Blute Blog

Blute's blog about evolutionary theory: biological, sociocultural and gene-culture.

A Debate Over Senescence

with 4 comments

The debate over theories of senescence (commonly defined as a decrease in function with age) that has gone on in the pages of TREE (Trends in Ecology & Evolution) is interesting but I will not try to summarize all the arguments here, see [1-6]. The key issue dividing champions of Hamilton [1,4,6] versus those of Williams [2,3,5] seems to be whether extrinsic mortality must be condition-dependent to select for senescence [1,4,6] or whether it just has to be extrinsic period [2,3,5]. Many points could be made about either (and indeed about both) sides of this argument. It seems strange to see two of the great evolutionary biologists of their time pitted against each other by others, especially since according to the first side at least, Williams eventually agreed with Hamilton anyway. The debate seems to be all about time but what about space? If the discussion is all about extrinsic mortality, what about intrinsic mortality? Is there such a thing? There must be believed to be, otherwise why the need to distinguish some mortality as extrinsic? Intrinsic mortality sounds like senescence itself, but then it is supposed to be extrinsic mortality that selects for senescence so . . .? Density dependence is mentioned but the classic works that initiated modern discussions of it are not mentioned or cited [7,8]. It seems obvious to me that senescence is indeed density dependent [9,10].

Small organisms (which also tend to have short, fast life cycles and many small offspring), because of their disproportionate surface area (for a sphere = 4π r2), tend to consume (eat and excrete) more, depleting and degrading the external environment, and hence to suffer mortality from extrinsic causes (predation, parasites, accidents etc.) Large organisms (which also tend to have longer, slower life cycles and fewer, larger offspring capable of producing grand offspring), because of their disproportionate volume (for a sphere = 4/3π r3), tend to digest (break down and build up) more, depleting and degrading the internal environment, and hence to suffer mortality from intrinsic causes (developmental, physiological, behavioural etc.) i.e. senescence. The argument is that the former are adapted to low density (in per capita cost and/or frequency) relative to resources i.e. plentiful resources within a population, or among populations, growing ones with a history of catastrophes and hence consume/produce more. The latter are adapted to high density (in per capita cost and/or frequency) relative to resources i.e. scarce resources within a population, or among populations, declining ones with a history of bonanzas and hence digest/reproduce more – struggling morphologically, physiologically and behaviourally to build up mechanisms of escape in time, space and/or niche. Of course, further distinctions could be drawn. Somatic and reproductive and temporal and spatial properties of life cycles are not perfectly correlated. Density relative to antagonists matters too, low in that case being bad conditions and high good ones. It matters whether the consumption is by means of parasitism or predation and so on.
 
Evidence? Well, we have long known experimentally that caloric restriction among the small fast, forcing them to devote fewer resources to consumption and hence by implication more to digestion, increases lifespan. But don’t we also know that caloric expansion among the large slow, devoting more resources to consumption and hence by implication less to digestion, decreases lifespan (e.g. obesity among humans)? The slogan for such a density dependent theory of senescence might be mice get eaten while men get cancer!
                                   
Now of course this argument is about different life histories rather than about stages within life histories. But given that juveniles are obviously smaller and adults obviously larger, surely the analogous inference can be drawn from one to the other. Humans after all lavish food on their young even as they sometimes go without themselves. As adult humans we know that our young children get bug after bug (most of which they thankfully do not die of at least these days). But what do our parents die of? Number one is heart disease and number two is cancer. Thereafter there is in order a list of things  [11] which similarly do not have obvious extrinsic causes.

References
1.  Moorad, J. et. al. (2019) Evolutionary ecology of senescence and a reassessment of Williams’ “extrinsic mortality” hypothesis. Trends Ecol. Evol. 34, 519-530
2.  Day, T. and Abrams, P.A. (2020) Density dependence, senescence and Williams’ hypothesis. Trends Ecol. Evol. 35, 300-302. 
3.  Kozlowski, J. et. al. (2020) Williams’ prediction will often be observed in nature. Trends Ecol. Evol. 35, 302-303.
4.  Moorad J. et. al. (2020) George C. Williams’ problematic model of selection and senescence: time to move on. Trends Ecol. Evol. 35, 303-305.
5.  da Silva, J. (2020) Williams’ intuition about extrinsic mortality was correct. Trends Ecol.  Evol. 35, 378-379.
6.  Moorad, J. et. al. (2020) Williams’ intuition about extrinsic mortality is irrelevant. Trends Ecol. Evol. 35, 379.                       
7.  MacArthur R.H. (1962) Some generalized theorems of natural selection. Proc. Natl. Acad. Sci. 48, 1893-1897.
8.  MacArthur, R.H. and Wilson, E.O. (1967) The Theory of Island Biogeography. Princeton  University Press.
9.  Blute, M. (2010) Darwinian Sociocultural Evolution: Solutions to Dilemmas in Cultural and Social Theory. Cambridge University Press.
10.  Blute, M. (2016) Density-Dependent Selection Revisited: Mechanisms Linking Explanantia and Explananda. Biological Theory 11, 113-121.
11.  National Vital Statistics Report. United States Life Tables (2019)
      https://www.cdc.gov/nchs/data/nvsr/nvsr68/nvsr68_07-508.pdf

Written by Marion Blute

September 21, 2020 at 1:39 pm

4 Responses

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  1. Pathogens cause a lot of heart disease and cancer, I think. I should think that they are high on the list of causes of density-dependent senescence as well.

    Tim Tyler

    October 12, 2020 at 12:33 am

    • Enjoyed your book on memetics Tim. There is no obvious evidence at least in the mortality data cited that what you think is the case. As I noted, low density relative to antagonists is a bad condition that favors escaping. Of course theory always depends on assumptions. For example, given that mortality is from antagonists, the small, fast would be most at risk from predators while the large, slow would be most at risk from parasites.

      Marion Blute

      October 14, 2020 at 2:47 pm

      • You are expressing scepticism about the links between parasites and cancer and heart disease? My understanding is that these are important and under-appreciated. The link between HPV and cervical cancer is well known, but it is also the tip of an iceberg. Cancer is caused by solar radiation, too, but viruses slicing and dicing DNA is another common cause of somatic mutations. For heart disease, consider this quote (from a review): “There is sound evidence that atherosclerosis is initiated in infancy and childhood and is associated with childhood infections that develop later age atheroma”.

        Tim Tyler

        October 19, 2020 at 10:32 pm

  2. I didn’t say never – the basic thesis is that the large slow-lived are more likely to suffer from senescence than the small short-lived.

    Marion Blute

    October 20, 2020 at 10:17 am


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