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Thread: A hypothesis on a novel and uncommon aging mechanisms localized in the nervous system

  1. #1 A hypothesis on a novel and uncommon aging mechanisms localized in the nervous system 
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    Dear forum,

    I would like to present a hypothesis on novel aging mechanism that promotets cellular aging in animals with nervous system.

    The text is quite long, therefore a the Tl;Dr:

    TL;DR: An extremely weak, but extremely often activated feedback mechanism in animal nervous systems creates a high number of very weak memories of a special type in the course of life (up to one billion in humans). Their combined, ever-increasing inhibitory effects on cellular repair processes, mediated from the memory system to the body by neuroendocrine signals, represent an important cell non-autonomous aging mechanism which enforces—against the existing potential for cellular self-repair—the accumulation of cellular damage and waste.

    The first section of the hypothesis follows here. Due to the limit of 10000 characters per posting, the rest of the hypothesis follows in my comments to this posting.

    START HYPOTHESIS (Posting 1)

    A Hypothesis on a Novel Aging Process Localized in the Nervous System


    Licensed under CC BY 4.0, 2019, Rudger Kanding




    INTRODUCTION
    Gabuzda & Yankner open their 2013 Nature article „Physiology: Inflammation links ageing to the brain“ with the statement: „One of the least-understood aspects of ageing is its coordinated and stereotyped progression in all organ systems.", PMID 23636321, p. 197.


    To shed light on this aspect of aging, the present text examines the possible effects of a hypothetical feedback mechanism localized in the CNS. It is shown that the feedback mechanism induces procatabolic and proinflammatory effects on the cellular level and that these effects inhibit cellular repair mechanisms. The text argues that these inhibitory effects on cellular repair mechanisms may cause an important part of the aspect of coordinated, organism-wide aging mentioned by Gabuzda & Yankner.


    To get an overview of the hypothesis, it is sufficient to read part 1 up to the corresponding marker (= 2300 words).

    PART 1: THE HYPOTHESIS

    The hypothesis is based on the following 3 premises:

    1 MEMORY OVEREXPRESSION

    A memory trace, once formed in the neuronal networks of the brain, is never fully inactive. Rather it is permanently active to a tiny extent (let’s say around a micro-percent) compared to its activity during memory recall.


    This premise is hypothetical and is thought to be caused by the following two mechanisms A and B:


    Mechanism A) Existing memory traces are constantly slightly activated both by intrinsic neuronal activities taking place within memory systems and by external neuronal signals entering the memory systems.


    This assumption is supported on the one hand by research data showing that synaptic and neuronal spontaneous activities induce permanent basic activity in neuronal networks (see PMIDs 18319728 and 10980021). These activities are theoretically able to permanently activate existing memory traces at a very low level.


    Furthermore, during the waking state strong activities predominate within the cortex, which are caused by permanent ongoing internal calculations (PMID 21715156). Quote:


    "Statistical measures … show that the impact of internal network state on spiking activity is major in awake animals. Thus, cortical activity cannot be considered as being driven by the senses, but sensory inputs rather seem to modulate and modify the [permanently ongoing] internal dynamics of cerebral cortex.", p. 717.


    These activities, which are far stronger than those induced by synaptic and neuronal spontaneous activities, also reach the memory systems and could theoretically activate the contained memory traces permanently in a slight way.


    Mechanism B) In particular, aversive memories tend to lose small portions of their inhibitory control over time. This leads to a slight, persistent overactivity of the memory traces affected by this phenomenon. The underlying mechanism is explained in Part 2 of this article.


    I call this tiny basic activity of (parts of) memory traces produced by the mechanisms A and B the “OVEREXPRESSION” of a memory.


    Effectively, the two mechanisms A and B induce a slight neuronal noise in the output of memory systems. This noise contains therefore constantly varying, tiny portions of memory traces, the minor effects of which on body and mind are usually negligible.


    Crucially, however, a certain type of memory can, through the feedback mechanism described below, raise this neuronal noise to a significant and harmful level throughout life.

    2 OVEREXPRESSION OF AVERSIVE MEMORIES TRIGGERS ANTI-HOMEOSTATIC BRAIN-BODY MECHANISMS

    The overexpression of an _aversive_ memory, e.g. a fear memory, exerts a variety of extremely weak, anti-homeostatic effects on body and brain.


    This follows from research results of brain-body medicine, which investigates the influence of emotions on physical health.


    The basic argument underlying this claim is that if a negative emotion has a proven anti-homeostatic effect, then the overexpressed memory of that emotion will have the same effect, only much weaker.


    For mammals, extensive research data exists to support the view that negative emotion, and therefore also their overexpressed memories, have a deleterious effect on health (details follow below). It is assumed here, and supported further below with argument, that this view applies not only to mammals but to all animal species with nervous systems. Due to the large amount of research data available for mammals on aging and brain-body mechanisms, the main argumentation is presented on the basis of this animal class.


    Decisive for the hypothesis presented here will be that among the brain-body mechanisms triggered by overexpressed aversive memories there are also those that inhibit cellular repair mechanisms. On this basis, the text will conclusively show that the overexpression of a unique type of very weak aversive memory, which is formed extremely frequently over the course of life, induces a significant part of the aging phenotype through its inhibitory effect on cellular repair mechanisms.


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    Ok, here Posting 2:

    3 RE-MEMORIZATION OF OVEREXPRESSED MEMORIES CREATES A VICIOUS CYCLE
    Now the crucial premise:


    The normal mechanisms of memory perception, present in all animals with nervous systems, lead to the unconscious perception of the OVEREXPRESSED EMOTIONAL COMPONENTS of aversive memories …


    ... AND TO THE CONTINUOUS AND UNCONSCIOUS RE-MEMORIZATION of these overexpressed emotional components as part of the emotionality of the normal, ongoing autobiographical events ... followed by their RE-OVEREXPRESSION, ... and subsequent re-memorization ... and so on ... moment by moment, the whole life long.


    Ok, that sounds really weird. Therefore again step by step, human-centered argued:


    Step 1, memory overexpression: All memories of aversive events of your life are permanently a little bit active (i.e., „overexpressed“), thereby slightly shifting your state of mood towards negativity.


    Step 2, re-memorization: This (consciously imperceptible) slightly negative state of mood is re-memorized as a new aversive emotional memory along with the current autobiographical event. Since this newly formed memory is also overexpressible, this step increases the total number of aversive memories that can be overexpressed.


    Step 3 is a return to step 1, re-overexpression: In this return to step 1, the existing aversive memories are again overexpressed. Since the number of aversive memories was increased by the previous step, this re-overexpression leads to a further slight increase in the negativity of your state of mind.


    This changed state of mind is then re-memorized again in step 2, which again increases the number of overexpressed aversive memories ... and so on and so forth, the whole life long.


    In this way, the number of aversive memories that are overexpressed, and likewise their combined anti-homeostatic effect (remember premise 2 above), is constantly increasing.


    This is obviously a vicious cycle (hereafter just called “VC”). Vicious, because it induces a steadily increasing anti-homeostatic effect in the body, which may react with potentially dangerous health problems (see below).


    Since in humans a new autobiographical event is generated and memorized roughly every second (actually when a new visual scene occurs after an eye movement), overexpressed memories are re-memorized also roughly every second. The VC creates therefore during a human life about one BILLION of extremely weak aversive memories - and every single one of them exerts an extremely weak anti-homeostatic effect on the body.


    (Yes, you read that right, one BILLION, 10 ^ 9, 1000 MILLIONS of memories ... no joke.)


    A side note: The VC basically works like the mechanism „compound interest with contributions” in the financial sector. It starts as soon as the first aversive memory has been formed. Aversive memories, which are subsequently formed by negative life experiences, are "contributions".


    Note that after the formation and subsequent overexpression of the first aversive memory, the VC progresses in extremely small steps: For better illustration, the strength of the first aversive memory is defined as "1", and the initial negativity of the state of mind as "0". The first aversive memory is initially overexpressed at an assumed rate of only 10 ^ -8 (see premise 1) and shifts the negativity of the state of mind to the value 10 ^ -8. The subsequent re-memorization and re-overexpression of this tiny negativity, again at a rate of only 10 ^ -8, therefore yields an overexpressed portion of only 10 ^ -16 of the first aversive memory. This shifts the negativity of the state of mind to the value (10 ^ -8) + (10 ^ -16). And the following steps are, at first, in the same order of magnitude.


    These are really extremely small steps. The VC therefore only has a significant effect over longer periods of time. Using the compound interest formula: A = P x (1 + R) ^ N, and assuming the formation of only one aversive memory at the beginning of life, a simple calculation of the negativity induced by the VC after 20, 40, 60 and 80 years of operation yields the following values:


    20y: 1.1 x 10 ^ -6, 40y: 1.2 x 10 ^ -5, 60y: 0.014, and 80y: 1.65.


    [Parameters are: P = principal investment = overexpression rate of one aversive memory of strength „1“ = 10 ^ -8; R = interest rate = overexpression rate = 10 ^ -8; N = number of compounding periods = (18h wake time per day)*60*60*#years (corresponds to a re-memorization frequency of 1/sec).]


    The value of 1.65 for 80y operation time would correspond to the more than full permanent activity of the first aversive memory. Under the assumption that the original aversive experience leading to the formation of the first aversive memory triggered clear physiological reactions, such as increased blood pressure, pulse and respiratory rate, this value would certainly have dangerous effects.


    However, this calculation is not realistic because it does not take into account the many factors that control the overexpression of memories and their effects. Its aim is only to demonstrate that, within a human life span, the feedback mechanism is theoretically able to rise the tiny effects of memory overexpression to a significant level.


    These were the three premises on which the hypothesis is based.
    AVERSIVE MEMORIES LAST FOR A LIFETIME
    Decisive for the strength of the effects caused by the VC is the decay rate of aversive memories. If this decay rate is higher than the VC's aversive memory rebuild rate, the VC's effects will disappear over time. This raises the question of the lifetime of aversive memories.


    In principle, aversive memories are of crucial importance for survival. Since it is impossible for an organism to reliably predict the long-term relevance of aversive memories, their high importance for survival demands that they never be forgotten, but must be stored permanently. Mechanisms that adapt aversive memories to a temporarily changing relevance must therefore be realized by evolution through their weighted inhibition.


    This theorized long lifetime of aversive memories is proven in animal experiments, see PMID 15084662. Quote:


    „The current study addressed this issue [the permanence of conditioned fear memory] by exposing rats to two [distinct] fear conditioning episodes separated by 16 months.“, p. 3811,


    „Sham-lesioned rats showed high and comparable levels of freezing across all context and tone tests [i.e., also to the unique context/tone pair conditioned 16 months before the test].“, p. 3810.


    This suggests that, at least in rats, aversive memories are preserved over the entire lifetime. In humans, traumatic memories are an example of the long lifespan of aversive memories.


    Thus, due to this long lifespan of aversive memories, the VC really creates the postulated high number of memories. But I suppose many of them lose a lot of their contextual information throughout life. For background information, google „silent engram“.


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    Time Lord Paleoichneum's Avatar
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    Im still not buying the assertion of memory having an effect on aging. For the myriad of reasond mentioned on the .org

    Im going to ask again, have you done any reading on intro level college biology about size reletive to life span in mammals. It's very well understood and has nothing to do with memory
    If more of us valued food and cheer and song above hoarded gold, it would be a merrier world. -Thorin Oakenshield

    The needs of the many outweigh the need of the few - Spock of Vulcan & Sentinel Prime of Cybertron ---proof that "the needs" are in the eye of the beholder.
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    Ok, here posting 3, which finishes part 1 of the hypothesis:

    THE VC EXISTS IN ALL ANIMAL SPECIES WITH NERVOUS SYSTEM

    Since the main explanations of VC were human-centered, here is a brief explanation of why the VC most probably exists in all species with nervous systems:

    The feedback mechanism that generates the VC consists of the three components "memory overexpression", "state of mind" and "memorization of the state of mind". Memory overexpression alters the state of mind, which in turn is re-memorized and re-overexpressed - this is the basic mechanism of the VC.

    What is crucial now is that the components of the VC most likely exist in all animals with nervous system, even in simple organisms such as the nematode C. elegans.

    Briefly explained using C. elegans: Memory overexpression certainly exists to a certain degree in the constantly active nervous system of this animal. Furthermore, the state of the neurons, which coordinate the main activities of this animal during wakefulness, can be regarded as a state of mind. And since the state of mind represents the survival critical assessment of the current life situation, simple mechanisms for its memorization must exist to enable the simple learning processes that C. elegans is capable of. See the article „An elegant mind: learning and memory in Caenorhabditis elegans.“, PMID 20335372. Quote: „The section on associative learning highlights the worm's ability to learn and remember relevant environmental stimuli, including smells, tastes, temperatures, and oxygen levels …“, p. 191.

    This argumentation for the existence of VC in C. elegans applies all the more to animal species with more complex nervous systems. Therefore, the VC and its anti-homeostatic effect might be present in all species with nervous systems.

    This leads to the decisive statement of the hypothesis, thought to be valid for all species with nervous system:

    MAIN ASSERTION OF THE HYPOTHESIS


    THE COMBINED ANTI-HOMEOSTATIC EFFECTS OF THE OVEREXPRESSION OF ALL THE MEMORIES FORMED BY THE VC, CREATE IN THE LONG RUN, MAINLY BY INHIBITING CELLULAR REPAIR MECHANISMS, THE MAIN PARTS OF THE AGING PHENOTYPE AND RELATED DISEASES.


    This assertion requires some clarifying remarks:

    1) The VC is not a cellular aging process, but a centrally controlled "aging inducer" that triggers evolutionary ancient cellular aging mechanisms such as apoptosis and cellular senescence through systemically acting neuroendocrine signals.

    The VC is not the only mechanism of this kind. Several phenomena and mechanisms are known in which the speed of aging is modulated by systemic signals. These may have been created by evolution to extend or shorten the lifespan of an individual under certain circumstances, with the aim of increasing the chances of survival of the species as a whole. Examples are "hypothalamic programming of aging" (PMID 23636330), caloric restriction (PMID 27338076), hormesis (PMID 23799363), and phenoptosis (PMID 10648966). Arguments suggesting that the VC is an important representative of this class of mechanisms and possibly regulates the important mechanism "hypothalamic programming of aging", follow below.

    2) The sudden, organism-wide aging and death of some plants after flowering indicates the existence of systemic aging mechanisms in plants. The VC hypothesis cannot explain these mechanisms. This does not pose a problem, because evolution in plants has most likely taken its own, nervous system independent path to the development of systemic aging mechanisms.

    [If you just wanted to get an overview of the hypothesis, you can stop reading here.]

    For all others we continue with the clarifying remarks ...

    3) The existence of the feedback mechanism that generates the VC (i.e., memory overexpression induces an altered state of mind that is re-memorized) is beyond question, since the necessary components, a) overexpression of emotional memories, b) induction of the overexpressed emotion into the state of mind, and c) the re-memorization of this changed state of mind, certainly exist in humans.

    The first effect is tiny, but unavoidable in neuronal networks. The second effect is a normal influence of active emotional memories on the state of mind: for example, remembering a sad event induces a slight sadness. And the third effect is part of the normal function of the human brain: the current state of mind is memorized together with the current autobiographical event.

    The crucial questions are therefore: under the assumption that aversive memories do not decay, are the effects of the memories created by the VC theoretically strong enough to have a significant effect after a few decades? And if so, are the extremely weak memories generated by the VC really long-lived enough to sustain these effects permanently?

    4) In addition to inhibiting repair mechanisms, VC also has a direct cell-damaging impact through its proinflammatory effect. Furthermore, it permanently exerts a diffuse, body-wide, tensioning effect on muscle fibers. In addition, VC triggers, directly and indirectly, a myriad of less important systemic and cellular mechanisms. To keep the presentation of the hypothesis short, these points are not discussed here.

    5) There is no simple relationship between how the VC is configured specifically in a species (i.e. number, strength and effects of the VC memories) and the lifespan of that species. Evolution used countless parameters to adjust the lifespan of a species (see e.g. PMID 25798145), the effects of which can mask the influences of the VC.
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    Quote Originally Posted by Paleoichneum View Post

    Im going to ask again, have you done any reading on intro level college biology about size reletive to life span in mammals. It's very well understood and has nothing to do with memory
    I’m quite deep in aging science, having printed and intensely read about 800 research and review articles and annotated them with thousands of remarks. From this base I created my original hypothesis comprising the horrible amount of around 50000 words and 300 references. My posting here is the short version of only the senescence part of this hypothesis.

    There is also a possible link between body size and memory, because larger animals have less predators and therefore need less fear reactivity, which results in a lower number of lifetime fear memories.

    But as mentioned in my hypothesis, there’s no simple relationship between the VC and species lifespan, because evolution adjusts species lifespan by means of many parameters.

    Naked mole rats, or bats are a good example, because they are small but live long.
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    If more of us valued food and cheer and song above hoarded gold, it would be a merrier world. -Thorin Oakenshield

    The needs of the many outweigh the need of the few - Spock of Vulcan & Sentinel Prime of Cybertron ---proof that "the needs" are in the eye of the beholder.
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    A couple of questions: are you here because you failed to find anyone who accepts your hypothesis on the other forum?
    Are you under the impression that posters here (a number of whom are also habitués of the forum where you last attempted to push this) will be less critical?
    "[Dywyddyr] makes a grumpy bastard like me seem like a happy go lucky scamp" - PhDemon
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    Quote Originally Posted by Dywyddyr View Post
    A couple of questions: are you here because you failed to find anyone who accepts your hypothesis on the other forum?
    Are you under the impression that posters here (a number of whom are also habitués of the forum where you last attempted to push this) will be less critical?
    I’m mainly here to get a little bit of feedback because well founded criticism is really invaluable. Because I read a lot of articles and found a lot of points that support my hypothesis to a certain degree, I’m now too much inside my hypothesis and need reflections to recognize the weak points of the hypothesis. The comments in .org helped me already a lot and i hope to get now more specific ones here.
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    How has your "theory" responded to the criticism you got on the other forum? You ignored most of it and responded with walls of text that did not address anything..
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    Quote Originally Posted by PhDemon View Post
    How has your "theory" responded to the criticism you got on the other forum? You ignored most of it and responded with walls of text that did not address anything..
    1) All important points explained in more detail

    2) Complete retraction of my position that the VC is the major driving factor of aging

    3) Added the relation of the VC to aging in plants

    4) Gave examples of other non-entropic aging mechanisms

    5) Added the decisive quotes of the mentioned studies

    6) Added an argumentation why aversive memories do not decay

    7) Added an argumentation why the VC might exist in all animals with nervous system

    8) Added a calculation of the effects of the VC

    Criticize my changes, but please don’t tell i didn’t respond to the criticism I got in the .org.

    All the listed changes try to address the criticism I got.
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    OK, you may have tried, but a lot of your clarifications did not address the core problem of the criticism, hence my "walls of text" comment.
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    If someone is interested, here an improved version of the core premise of the hypothesis:

    3 RE-MEMORIZATION OF OVEREXPRESSED MEMORIES CREATES A VICIOUS CYCLE


    Now the crucial premise:

    The normal mechanisms of memory perception, present in all animals with nervous systems, lead to the unconscious perception of the OVEREXPRESSED EMOTIONAL COMPONENTS of aversive memories …
    ... AND TO THE CONTINUOUS AND UNCONSCIOUS RE-MEMORIZATION of these overexpressed emotional components as part of the emotionality of the normal, ongoing autobiographical events ... followed by their RE-OVEREXPRESSION, ... and subsequent re-memorization ... and so on ... moment by moment, the whole life long.
    Ok, that sounds really weird. Therefore again step by step, human-centered argued:


    Step 1, memory overexpression: Due to the mechanisms described in premise 1, all aversive memories of your life are permanently a little bit active, i.e. "overexpressed".

    Step 2, Slight induction of the aversive components of overexpressed memories: The memory overexpression that took place in the previous step virtually seamlessly activates a standard function of the brain:

    Activated brain function: Those neuronal mechanisms that feed the content of a recalled memory into the mind, induce to some extent the emotion stored with the memory. For example, remembering a sad event induces a slight sadness into the mind.

    This function causes the aversive components of overexpressed memories to be slightly induced into the mind, which corresponds to a slight (not consciously perceivable) shift in the state of mind towards negativity.

    Step 3, re-memorization: A further standard function of the brain activates the next step:

    Activated brain function: An autobiographical event is memorized together with the accompanying emotions.

    This function causes the slightly negative state of mind induced in the previous step to be memorized as a new aversive memory along with the current autobiographical event. Since this newly formed memory is also overexpressible, this step increases the total number of aversive memories that can be overexpressed.

    Return to step 1, re-overexpression: In the return to step 1, the existing aversive memories are again overexpressed. Since the number of aversive memories was increased by the previous step, this re-overexpression leads in step 2 to a further slight increase of the negativity of your state of mind. This changed state of mind is then re-memorized again in step 3, which again increases the number of overexpressed aversive memories ... and so on and so forth, the whole life long.


    In this way, the number of aversive memories that are overexpressed, and likewise their combined anti-homeostatic effect (remember premise 2 above), is constantly increasing.
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    Now that you've narrowed the scope so much, why do you feel its a viable hypothesis that humans alone would have this proposed problem, and no other organism, all of which age and die? (please no waffle about "immortal" germ lines or bacteria, as that is fallacious)

    *[Repeat of my post from the .org]
    If more of us valued food and cheer and song above hoarded gold, it would be a merrier world. -Thorin Oakenshield

    The needs of the many outweigh the need of the few - Spock of Vulcan & Sentinel Prime of Cybertron ---proof that "the needs" are in the eye of the beholder.
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    Quote Originally Posted by Paleoichneum View Post
    Now that you've narrowed the scope so much, why do you feel its a viable hypothesis that humans alone would have this proposed problem, and no other organism, all of which age and die? (please no waffle about "immortal" germ lines or bacteria, as that is fallacious)

    *[Repeat of my post from the .org]
    In order to cover this point I added the following argument to the hypothesis:


    THE VC EXISTS IN ALL ANIMAL SPECIES WITH NERVOUS SYSTEM


    Since the main explanations of the VC were human-centered, here is a brief explanation of why the VC most probably exists in all species with nervous systems:


    The feedback mechanism that generates the VC consists of the three components "memory overexpression and induction", "state of mind" and "memorization of the state of mind". Memory overexpression induces a changed state of mind, which in turn is re-memorized and re-overexpressed - this is the basic mechanism of the VC.


    What is crucial now is that the components of the VC most likely exist in all animals with nervous system, even in simple organisms such as the nematode C. elegans.


    Briefly explained using C. elegans: First, the state of the neurons, which coordinate the main activities of this animal during wakefulness, can be regarded as a state of mind. And since the state of mind represents the survival critical assessment of the current life situation, simple mechanisms for its memorization must exist to enable the simple learning processes that C. elegans is capable of. See the article „An elegant mind: learning and memory in Caenorhabditis elegans.“, PMID 20335372. Quote: „The section on associative learning highlights the worm's ability to learn and remember relevant environmental stimuli, including smells, tastes, temperatures, and oxygen levels …“, p. 191. And finally, there is certainly some degree of memory overexpression and induction in the constantly active nervous system of this animal.


    This argumentation for the existence of the VC in C. elegans applies all the more to animal species with more complex nervous systems. Therefore, the VC and its anti-homeostatic effect might be present in all species with nervous systems.
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    Plants, bacterium, fungi, etc all age and die as well, most at a similar rate as animals with nervous systems in many/most cases.

    Nemotodes learning is not support for your assertion of bad memories cause aging
    If more of us valued food and cheer and song above hoarded gold, it would be a merrier world. -Thorin Oakenshield

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    Quote Originally Posted by Paleoichneum View Post
    Plants, bacterium, fungi, etc all age and die as well, most at a similar rate as animals with nervous systems in many/most cases.

    Nemotodes learning is not support for your assertion of bad memories cause aging
    This is covered in the clarifications part, directly after the main statement of the hypothesis:

    1) The VC is not a cellular aging process, but a centrally controlled "aging inducer" that triggers evolutionary ancient cellular aging mechanisms such as apoptosis and cellular senescence through systemically acting neuroendocrine signals.

    The VC is not the only mechanism of this kind. Several phenomena and mechanisms are known in which the speed of aging is modulated by systemic signals. These may have been created by evolution to extend or shorten the lifespan of an individual under certain circumstances, with the aim of increasing the chances of survival of the species as a whole. Examples are "hypothalamic programming of aging" (PMID 23636330), caloric restriction (PMID 27338076), hormesis (PMID 23799363), and phenoptosis (PMID 10648966). Arguments suggesting that the VC is an important representative of this class of mechanisms and possibly regulates the important mechanism "hypothalamic programming of aging", follow below.

    2) The sudden, organism-wide aging and death of some plants after flowering indicates the existence of systemic aging mechanisms in plants. The VC hypothesis cannot explain these mechanisms. This does not pose a problem, because evolution in plants has most likely taken its own, nervous system independent path to the development of systemic aging mechanisms.


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    Quote Originally Posted by Paleoichneum View Post
    Plants, bacterium, fungi, etc all age and die as well, most at a similar rate as animals with nervous systems in many/most cases.

    Nemotodes learning is not support for your assertion of bad memories cause aging
    This section is also related to the issue:

    To what extent does the VC contribute to aging?

    The extent to which VC contributes to the aging process, relative to purely entropic cellular aging processes and relative to other possibly existing centrally controlled aging inducing mechanisms, is very difficult to estimate.

    However, the life span of vertebrates varying by a factor of 2000 (PMID 29074821) suggests that there exist other mechanisms besides purely entropic ones that control the lifespan of an animal species. Furthermore, the long life of some animals (up to 11000 years in sponges) and the proliferative immortality of bacteria (PMID 31120870), the germline (PMID 15546980) and HeLA cells suggest that pure entropic cellular aging is much slower than normal aging of most animals. This means that non-entropic aging processes, such as „hypothalamic programming of aging“ (PMID 23636330), or the hypothetical VC, may be significantly involved in the aging process of animals.
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    "Immortality" you keep using this word, I do not think it means what you think it means. They still DIE is a very short time, they just happen to clone. And germ line would DIE as soon as humans stopped providing the ideal conditions. So stop trying to use them as examples.
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    Quote Originally Posted by Paleoichneum View Post
    "Immortality" you keep using this word, I do not think it means what you think it means. They still DIE is a very short time, they just happen to clone. And germ line would DIE as soon as humans stopped providing the ideal conditions. So stop trying to use them as examples.
    Thats why i changed “immortality” into “proliferative immortality”, indicating that not individual cells, but the cell line is immortal (of course only when the necessary conditions are provided).


    I do not infer from this proliferative immortality a potential immortality for multicellular organisms. For me it only indicates that aging is not only caused by entropy but that additional mechanisms must be at work.
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    But they ARE subject to entropic aging at the same rate as other cells. Tge use of the term here seems to be a weasel word to make a point that isnt actually valid
    If more of us valued food and cheer and song above hoarded gold, it would be a merrier world. -Thorin Oakenshield

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    Quote Originally Posted by Paleoichneum View Post
    But they ARE subject to entropic aging at the same rate as other cells. Tge use of the term here seems to be a weasel word to make a point that isnt actually valid
    My argument is not really watertight, but as an INDICATOR that besides entropy additional mechanisms must be involved in aging of multicellular organisms, it’s not too bad.

    Here an interesting excerpt of the Wikipedia article on „biological immortality“:

    Many unicellular organisms age: as time passes, they divide more slowly and ultimately die. Asymmetrically dividing bacteria and yeastalso age. However, symmetrically dividing bacteria and yeast can be biologically immortal under ideal growing conditions.[14] In these conditions, when a cell splits symmetrically to produce two daughter cells, the process of cell division can restore the cell to a youthful state. However, if the parent asymmetrically buds off a daughter only the daughter is reset to the youthful state—the parent isn't restored and will go on to age and die. In a similar manner stem cells and gametes can be regarded as "immortal".
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