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There seem to be a number of ideas about why we age. Hypotheses include the gradual accumulation of cell metabolic products affecting organism function and the reduction of telomere length during cell division. My hand-wavey idea would be "wear and tear".

Are we anywhere near a consensus theory of senescence?

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    $\begingroup$ This is one of the subjects where -- in my opinion -- there can't be just a single dominating theory, at least not now. As in many other areas of biology, many different theories do co-exist here and the reality seems to be a mix-up of them all. $\endgroup$
    – Alexander Galkin
    Dec 27, 2011 at 11:00
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    $\begingroup$ Can you explain why there can't be a single dominating theory? Your comment suggests that in the future we might have one. I find this a fascinating subject - since so many pathologies are age related, surely a "theory of senescence" should be one of the primary focuses of medicine..? $\endgroup$
    – Poshpaws
    Dec 27, 2011 at 12:02

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The 'wear and tear' argument is most likely true but it is also interesting to reason about ageing as inevitable from the evolutionary point of view.

To set up the argument, we need two things: First, each individual has got a 'reproductive potential' which is realised throughout life. This means a deleterious mutation which has an effect in early life, will affect reproductive value more than a mutation which manifests itself in later life, after the individual has already had offspring. Thus selection will act strongly on genes which are expressed in early life than on those which are expressed later. For that reason, there's no strong selection against diseases such as diabetes or cancer. This argument can be applied not only to occurrence of disease but also to decay of ordinary functions of the body.

Secondly, cells in the body are constantly renewed and defects such as telomeric breaks are repaired. Mutations in the soma are taken care of by the immune system and can be in principle avoided. The fact that they tend to accumulate in later life can be explained by the first point: selection is weaker to oppose telomeric breaks and mutations in later life.

I was trying to be brief here, but there are more sides to the argument (e.g. Williams' antagonistic pleiotropy). Modular Evolution (Vinicius, CUP 2010) provides a good overview of the evolutionary aspect of theory of senescence (and many other interesting evolutionary arguments).

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  • $\begingroup$ Thanks @Greg Slodkowicz. Would it then be true to say that all sexually reproducing species age? I ask this because some bacteria do not exhibit senescence. $\endgroup$
    – Poshpaws
    Dec 27, 2011 at 17:25
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    $\begingroup$ en.wikipedia.org/wiki/Turritopsis_nutricula is a famous example. In case of bacteria, they are said to be immortal as a colony, since they can divide indefinitely. But for single-cell organisms which reproduce asexually even the notion of an individual is blurred, since each cell splits to form two identical daughter cells. $\endgroup$
    – Greg Slodkowicz
    Dec 27, 2011 at 21:51
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    $\begingroup$ I’ve never been completely convinced by the wear & tear argument: germ cells (and all unicellular organisms) are direct descendants of the “arch” cell. Not just genetical, but cytoplasmatic, through cell division. If the wear & tear argument were naively true, germ cells would long have ceased working. Now, it may be that preventing wear & tear is so expensive that metazoa have disbanded it in somatic cells (where it’s expendable). But I’ve never heard that mention. $\endgroup$
    – Konrad Rudolph
    Dec 29, 2011 at 9:20
  • $\begingroup$ Maybe recombination prevents the accumulation of defects that you would expect from germ cells by providing other alleles that may be functional. $\endgroup$
    – Armatus
    Jun 21, 2012 at 15:49
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Once could argue that we die because it is advantageous to get rid of mature individuals once they have reproduced. Because mature individuals have no more offspring to convey beneficial genes, those offspring which will benefit from knocking off their ancestors will have an evolutionary advantage.

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    $\begingroup$ Actually, you want them to stick around long enough to take care of their offspring. $\endgroup$
    – Greg Slodkowicz
    Jan 1, 2012 at 12:08
  • $\begingroup$ But not too much longer ofter that. Any post-reproductive beneficial traits will not be selected for, and will die out. $\endgroup$
    – dar7yl
    Jan 2, 2012 at 8:01
  • $\begingroup$ @dar7yl Except for post-reproductive lifespan in women. Not sure how strongly it is selected for, but it clearly has an advantage. See here. Awesome results! $\endgroup$
    – kasia
    Jan 5, 2012 at 2:15
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    $\begingroup$ That doesn't explain why we don't just reach sexual maturity and then stop aging - it can't be the primary explanation, although it would be a selective pressure once aging existed in the first place. $\endgroup$
    – Rik Smith-Unna
    Feb 3, 2012 at 18:23
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There is a pretty good discussion on this topic in chapter 2 of Geriactric Medicine - An Evidence Based Approach (4th ed) by Cassel. This is the main reference for the info below which can hopefully add something to the answers already given.

In terms of views on ageing, there's evidence to support both:

  • general principles that may apply to it; and
  • it being a consequence of a collection of degenerative processes (this is apparently the more supported view).

Since almost all biological systems in the body degenerates with age and this happens seemingly at random, it's been difficult to identify particular catalysts that cause this. Consequently, biologists apparently steer away from a general theory or mechanism.

However, there are two classes of theories that have been floating around. That is 'loose cannon' and 'weak link'.

Loose Cannon encompasses theories that support the 'wear and tear' proposition. Two popular theories under this banner are free radicals and glucose.

Weak Link suggests that particular physiological systems are vulnerable during senescence and if a system fails, the whole body begins to decline. It's suggested that the neuroendocrine and immune systems are particularly vulnerable.

There is also a limit on the ability of cells to replicate - this is called the Hayflick Phenomenon (or limit). The reduction of the enzyme Telomerase, which lengthens telomeres during mitosis, is implicated in limiting a cell's ability to replicate indefinitely.

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  • $\begingroup$ The link to springerlink.com is broken. I'm also unable to find any copy saved on the Wayback Machine. $\endgroup$
    – user70723
    Jun 7, 2022 at 16:12
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"WHY" we age is a different question from "HOW" we age. The "WHY" refers to ageing from an evolutionally standpoint, whereas the "HOW" refers to biology of ageing. As for the "WHY" I would read a few papers on the antagonistic pleiotropy hypothesis (click here). As for the "HOW", there is no definitive understanding of mechanisms of ageing. However, the role of cellular senescence in ageing and age-related disease is a major player in the biology of ageing (click here for example). When cells become senescent (due to either telomere shortening/DNA-damage) they can no longer divide to regenerate damaged tissue. Additionally, senescent cells are highly pro-inflammatory and so have the potential to damage the surrounding tissue if the are not removed. In younger organisms, senescent cells are most likely removed my the immune system, but as organisms age, the immune system also ages and can no longer effectively remove senescent cells.

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I know this question has closed out, but I wanted add this recent reference. The reactivation of telomerase (which inhibits telomere shortening) seems to have rejuvinated mice, including neuronal growth in the brain. This is crazy awesome for a couple of reasons.

One being that we may all get to see our 140th birthday.

But since there were a reversal of aging from telomere extension, that implies that aging is adaptive and not a 'wear and tear' phenomenon, at least in animals like mice (and hopefully humans). hard to believe.

i.e. If there was a mutant that turned on telomerase, why is it not a ubiquitous trait?

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  • $\begingroup$ Interesting, but the Guardian article is not really a reference - better to go to the original paper. Also, a concern with telomere-lenghtening strategies would be carncer surely. $\endgroup$
    – Poshpaws
    Jun 30, 2012 at 13:09
  • $\begingroup$ cancer is mentioned in the article... $\endgroup$
    – shigeta
    Jun 30, 2012 at 14:35
  • $\begingroup$ I was think about this. I have same idea, so i think to be immortal we should resolve cancer first. So i'm still researching about cancer... $\endgroup$
    – DucFabulous
    Jul 8, 2013 at 13:18
  • $\begingroup$ are you aware of Aubrey De Gray? His thinking is theoretical at this point, but well articulated. ted.com/talks/aubrey_de_grey_says_we_can_avoid_aging.html $\endgroup$
    – shigeta
    Jul 8, 2013 at 20:58

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