection at the expense of temporary population thriving reduction in order to surpass the threatening obstacle via evolving. Sacrifice of population speed for fitness speed in order to gain a long term population speed increase.

Each "ageing aided death/loss of nutrients" of the extincting species lifeforms degenerates the fittness of the predating/competeing species.. The predatory or competeing species fitness is evolved by the extincting species competition or ability to avoid capture/being eaten. If they (falsely) degenerate on purpose (ageing isnt infact degeneration, just a weakness factor, a selfimposed penalty) they will degenerate their attacker. In the process they will achieve more selection for themselves(as explained ageing + sexual reproduction) and less selection for their predator at the expense of population size, hoping that it will result in a change of genome/behavior allowing them to replenish the population numbers sacrificed.

I did already note the importance of the "life source" and "death source" of the species causing fitness evolution from two or more sides.

I dunno if I'm losing my mind, but it seems to me that "uneducation" is exactly what science needs these days.

The entire tree/foodchain of eukaryotic life is balanced this way.

Too simple to be true? Did anyone of scientific background actually claim my claims and get peer reviewed?

Edited by addx, 02 April 2014 - 12:42 PM.

[addx]

Oh yes, I forgot one other important thing of sexual reproduction.

The roles of male and female phenotypes infact provided evolutionary purpose. The male is traditionally(although not a rule) subject to more "evolutionary challenge of thriving" while the female is subject to more "evolutionary challenge of extinction". The male risks his life to thrive the species by acquiring/protecting more of the species life source. The female phenotype risks less for acquiring, but more for survival in order to survive to be fertilized by the smaller number of surviving males. This ensures reproduction and ensures more focused evolution through phenotypes.The male evolves thriving genes and passes them on to females. The female evolves extinction avoidance/survival genes and passes them on to males. Evolution is thus faster via divide and conquer of obstacles. This relationship is conserved by evolution to this day even in humans where females still, on average, provide the survival brakes to males instinct to acquire.

I would really like to know how this fundamental truth did not find its way into evolution theory. When I open up wiki on sexual reproduction it is still questioned how and why it evolved and how it produces an advantage. Ageing isnt even considered to be a mechanism of evolution but an imperfection that bothers only us humans at the top of the foodchain.

All of such obviousness are being explained by inceasingly complex "synthesis" theories that are mostly based on genetics. (why not quantum theory... that might provide even more confusing and complex data to eagerly misinterpret for scientists). The misinterpreted or overlyinterpreted data is combined with some common sense observations alas made from the wrong perspective providing a theory that can choose any of the subtheories as tools to explain any of the phenomena and thus can hardly be beat by anything but the real truth.

It is still a matter of debate how sexual reproduction produces an evolutionary advantage even within the genetics department. They can't really find much meaning in the data, can they? Especially from the gene-centric view.

Noone is actually able to figure out the "natural laws" and figure out that all these genes and chemicals are just a manifestation of "system evolution tendency laws" that exist and can be described without concrete matter on which it acts. Evolution is a principle, a fundamental truth of time elapsing that holds true in all systems with changes bound by fixed rules and time.

Evolution can be explained abstractly and predict all the mechanisms that appeared in an abstract way.

Edited by addx, 02 April 2014 - 02:31 PM.

[Brett Black]

Addx, not every characteristic that an organism posseses has to impart a benefit or cost upon its survival. Some characteristics may have no impact upon survival, and thus some characteristics have no adaptive "explanation."

[Jeoshua]

Also, there are some characteristics that have a marked disadvantage in some realms and a benefit in others. A good example of this is the coloration of male birds, often very showy and bright. Very noticeable, and it attracts predators. But the ladies seem to like it, and that increases their chance of finding a mate. It has been argued that it is seen as a desirable trait since, if the bird can survive being that showy and noticeable to predators, then that bird must be an extremely fit one in other ways, and therefore would be seen as a better mate. I personally doubt that the lady birds look too deeply into the actual mechanics of it, and just respond to how beautiful the male birds are.

[Brett Black]

Antagonistic pleiotropy:
http://en.wikipedia....ropy_hypothesis

[addx]

Antagonistic pleiotropy:
http://en.wikipedia....ropy_hypothesis

Good link, followed it and found this:

http://en.wikipedia....ution_of_ageing

and then this:

http://en.wikipedia....ki/Evolvability


So I'm not the first one to play around with these ideas but I can fortify them like noone.

From the last link:

The study of evolvability has fundamental importance for understanding very long term evolution of protein superfamilies^[32][33] and organism phyla and kingdoms.^[34][35][36] A thorough understanding of the details of long term evolution will likely form part of the Extended Evolutionary Synthesis (the update to the Modern Synthesis).^[

So, there we go. My work is predicted



More from the last link:

Ageing theories based on evolvability[edit]

Goldsmith^[28] proposed that in addition to increasing the generation rate and thereby evolution rate a limited life span improves the evolution process by limiting the ability of older individuals to dominate the gene pool. Further, the evolution of characteristics such as intelligence and immunity may specially require a limited life span because otherwise acquired characteristics such as experience or exposure to pathogens would tend to override the selection of the beneficial inheritable characteristic. An older and more experienced but less intelligent animal would have a fitness advantage over a younger more intelligent animal except for the effects of ageing.
Skulachev^[29] has suggested that programmed ageing assists the evolution process by providing a gradually increasing challenge or obstacle to survival and reproduction and therefore enhancing the selection of beneficial characteristics. In this sense ageing would act in a manner similar to that of mating rituals that take the form of contests or trials that must be overcome in order to mate (another individually adverse observation). This suggests an advantage of gradual ageing over sudden death as a means of life span regulation.
Weissmann's 1889 ageing theory was essentially an evolvability theory. Ageing or otherwise purposely limited life span helps evolution by freeing resources for younger, and therefore presumably better adapted individuals.
Yang (2013)'s model^[2] is also based on mechanisms of evolvability. Aging accelerates the accumulation of novel adaptive genes in local populations. However, Yang changed the terminology of "evolvability" into "genetic creativity" throughout his paper to facilitate the understanding of how aging can have a shorter-term benefit than the word "evolvability" would imply.



More:


Summary of empirical evidence favouring programmed ageing[edit]


This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2011)

• Existence of complex programmed death mechanisms exist in semelparous species (e.g. octopus) including hormone signalling, nervous system involvement, etc. If a limited life span is generally useful as predicted by the programmed ageing theories, it would be unusual for an octopus to possess a more complex mechanism for accomplishing that function than a mammal.
• Discovery of "ageing genes" with no other apparent function.
• Caloric restriction effect: reduction of available resources increases life span. This behavior has a plausible group benefit in enhancing the survival of a group under famine conditions and also suggests common control.
• Progeria and Werner syndrome are both single-gene genetic diseases that cause acceleration of many or most symptoms of ageing. The fact that a single gene malfunction can cause similar effects on many different manifestations of ageing suggests a common mechanism.
• Although mammal life spans vary over an approximately 100:1 range, manifestations of ageing (cancer, arthritis, weakness, sensory deficit, etc.) are similar in different species. This suggests that the deterioration mechanisms and corresponding maintenance mechanisms operate over a short period (less than the life span of a short-lived mammal). All the mammals therefore need all the maintenance mechanisms. This suggests that the difference between mammals is in a common control mechanism.
• Life span varies greatly among otherwise very similar species (e.g. different varieties of salmon 3:1, different fish 600:1) suggesting that relatively few genes control life span and that relatively minor changes to genotype could cause major differences in life span—suggests common control mechanism.

So, it's not just my uneducated ass now. But my uneducated ass is smart enough to figure all this out with scraps of data


Brett, thanks! Seriously!


So, how does programmed ageing look now substantiated a bit by something that's not my ramblings?


Everything I thought of here of the top of my head simply provoked by you guys questioning me is on that wiki page. That seriously made my day. Brett thanks again.

Edited by addx, 03 April 2014 - 07:35 AM.

[addx]

Ageing is infact the primary driver of eukaryotic life form evolution. The great variety of life spans even among same families of species while at the same time causes of age related death are quite similar strongly suggests that it's an artificial driver of evolution. If one looks from the macro perspective its infact a way to balance and grow the eukaryotic food chain/tree suggesting again that it's a mechanism.


Life form(species) is a "meta organism"(think of ants and their phenotypes representing differentiated organs) represented by its carriers(organisms) and in a "loose binding" schema.

This is basicly identical to the way differentiated cells in the sack that represent the body of the organism are infact carriers of the genome, that a bit tighter binding but cells are still relatively autonomous within the body.

Life forms as single entities compete with each other for acquiring and keeping their portion of available "life source". Life forms compete using their carriers. They compete through population growth which increases momentary "life source" possession. Too much competition for "life source" causes evolution. Evolution extends available "life source" for life forms to compete for either by evolving more economic use(increasing complexity of the foodchain, evolving predators or parasites) or evolving ability to exhaust untouched resources(enabling migration to further/harder parts of the world or use of new kind of raw resources). Evolution is forced by ageing , mutation and replication selection mechanisms installed into the life form carriers through "loose binding" schema. The "loose binding" schema was conceived on top of sexual reproduction which requires "inter life carrier" signalling and guiding instinct(communication) which provided the neccessary scaffold.

That's your definition of life and evolution. Neither can be defined without the other. It's the same thing. It's a single thought that doesn't have a word for it.


Would anyone like to change their vote at this point or did anyone become indecisive?

Edited by addx, 03 April 2014 - 08:37 AM.

[Vardarac]

But the refrigerator did not evolve from an immortal amoeba that could repair itself indefinitely.

It's true that on a population level, the amoeba is immortal, just like our seed line is technically immortal. But there are at least two reasons I can think of to not bet the farm on aging being orchestrated disabling of repair mechanisms:

1. Consider that there may be a fitness cost for repair depending on the context. Calorie restriction increases longevity at least in part because it causes the body to recycle existing proteins and break down old cells, destroying potentially damaging garbage and possibly senescent cells in the process. However, longevity of this kind comes at a cost: It may cause a drop in sexual selection for the restricting organism; it can result in the organism's loss of fertility; or it may render the organism weaker, both to disease and to predation.

The failure of repair mechanisms to consistently work well, then, might have arisen evolutionarily as a way to make short-term gains for long-term benefit on an individual level (or, as you said, on the population level).

What is important to recognize is that this failure does not have to come from active suppression of "perfect" (assuming they once really were) repair mechanisms, but the simple decay of such mechanisms. Consider our defunct vitamin C synthesis gene. The selective pressure to have vitamin C synthesis dropped when we began eating fruit, hence it was allowed to decay through mutation; similarly, there was not, and may never have been, an ability to or evolutionary need for an individual to divide indefinitely or repair perfectly.

Now, on the other hand, there are examples where there is active suppression of repair mechanisms, like telomerase. However, telomerase is a particularly wonky example because its activation is frequently observed in cancer cells. It may be suppressed because its activation removes a check on unregulated or cancerous cell division and growth, a fitness cost and the underlying theory behind ADG's WILT proposal.

Together, these concepts suggest that we have reason to believe that aging may (at least in part or in majority) be the result of allowing repair mechanisms to decay by mutation (or perhaps remain insufficient) for short-term fitness gains. This holds with your idea that aging is advantageous yet still allows the "mechanism" to be passive failure rather than orchestrated failure, hence the popularity of the idea that it is a "mistake;" a "purposeful mistake", if you will.

However, like Brett has said, the ideas of passive failure versus evolved, active suppression of mechanisms that might otherwise keep us young are not mutually exclusive. I think this is the heart of the issue in this discussion. I think both should be researched and considered.

2. Immortality of the population does not necessarily entail immortality of the individual. This holds especially true in a multicellular organism, where the aforementioned cost of repair could critically decrease the organism's fitness. Do we really have evidence of observations of amoeba dividing indefinitely? By that I mean, if you were to make one permanently labeled amoeba (theoretically possible due to semiconservative DNA replication), give it perfect nutrition, and practically infinite room, would it go on dividing forever, or would it eventually die?

Check it out for yourself. Check out the functions of mu-opioid and kappa opioid receptors on the cellular level and then psychological. Then check out age-wise how the balance proceeds through life, check out sliced old rats or whatever. Mu opioid receptors enable subsequent growth of cells in exchange for sacrifice(for the CNS higher idea) if other factors align(growth hormone, insuline factors etc). Kappa opioids do the same thing - but they work differently, they alow just the sacrifice and mostly degrade the cell also depending on factors.

Certainly I would entertain your hypothesis as a co-cause, but there could be many other "primary drivers" of aging that work independently of this. Only experimental evidence will elucidate that. What are you suggesting - antagonize K-opioid receptors and watch the effect on overall health and on lifespan?

Edited by Vardarac, 03 April 2014 - 08:53 AM.

[addx]

But the refrigerator did not evolve from an immortal amoeba that could repair itself indefinitely.

It's true that on a population level, the amoeba is immortal, just like our seed line is technically immortal. But there are at least two reasons I can think of to not bet the farm on aging being orchestrated disabling of repair mechanisms:

1. Consider that there may be a fitness cost for repair depending on the context. Calorie restriction increases longevity at least in part because it causes the body to recycle existing proteins and break down old cells, destroying potentially damaging garbage and possibly senescent cells in the process. However, longevity of this kind comes at a cost: It may cause a drop in sexual selection for the restricting organism; it can result in the organism's loss of fertility; or it may render the organism weaker, both to disease and to predation.


The failure of repair mechanisms to consistently work well, then, might have arisen evolutionarily as a way to make short-term gains for long-term benefit on an individual level (or, as you said, on the population level).

What is important to recognize is that this failure does not have to come from active suppression of "perfect" (assuming they once really were) repair mechanisms, but the simple decay of such mechanisms. Consider our defunct vitamin C synthesis gene. The selective pressure to have vitamin C synthesis dropped when we began eating fruit, hence it was allowed to decay through mutation; similarly, there was not, and may never have been, an ability for or evolutionary need for an individual to divide indefinitely or repair perfectly.

Now, on the other hand, there are examples where there is active suppression of repair mechanisms, like telomerase. However, telomerase is a particularly wonky example because its activation is frequently observed in cancer cells. It may be suppressed because its activation removes a check on unregulated or cancerous cell division and growth, a fitness cost and the underlying theory behind ADG's WILT proposal.

Together, these concepts suggest that we have reason to believe that aging may (at least in part or in majority) be the result of allowing repair mechanisms to decay for short-term fitness gains. This holds with your idea that aging is advantageous yet still allows the "mechanism" to be passive failure rather than orchestrated failure, hence the popularity of the idea that it is a "mistake."

But like Brett has said, the ideas of passive failure versus active suppression of mechanisms that might otherwise keep us young are not mutually exclusive. Both should be researched and considered.

2. Immortality of the population does not necessarily entail immortality of the individual. This holds especially true in a multicellular organism, where the aforementioned cost of repair could critically decrease the organism's fitness. Do we really have evidence of observations of amoeba dividing indefinitely? By that I mean, if you were to make one permanently labeled amoeba (theoretically possible due to semiconservative DNA replication), give it perfect nutrition, and practically infinite room, would it go on dividing forever, or would it eventually die?

Check it out for yourself. Check out the functions of mu-opioid and kappa opioid receptors on the cellular level and then psychological. Then check out age-wise how the balance proceeds through life, check out sliced old rats or whatever. Mu opioid receptors enable subsequent growth of cells in exchange for sacrifice(for the CNS higher idea) if other factors align(growth hormone, insuline factors etc). Kappa opioids do the same thing - but they work differently, they alow just the sacrifice and mostly degrade the cell also depending on factors.

Certainly I would entertain your hypothesis as a co-cause, but there could be many other "primary drivers" of aging that work independently of this. Only experimental evidence will elucidate that. What are you suggesting - antagonize K-opioid receptors and watch the effect on overall health and on lifespan?

I agree with most of your reasoning. I do have an issue thinking about the mechanism as active or passive. It doesn't really matter, it is a mechanism, meaning not a mistake.

Maturing(growing to a final form) requires growth stopping mechanisms, meaning cell division inhibition. The same mechanisms purportate ageing after final form is reached. "Using cells" for their function but not allowing them to divide(be replaced) eventually kills you, depending on how well you provided for the ones that exist.

Antagonizing k opioid receptors proved much useful function in animal tests, but I don't think it's that simple. Opioids work in tandem with other factors and their receptors perform different functions depending on the ligand that activates them and the presence of arrestins which are controlled by something else etc. They have restored stem cells by manipulating a stress pathway operated by kappa opioids, so my idea is that they research kappa opioid receptors as much as they can and the spread out from there. I think opioidergic functioning is extremely important to elucidate and I think they don't have a chance to elucidate it without this complex evolutionary/sack of cell thought concept providing a road map.

I think cellular stress pathways need to be researched and processes controlling opioidergic gene expression meaning opioid receptors and all ligands.

In short I do beleive the opioids purpose is to "modulate/translate" the effects of behavior/interaction of organism with environment on ageing(instrinsic death source). Stress increases ageing, thriving decreases. In order to find what that exactly means - follow the opioids

The organism isnt repaired after maturation just the same as fear memories are never forgotten(after I think a few weeks in developement a protein blockade in amygdala blocks LTD processes). Why should they be forgotten? What would then force evolution? What would force the parent to tell the child of its fear? What would tell the female that the male is weak and keeps getting damaged and wasting resources on his misevolved behavior?

It's not a mistake or an imperfection. It infact it is the single most important thing we have to thank for our existance along with sexual reproduction.

Edited by addx, 03 April 2014 - 09:08 AM.

[addx]

The mechanism of ageing can't really be "active" because it is supposed to be operated by experience of the organism. The experience of the organism is sublimated from its atomic units cells - that evolved the body as a cooperating sack of cells to experience and spread accross the world better through it.

The body is as a very confined symbiotic group of localy phenotyped(differentiated) cells which orchestrate each other phenotyping through developement and cooperate to provide a beneficial advantage of survival and thriving that the body as a sack of cells provides.

The cooperation has a vague set lifetime decided by the fact how much the cells in the sack are "happy in the sack". If there is a higher purpose(the organism providing more survival and thriving than invdividual cells would have alone) there is always a sacrifice(ageing).

Ageing makes sure that the cells stay in the sack providing the higher purpose. If the organism fails to provide a survival advantage it is destroyed by the survival desire of the cells. Each "new(mutated) instance of a body/organism" created from the zygote is a chance at reducing future cell species sacrifice for thriving without endangering survival of the cell species.

Evolution of society is based on the same principles of unhappy individuals causing destruction through selfdestruction - evolving the able individuals to survive it.

Work out the same reasoning on all "major grouping levels" and you have proper evolution synthesis. And there's basicly no genetics involved.

Cells evolving new tiers of more intelligent behavior enabling more "intelligent"(beneficial for population, compromising for individual) organisation into groups. Types of groups depend on organs/nervous system layers that evolved from the basic sexual reproduction mechanism. There are 3 main direction of evolution, sexual reproduction, "acquring lifesource" behavior and "extinction avoiding" behavior in balance with each other. What evolves is form that results in behavior - infact meaning behavior - in 3 distinct directions. Behavior may be performed by common form(muscles) but infact it's the behavior that is selected for and the form follows. This allows evolution theory to nicely pass over into the "ether" of mammals which can pass on behavior without any "form" being exchanged. That's synthesis.

Edited by addx, 03 April 2014 - 11:27 AM.

[addx]

Everything I read feeds into this. (Which is also a symptom of acute mania)


From another thread http://www.longecity...hrenia-in-mice/

An experimental cancer drug appears to be able to reverse schizophrenia in mice, researchers at Johns Hopkins Medicine have found.
The team say an experimental anticancer compound can reverse behaviours associated with schizophrenia in adolescent mice with the rodent version of the disease.
They also discovered some of the lost brain cell function was restored in mice being administered the cancer drug.
Published in the Proceedings of the National Academy of Sciences, the researchers discovered the compound - FRAX486 – appears to halt a pruning process in the schizophrenic brain in which vital neural connections are destroyed.
The drug is one of a class of compounds called PAK inhibitors which provide some protection from brain damage caused through inherited disease. There is also evidence to show the drug could be used to treat Alzheimer's, while previous studies have found the PAK protein can initiate cancer and cell growth, meaning inhibitors could be developed to fight cancers.
The team said they were able to restore disabled neurons in adolescent and young adult mice with schizophrenia through FRAX486.
Study leader Akira Sawa said: "By using this compound to block excess pruning in adolescent mice, we also normalised the behaviour deficit. That we could intervene in adolescence and still make a difference in restoring brain function in these mice is intriguing."
In their experiments, the researchers reduced the expression of a gene called Disrupted-in-Schizophrenia 1 (DISC1), which appears to regulate the fate of neurons involved in higher order functions like information processing.
The deficit in DISC1 caused deterioration of parts of the brain that help neurons to communicate with one another. It also means the regulation of another protein, Rac1, cannot be controlled. Excess Rac1 leads to excess PAK in mice.

Does anyone read this like I do?

The subconscious <-> conscious tiers age/stress each other. The conscious tier is evolved by the subconscious tier and thus determines its fate in maturation/developement. The proteins involved in this story regulate this relationship.

Stress of the subconscious tier during developement causes early maturing of the upper, conscious tier, the one that's supposed to help it. Makes sense, does it not? Stress of the upper tier/conscious tier causes ageing of the subconscious tier(which already matured to start developing the conscious tier, so it means it can only age now). "Tiers" are allowed to thrive as they mature to provide cell division and differentiation and protein guided development of more advanced tiers. After that they are not allowed to grow any more by the tier that evolved/developed after them.

Now, does that explain ageing or what?

Top-down supression(of subconscious emotion/pain -> subconscious behavior) is probably facilitated by opioids which supress subconscious behavior, project(sublimate) the "needs for outcome"(which enables the conscious to project the solution outward or inward depending on positive or negative - causing paranoid-schizoid reasoning described best by m. klein) to the conscious to produce a behavior adaptation as the subconscious is "scared" of what is about the happen the conscious is set to avoid it in a smarter way(that is conscious of group ally behavior and enemy behavior and can provide better guidance than subconscious guidance).

This is how the body evolves and how tissues develop, mature and age each other depending on how the later evolved/developed parts serve the earlier evolved/developed parts. This provides a mechanism that only the later evolved parts are easily mutated or degenerated by not even developing them in the offspring.

Edited by addx, 03 April 2014 - 01:26 PM.

[Vardarac]

There is a lot of verbiage and at some points use of (unique?) terminology here that I'm not familiar with. A clear, very concise review of your theory, citations of the specific evidence you've used to construct it, and a clarification or simplification of terms where possible would be quite helpful. It's difficult to provide useful feedback on lots of text without a lot of studies or specific illustrative examples in accompaniment.

In particular, there are several claims you've made that I'm not sure I agree with that I think would be helpful to review:

It doesn't really matter, [the selection of aging] is a mechanism, meaning not a mistake.

The point I was trying to make here is that even though I think you have made a good hypothetical case for the evolutionary selection of aging organisms (indeed, we have many theoretical examples of this, such as salmon that die rapidly after spawning so as not to compete with their newly hatched fry), the manner through which aging originated could merely be senescence and loss of genetic fidelity over time to a level that hinders late-life fitness but not early-life fitness.

In other words, the primary mechanism of aging could be genetic or cellular mistakes, that is, random inherited or acquired errors (or for chemical/cellular process errors the late-life inability to remedy or compensate for these), but the selection of the mistakes or the propensity to make them is not accidental.

The proper function of the BRCA genes, for example, is as tumor suppressors. Errors in these or other tumor suppressors lead to cancer, but this does not necessarily mean development or fatality of that cancer by reproductive age, especially if the mutation is acquired in somatic cells rather than inborn. It does, however, increase the chance that disease and degradation will come later. Under your theory, such damaged genes might be selected perhaps when more rapid evolution or population turnover becomes necessary.

Maybe I'm reading you wrong, but from what I'm seeing there is (and this seems to be another central point of the debate) no reason to believe that selection for aging phenotypes is incompatible with popular senescence theories.

Maturing(growing to a final form) requires growth stopping mechanisms, meaning cell division inhibition.

Inhibition and/or lack of signal to divide. Effectively the same thing with respect to what you say next, but important to recognize for a reason I'll go into later.

The same mechanisms purportate ageing after final form is reached. "Using cells" for their function but not allowing them to divide(be replaced) eventually kills you, depending on how well you provided for the ones that exist.

The thing is, we know that stem cells (are these, as you say, functionally indistinct from the fully differentiated cells? I think they are IIRC since they have to not be differentiated before they divide, but correct me if I'm wrong) continue to divide and then differentiate into adulthood; they have to, or we wouldn't be able to continually renew our skin or intestinal epithelium well into old age. This is particularly apparent in radiation poisoning, which causes such a huge degree of DNA damage that cells stop dividing. Cancer patients and nuclear accident fatalities are both a testament to this.

Maturation-related growth certainly arrests well before old age and death in most humans, but maintenance division merely peters out as time goes by. The big question here is, what causes that, and what reason do we have to believe that cause? Is it inhibition or lack of signal, as you suggest? Is it senescence, or acquired or accumulated damage to the cell? Could it be a combination of both?

Studies to back up any of these hypotheses would be helpful. I would appreciate it if anyone could jump in here if they're aware of these.

The organism isnt repaired after maturation just the same as fear memories are never forgotten(after I think a few weeks in developement a protein blockade in amygdala blocks LTD processes).

So, are you saying here that stress, which causes fear, also causes cellular repair to stop? I don't really have a problem with that idea, although implying that it is almost a "behavior" that becomes increasingly ingrained in response to stress I am less keen on.

Why should they be [repaired]? What would then force evolution?

I think this goes back to what I was saying earlier, that you don't need to have a forced or sophisticated shutdown mechanism. All you need is selected imperfections sufficient to kill the organism on a timescale that brings about population balance or sufficiently quick evolutionary generation time.

By the same token, inhibition or lack of growth may be needed to actually preserve rather than decrease fitness; telling cells to continue dividing after they've taken a certain amount of damage is a bad thing. Here is a good review of the evidence for this point.

None of this is to bust your chops, but if you do not have a formal background in the sciences and have not written a clear, concise review of evidence to build a better case for your theory than for a potentially competing theory, then it will be very difficult for you to secure research interest or funding, especially when you want to tell scientists that they've been barking up the wrong aging tree. This is coming from a bachelor's-level peon who doesn't control the purse strings - smarter, more knowledgeable, and better-paid people than me will be much harder to convince!

[adamh]

addx, the central point of your thesis seems to be the belief that senescence is needed for evolution to work properly. You have not given anything to back that up besides your statement that otherwise, young animals would not be able to establish territories, or in the example of male lions, to take the head position in a pride. You believe that superior or more adaptive animals will not be able to survive unless the dominant animals first die off. Is that a fair summation of what you are saying?

However, a species does not start off by being dominant in its niche. All species are in competition with other species either through a prey - predator relationship or competition for food and space. Only in a few rare cases in which a species has become so dominant that other species can't meaningfully compete with it would give a situation in which the young might not be able to take territory from a non-aging group of adults. I'm not sure we have ever seen an example of such dominance, lions for example compete with many other predators, some of which hunt in packs and lions by and large stay away from them or from each other. A pack of 10 to 20 hyenas is more than a match for a lion.

If that's the case, then why would a young animal not be able to compete unless older animals of the same species die of old age? He or she would still have to compete with all those other species even if their own species graciously died off and made room for them. Dying off and making room makes it easier for competing species to take over the food or territory of the ones dying out. Therefore, not aging would give an evolutionary advantage to the individuals, and then to the species that was able to do it.

My theory is that aging is extremely hard to avoid and requires whole systems to be developed to sustain it. We have already a strong multifaceted immune system showing that we have a will to live. Incompetent cells and tissues are taken out by apoptosis or by other mechanisms and replaced with new. Damage due to trauma is repaired, even well into old age but the sum total of damage ranging from cross linking, dna damage which is improperly repaired to diseases, all the way up to malfunctioning systems overcomes the repair.

Why on earth would a species program aging into its makeup when nature does the job for us? What we have seen is the opposite, fighting with all we've got to keep it from happening. What advantage would there be for a species to basically self destruct? To make room for the young? That would make room for other species more so than for the young of the same species.

I think its a balance between survival strategies. Resources spent on keeping older animals alive could be spent on higher rates of reproduction which is another way for the species to survive. If the older animals die before they can reproduce that obviously is a dead end but since most animals will die of disease, injury or predation even if they have immortal genes, the payback for the species to have those immortal genes is not worth the effort. Better to concentrate on other survival traits. Better camouflage may give more benefit to the species than a theoretical immortality in which the animal will die anyway sooner or later. I see this as much more likely than programmed suicide.

[addx]

I do realise I can't just ramble if anyones going to listen, I have started working, building concepts, first theoretically working out evolution through logic and system developing to predict and define life behaviour in abstract but well defined terms. Ive done a very good job at this I think as this is in my nature. Ill have much more trouble as I move on as most of the facts that just merged into an "idea" in my head were simply picked up from reading various unrelated material, I didn't keep track, I have to refind much stuff and I have to research a lot more stuff in order to make a structured all encompassing theory from start of life to us. I did not give much attention to some facts which I will have to explain why I don't find important and so on. It will be an effort, so Im really still just at the start, trying to see if Ive bitten more than my share, probably have, but still, if it makes some sense, Ill work on it, it'll be good, but I guess I just can't get anyone actually in the field to discuss this with, I don't know anyone...

I don't need any funding. I just need to invest my time, research, note and think and write. I only want to put it out and there and try not to over extend or overproject some ideas and invalidate it all because I know theres a lot of sense to it, but I also know Im too uneducated-insecure and I can make blunders. I would appreciate someone to discuss with constructively from time to time from the fields involved and of more as I make progress, thats all.

As for the pharmacology research I mentioned, I don't want to carry it out myself, I just want to write what I think life is in a theory-book format and hope it is the truth and people recognise it, science recognises it regardless of its pedigree. I hope that if it is true that my pedigree won't matter, if it isn't, Ill be glad I got that out of my head, Im sure there is some truth in it.

I will answer other parts of your post tomorrow when I can think better, gtg sleep now.

[Brett Black]

There is a lot of verbiage and at some points use of (unique?) terminology here that I'm not familiar with. A clear, very concise review of your theory, citations of the specific evidence you've used to construct it, and a clarification or simplification of terms where possible would be quite helpful.

I agree with this. I've only been skimming over Addx's posts because I repeatedly run into parts that are difficult for me to make sense of.

[addx]

Ok, fair enough, since most of you asked the same questions this time Ill try to ramble less and be more concise.

But I have to start-evolve from scratch. Ill try and be as short as possible and precise.

-------------

Anyway, here goes.

Life is observed as a phenomena of integrating matter into self-replicating schemas.

Matter is integrated by self-replication itself, so making it a part of the self-replicating schema and increasing its growth rate.

Replicator is a form of matter facilitating a self-replication schema.

Life source is all the specific forms of matter and energy required for sustaining the behaviour of replicators of a specific self-replicating schema.


Life source is represented by nutrients and energy such as the minerals from the soil or the sun, or water from a river-rain or another plant or animal.


Death source represents all the specific conditions and that cause irreparable damage to replicators in terms of facilitating a specific self-replicating schema.

A death source can a difficult obstacle causing injuries, climate-chemical-radiational conditions and also another plant or animal by making it its life source.


The behaviour of the replicator through which it facilitates a self-replication schema can be observed to fall into following categories.

Acquiring is the observed behaviour of the replicator which serves the purpose of acquiring life source in order to replicate.

Avoidance is the observed behaviour of the replicator which serves the purpose of death source avoidance in order to survive to acquire and replicate.

All this doesn't really discern robot replicators from the ones we consider life so we must discern further.

Mutation is observed as a change of the form of a replicator inducing a chance of generating a new self-replicating schema via the newly formed replicator.

In order to reduce risk of all the replicators of a given schema losing replicating ability through spontaneous mutation, it is best set to happen during replication and it is observed to be so in most cases(simple life has methods of exchanging genetic material between replicators, this is a weak violation of this rule with some safety mechanism probably). This ensures that the original replicator will still keep an ability to self-replicate even if the mutated replicator fails to spawn a successful self-replicating schema.

Selection of self-replicating schemas is observed to result from population reduction of those self-replicating schemas whose replicators fail to avoid their death source and is also observed to result from lack of growth of those self-replicating schemas whose replicators fail to acquire the required life source(due to competition or otherwise caused failure).

Evolution of life is observed as increased integration (increased life sourcing) or reintegration (recycling - food chain) of matter resulting from mutation and selection generating new distinct self-replicating schemas over time.

Selection mechanisms as explained cause evolution to generate new distinct self-replicating schemas or replicators that are relatively more successful from old ones in terms of acquiring and/or avoiding in order to replicate.

This means that either:

a) acquiring for replication is relatively sacrificed to provide energy/time for increased avoidance mechanisms and this results in better survival of existing population at the cost of replication or reduced population growth.

b) avoidance is relatively sacrificed to provide for increased acquiring and replication resulting in increased population growth but increased risk to existing population.

It is immediately obvious that increased selection pattern a) results from the self-replicating schema being overwhelmed by its death source while increased selection pattern b) results from the self-replicating schema being overwhelmed by competition for its life source

This is enough to define the basic balances of simple life, but is not what we're after really. As said, complex life was enabled by sexual reproduction and ageing so let us try and explain that now.

The biggest event in evolution is the creation of the eukaryotic cell which features sexual reproduction.

Sexual reproduction spawned a meta entity called gene pool. From the perspective of the gene pool, its replicators refresh it every now and then with beneficial and less beneficial genes..

Sexual reproduction inverted the replicator to become a pawn of the newly evolved organisation of life called the gene pool rather than its own "master".

The organisation of life is upheld by the need of replicators to find each other to sexually reproduce and thus each time make a deposit into the gene pool.

It seems like this is a maladaptation as the replicators need to find each other results in fewer replications, so what is the tradeoff for such an organisation to evolve?

The tradeoff is obviously the gene pool - the organisation itself, but how does it prove to be an advantage for life?

It provides for "conditions" for depositing genes in the pool which keep it filled with healthier genes.

A replicator is forbidden to deposit genes before reaching "maturity". This proves he has minimum function to survive "long enough" to "prove" himself worthy of depositing genes and replicating (could be seen as reward from the gene pool, just to illustrate better how the flow of life flows).

Single cell and even some multi cell eukaryotic life forms preserved asexual reproduction but most didn't due to the following:

As sexual reproduction of cells evolved, asexual reproduction could be "sidetracked" towards building a body of cells. This is the evolution of multicellular life form. A cell divides asexually and coordinated via various mechanisms into a body of differentiated cells performing a different task.

The body of a multicellular life form is simply more evolved acquiring and avoiding behaviour resulting from "hijacking" the now optional asexual reproduction method.

The single cell instead of immediately beginning replication starts to build a body around it that will eventually help it survive to sexually reproduce with another such life form. The multicellular body enables acquiring of new life sources and avoidance of more death source.

The protein guided body development out of a single cell is a complex timed process which can easily go wrong(errors integrate over time), again causing a need to reject undeveloped bodies from allowing them to deposit in the gene pool as a gene that disrupts multicellular body producing processes would prove to be very unhealthy for the subscribers of the gene pool.

Remember, growing of the body is an evolution of tools support both acquiring and avoiding behaviour. It is in fact an evolution of the old replicating ability - asexual reproduction.

It seems that multicellular life forms invest quite the resource into their acquiring and avoiding behaviour tools. This causes quite a delay in reproduction compared to unorganised life. But the payoff of new life sources and avoidance of death sources seems worthy. The gene pool provides a payoff in terms of providing essential selection mechanisms for this newly evolved behaviour of growing bodies.

The growing bodies are investment into the future ability of a replicator to survive and replicate but how much should be invested? A body could be set to grow indefinitely before allowing time and resources to reproduce instead of growth. This may make it more sturdy in terms of avoidance but if it still somehow dies before replicating all the investment is literally lost. So,


the gene pool needs to regulate time to mature to make sure it gets enough deposits or in other words to make sure its subscribers deposit before a death source gets them but after maturation of the body.

If a "bad behaviour gene" survives development of the body there is nothing stopping it from polluting the gene pool. For example, a gene that causes worse acquiring after maturing would persist indefinitely if the species did not have a death source. The reduced replication this would cause wouldn't extinct the gene from the pool. Such subscribers would still make regular albeit slower deposits and the bad gene might infest the entire population of the gene pool subscribers before a death source pressures it out. So,

an artificial death source is provided through ageing of the mature body. Giving it a time limit for making deposits to the gene pool.

A gene infests the pool if it replicates more often than its replicators die out. In order to reduce this tendency ageing causes artificial timed deaths.

This makes sure that bad genes will be pressured out. Only genes whose ability doesn't impair the life form to make enough deposits to overcome the ageing vs. reproduction balance will spread.

If the gene pool provides steady evolution in this way that also means it is worthwhile to induce death of bodies which will become more and more obsolete relative to new ones being created. It then also makes sense kill the old bodies to allow more life source for new better ones.

Mutations are more often degenerating that beneficial so a gene pool can afford to age its bodies only if its population is large enough to guarantee a beneficial mutation among future generations and enough replicating speed to make up for age related deaths. If this doesn't happen the population and the gene pool will in fact start to degenerate.

Remember, selection process as defined before mostly selects for survival (which provides for many hardly alive species of simple life). Ageing setting a time limit for reproduction in fact causes a shift in balance of the selection process to select for acquiring and reproduction. Those who acquire and reproduce most in a time limit are selected for. Of course avoidance is still selected for, but secondary now.

This whole setup now superpowers evolution. Bodies allow new life sources and evasion of death sources. Selection mechanisms now force evolution through subscription to an organisation(for driving evolution/selection) rather than wait for it to happen spontaneously.

The fact that this whole setup is enabled through sexual reproduction and sexual reproduction requires coordination meaning signalling and understanding signals - sets the platform for evolution of more advanced organisations(for driving of evolution/selection) of later life, harems, mammal groups and even social/business organisations of humans.

It is obvious that unicellular eukaryotic life and simple is still "on the verge" of this mechanism providing a payoff. But the body building multicellular life depends on the gene pool to select properly for body building behaviour.

Ever growing plants basically lack ageing so their deaths are truly provided by senescence and or disease/parasites/other damage/violence. Ever growing plants are basically only limited by their ability to rise from the land level or in other worse to push nutrients to required heights. The static nature of plant bodies stemming from a lack of nervous system makes this feasible and the payoff of large bodies for getting at the sun and deep into the ground is obvious. This violates ageing payoff for this kind of life but as said, it looks less "lively". But even so, many plants have various ageing mechanisms and many of them are seasonal proving a fixed age limit.

Animal life with nervous systems on the other hand develops increasing difficulties to sustain an ever-growing body. The ever growing body would have to adapt behaviour and life sources to its size providing a complex goal for evolution. The more complex the nervous system is, the bigger the problems are if the body doesn't reach a final mature state to tune behaviour in. It is seen as evolution progressed that the final mature state of newer life forms evolved to a more and more fixed size or differentiation level for maturity.

Stress during maturing is detected by the nervous systems and quickens maturing in order to make sure the life form survives to replicate and deposit. Increased stress is matched by reduced maturing time keeping the selection of maturing proving worthiness intact.

Stress during ageing is also detected by the nervous system and increasingly degenerates the body and causes faster ageing as repair mechanism are increasingly shut down to facilitate death by anything that damages/stresses the body further. While ageing did shift the balance of selection towards acquiring, the way it is implemented(shutting down repairs) also provides selection for avoidance to still depend on external death sources rather than a precisely timed death.

A species without a serious death source and with unlimited access to life source will evolve its immune and repair systems to prolong its life past maturing. This is allowed as such species has no competition but obviously it can't result in spectacular life prolongation any time soon, and by the time it does the species will compete with itself for life source due to a rapidly growing(undieing) population again causing a reduction in life time.

As evolution went on new organisations of evolution/selection/life evolved out of the old ones, providing even more selection of even more advanced behaviour. The gene pool provides basic body building selection. The nervous system upgrades the gene pool to provide advanced behaviour selection. Then it upgrades again to provide behaviour learning uncoupling it from the gene pool into a new meta-entity that carries the "behaviour pool" - the group. Groups compete via their behaviour, part of which derives from the gene pool and part from the knowledge of the group.

Uhmm... too tired now to go on, shortened it a bit at the end so... I have a lot more if I go into the nervous system adaptations, I just quickly summarised them in the last paragraph. I hope we can discuss this part before going into detail about the nervous system. As timed maturing and ageing is modulated by the nervous system(which matures and ages as well) responding to responding to various types of stress at various levels, this provides for the n-tier sublimating complexity of ageing.

Anyway, I hope this is readable and understandable. The last paragraph probably isn't but that can be resolved after discussing this.

Edited by addx, 05 April 2014 - 09:12 PM.