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The relationship of mammal survivorship and body mass modeled by metabolic and vitality theories

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  • Evolutionary demography: the dynamic and broad intersection of ecology and evolution
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Population Ecology

Abstract

A model describes the relationship between mammal body mass and survivorship by combining replicative senescence theory postulating a cellular basis of aging, metabolic theory relating metabolism to body mass, and vitality theory relating survival to vitality loss and extrinsic mortality. In the combined framework, intrinsic mortality results from replicative senescence of the hematopoietic stem cells and extrinsic mortality results from environmental challenges. Because the model expresses the intrinsic and extrinsic rates with different powers of body mass, across the spectrum of mammals, survivorship changes from Type I to Type II curve shapes with decreasing body mass. Fitting the model to body mass and maximum lifespan data of 494 nonvolant mammals yields allometric relationships of body mass to the vitality parameters, from which full survivorship profiles were generated from body mass alone. Because maximum lifespan data is predominantly derived from captive populations, the generated survivorship curves were dominated by intrinsic mortality. Comparison of the mass-derived and observed survivorship curves provides insights into how specific populations deviate from the aggregate of populations observed under captivity.

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Notes

  1. A body of literature discusses where the coefficient is between 2/3 and 3/4 (Dodds et al. 2001; da Silva et al. 2006; Banavar et al. 2010; Lee 2015). For the model, the value of the exponent is not germane.

  2. Leukocytes, the central actors of the immune system, are produced from hematopoietic stem cells in the bone marrow and the lymph system. The leukocytes circulate as a component of blood to detect and remove pathogens from the body and repair damaged tissue. The gradual reduction of immune system function with age involves essentially all the aging hallmarks but of particular importance are the loss of proteostasis and the reduction in the number of naïve T cells and stem cells with age (Ponnappan and Ponnappan 2011). Collectively these processes are known as immunosenescence (Weiskopf et al. 2009) and result in inflammaging, both of which are hallmarks of aging leading to death (Franceschi et al. 2007). While immune system function is an index of aging, degradation of other processes working across the molecular, cellular and system levels are also important (López-Otín et al. 2013).

  3. This is an upper limit of cell replication, determined by the attrition of the protective telomeres end caps on chromosomes (Hayflick and Moorhead 1961). Once the telomere reaches a critical length, cell replication stops. However, telomerase can maintain TL (Blackburn et al. 2015). Evidence suggests that TL declines with lifespan in some species but not others. Telomerase varies with body size but not life span (Monaghan 2010).

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Acknowledgements

I wish to acknowledge the two reviewers whose comments greatly improved the analysis and organization of the manuscript. This work was supported by National Institute of Health Grant R21AG046760.

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Correspondence to James J. Anderson.

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Anderson, J.J. The relationship of mammal survivorship and body mass modeled by metabolic and vitality theories. Popul Ecol 60, 111–125 (2018). https://doi.org/10.1007/s10144-018-0617-6

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