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Population Cycles Causes and Analysis

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Ever since Elton’s classic book Voles, Mice and Lemmings (Elton 1942), understanding and explaining the causes of regular multiannual cycles in animal populations has been a central issue in ecology. Many hypotheses have been erected and incessantly argued about, but no clear picture has emerged. Below I briefly sketch the major hypotheses without any attempt to be complete or to comment on their relative merits or demerits. Detailed reviews and discussion can be found in Keith (1963), Krebs and Myers (1974), Finerty (1980), Myers (1988), Royama (1992), and Stenseth (1999). (H1) Physical effects (e.g., Elton 1924, Bodenheimer 1938). Perhaps the most obvious hypothesis is that cycles in animal populations reflect the response of birth and death rates to an external physical factor that is itself cyclic. Two of the more specific physical hypotheses involve periodic climatic factors and sunspot activity. (H2) Predator effects. Lotka (1924) and Volterra (1926) demonstrated that cyclic dynamics are inherent in simple predator-prey models, leading to the hypothesis that regular cycles can result from interactions between predator and prey populations. (H3) Pathogen effects. Anderson and May (1980) showed that, under certain conditions, simple models of infectious disease transmission can generate cycles in host and pathogen populations. This is similar to H2 with the pathogen as a predator. (H4) Plant effects. Several hypotheses have been proposed for the possible role of plants in generating population cycles of herbivores. One is a generalization of H2 in which the plant is considered the prey and the herbivore the predator (Elton 1924, Pitelka 1957). Another involves nutrient cycling: In this hypothesis, nutrient deficiencies are assumed to reduce the resistance of plants, resulting in larger herbivore populations, but nutrients released in feces and decaying animal and plant matter cycle back to the plants, increasing their vigor and resistance, and resulting in reduced herbivory (e.g., White 1974). Another hypothesis argues that herbivore feeding induces sustained chemical and/or physical changes in the plant (delayed induced resistance), which then reduce the reproduction and/or survival of future herbivore generations (Benz 1974, Haukioja and Hakala 1975).
Oxford University Press
Title: Population Cycles Causes and Analysis
Description:
Ever since Elton’s classic book Voles, Mice and Lemmings (Elton 1942), understanding and explaining the causes of regular multiannual cycles in animal populations has been a central issue in ecology.
Many hypotheses have been erected and incessantly argued about, but no clear picture has emerged.
Below I briefly sketch the major hypotheses without any attempt to be complete or to comment on their relative merits or demerits.
Detailed reviews and discussion can be found in Keith (1963), Krebs and Myers (1974), Finerty (1980), Myers (1988), Royama (1992), and Stenseth (1999).
(H1) Physical effects (e.
g.
, Elton 1924, Bodenheimer 1938).
Perhaps the most obvious hypothesis is that cycles in animal populations reflect the response of birth and death rates to an external physical factor that is itself cyclic.
Two of the more specific physical hypotheses involve periodic climatic factors and sunspot activity.
(H2) Predator effects.
Lotka (1924) and Volterra (1926) demonstrated that cyclic dynamics are inherent in simple predator-prey models, leading to the hypothesis that regular cycles can result from interactions between predator and prey populations.
(H3) Pathogen effects.
Anderson and May (1980) showed that, under certain conditions, simple models of infectious disease transmission can generate cycles in host and pathogen populations.
This is similar to H2 with the pathogen as a predator.
(H4) Plant effects.
Several hypotheses have been proposed for the possible role of plants in generating population cycles of herbivores.
One is a generalization of H2 in which the plant is considered the prey and the herbivore the predator (Elton 1924, Pitelka 1957).
Another involves nutrient cycling: In this hypothesis, nutrient deficiencies are assumed to reduce the resistance of plants, resulting in larger herbivore populations, but nutrients released in feces and decaying animal and plant matter cycle back to the plants, increasing their vigor and resistance, and resulting in reduced herbivory (e.
g.
, White 1974).
Another hypothesis argues that herbivore feeding induces sustained chemical and/or physical changes in the plant (delayed induced resistance), which then reduce the reproduction and/or survival of future herbivore generations (Benz 1974, Haukioja and Hakala 1975).

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