Posts Tagged ‘density-dependent selection’
A Debate Over Senescence
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
Density-dependent natural selection may have implications for the coming decline side of the COVID-19 pandemic
Chapter 3 of Darwinian Sociocultural Evolution on “Necessity: why did it evolve” discussed principles of evolutionary ecology, notably density dependence relative to resources in section 3.3.1., and applied them illustratively to the sociology of science. Subsequently Blute (2016) reviewed the history of, and greatly extended the theory. The extensions included its applicability to selection in space and/or time, to somatic functions as a cause and not just an effect (as in Fisher’s sex allocation theory for example), and to selection within and between, not just growing populations, but also declining ones. These may have implications for the coming declining side of the COVID-19 pandemic.
Where/when density measured in cost per capita relative to resources is low within a population, or in growing populations with a history of catastrophes, natural selection favours spending on consumption (eating and excreting) whereas where/when it is high or in declining ones with a history of bonanzas, selection favours investing in digestion (breaking down and building up). What should be built up? In a homogeneous environment it is mechanisms of social interaction whether cooperative, antagonistic or a mixture of both but in a patchy environment it is mechanisms of dispersal in time (maintenance), in space (motility), and/or in niche (mutability) – the 3 M’s. Similarly, low density measured in frequency or in growing populations with a history of catastrophes, natural selection favours production (many small offspring) whereas high densities or in declining ones with a history of bonanzas, selection favours “reproduction” (fewer larger offspring, ones capable of social interaction or their own 3M’s).
Both these somatic and reproductive distinctions are quantity versus quality ones with the former in each case depleting and degrading the external environment while the latter depletes and degrades the internal environment. As well, the former in each case is associated with a small size because of the disproportionate surface to volume ratio there and the latter of each associated with a large size because of the disproportionate volume to surface ratio there. Under the simplest set of conditions if both somatic and reproductive functions utilize the same or positively correlated resources and the two functions interact synergistically, then at low densities the more one consumes the more one can produce and vice-versa whereas at high densities the more one digests the more one can reproduce and vice-versa.
What then of COVID-19? Our culture is coevolving in interaction with their genes (gene-culture or culture-gene coevolution, between species in this case) and our culture has evolved favouring social distancing etc. in some places – depleting viral resources and causing a levelling off and decline in the viral population(s). But our culture is now on the edge of reversing itself at least somewhat. What are the implications of that for the virus? Given that surely humans are a heterogeneous environment, selection on the viruses should then favour:
i) maintenance: those which live longer (e.g. making the recovered or infected but symptom free contagious for longer)
ii) motility: those which move further (e.g. placing themselves in small droplets which disperse further rather than just in large drops which tend to fall) and/or
iii) mutability: those which increase their blind mutation rate seeking a new niche (e.g. infecting organs other than respiratory systems such as kidneys, nervous systems etc.)
It is at least possible therefore that changes in their genes and not just in our culture will in the future be contributing to one or more further spikes in the pandemic until a vaccine is widely available or until the 70 or 80% infection rate required for herd immunity is reached.
Blute, Marion. 2016. “Density-dependent selection revisited: Mechanisms linking explanantia and explananda.” Biological Theory 11(2) 113-121.
Resource depletion and environmental degradation
I have suggested (e.g. in Darwinian Sociocultural Evolution Chpt. 4 and this blog, Evolutionary Myth 8 posted in August 2010) that resource depletion and environmental degradation do not necessarily go hand in hand as is commonly thought. Specifically, I argued that low densities relative to ecological resources favour consuming/producing more and are associated with small sizes and resource depletion, while high densities favour digesting/re-producing more and are associated with large sizes and environmental degradation. (The size association is because of the greater surface area/volume ratio useful in the former case and the greater volume/surface area ratio useful in the latter case). The associations however can vary depending upon how the four terms are further interpreted. Hanging out sometimes with philosophers who are experts at analysing concepts, including scientific ones, encourages one to pay attention to and dig out these kinds of distinctions.
Consider only somatic functions as illustrated in the abstract in Figure 1. If consumption is understood as eating and excreting more (outer arrows 1 and 2) while digestion is understood as breaking down (degradative metabolism) and building up (biosynthetic metabolism) more (inner arrows 3 and 4), then sizes should be as stated – small versus large, but the former deplete and degrade the external environment while the latter deplete and degrade the internal environment. On the other hand, if consumption is understood as eating and breaking down more (left arrows 1 and 3) while digestion is understood as building up and excreting more (right arrows 4 and 2), then depletion and degradation should be as stated with the former depleting (the external and internal environments) and digestion degrading (the internal and external environments) but both sizes should be intermediate (although cost differences could shove both smaller or larger for example). An analogous break down can be applied to offspring production and re-production.
Such philosophical analysis of concepts can potentially be theoretically useful in the scientific sense. For example, the different interpretations described can be understood not just as different ways of analysing concepts, but as different ways in which genes specifying different components of life history strategies may be linked differently. For example, as originally suggested, the first breakdown could characterize heterospory or proto-genders with anisogamy while the second could characterize homospory or mating types with isogamy.
Blute Blog 