Habitat saturation and the spatial evolutionary ecology of altruism

Under which ecological conditions should individuals help their neighbours? We investigate the effect of habitat saturation on the evolution of helping behaviours in a spatially structured population. We combine the formalisms of population genetics and spatial moment equations to tease out the effects of various physiological (direct benefits and costs of helping) and ecological parameters (such as the density of empty sites) on the selection gradient on helping. Our analysis highlights the crucial importance of demography for the evolution of helping behaviours. It shows that habitat saturation can have contrasting effects, depending on the form of competition (direct vs. indirect competition) and on the conditionality of helping. In our attempt to bridge the gap between spatial ecology and population genetics, we derive an expression for relatedness that takes into account both habitat saturation and the spatial structure of genetic variation. This analysis helps clarify discrepancies in the results obtained by previous theoretical studies. It also provides a theoretical framework taking into account the interplay between demography and kin selection, in which new biological questions can be explored.     

The robustness of altruism as an evolutionary strategy

Kin selection, reciprocity and group selection are widely regarded as evolutionary mechanisms capable of sustaining altruism among humans andother cooperative species. Our research indicates, however, that these mechanisms are only particular examples of a broader set of evolutionary possibilities.In this paper we present the results of a series of simple replicator simulations, run on variations of the 2–player prisoner's dilemma, designed to illustrate the wide range of scenarios under which altruism proves to be robust under evolutionary pressures. The set of mechanisms we explore is divided into four categories:correlation, group selection, imitation, and punishment. We argue that correlation is the core phenomenon at work in all four categories.     

Genetic hitchhiking can promote the initial spread of strong altruism

Background  

The evolutionary origin of strong altruism (where the altruist pays an absolute cost in terms of fitness) towards non-kin has never been satisfactorily explained since no mechanism (except genetic drift) seems to be able to overcome the fitness disadvantage of the individual who practiced altruism in the first place.     

An evolutionary analysis of the relationship between spite and altruism

We investigate the selective pressures on a social trait when evolution occurs in a population of constant size. We show that any social trait that is spiteful simultaneously qualifies as altruistic. In other words, any trait that reduces the fitness of less related individuals necessarily increases that of related ones. Our analysis demonstrates that the distinction between Hamiltonian spite and Wilsonian spite is not justified on the basis of fitness effects. We illustrate this general result with an explicit model for the evolution of a social act that reduces the recipient's survival (harming trait). This model shows that the evolution of harming is favoured if local demes are of small size and migration is low (philopatry). Further, deme size and migration rate determine whether harming evolves as a selfish strategy by increasing the fitness of the actor, or as a spiteful/altruistic strategy through its positive effect on the fitness of close kin.     

On the relationship between evolutionary and psychological definitions of altruism and selfishness

I examine the relationship between evolutionary definitions of altruism that are based on fitness effects and psychological definitions that are based on the motives of the actor. I show that evolutionary altruism can be motivated by proximate mechanisms that are psychologically either altruistic or selfish. I also show that evolutionary definitions do rely upon motives as a metaphor in which the outcome of natural selection is compared to the decisions of a psychologically selfish (or altruistic) individual. Ignoring the precise nature of both psychological and evolutionary definitions has obscured many important issues, including the biological roots of psychological altruism.     

The evolutionary interplay of intergroup conflict and altruism in humans: a review of parochial altruism theory and prospects for its extension

Drawing on an idea proposed by Darwin, it has recently been hypothesized that violent intergroup conflict might have played a substantial role in the evolution of human cooperativeness and altruism. The central notion of this argument, dubbed ‘parochial altruism’, is that the two genetic or cultural traits, aggressiveness against the out-groups and cooperativeness towards the in-group, including self-sacrificial altruistic behaviour, might have coevolved in humans. This review assesses the explanatory power of current theories of ‘parochial altruism’. After a brief synopsis of the existing literature, two pitfalls in the interpretation of the most widely used models are discussed: potential direct benefits and high relatedness between group members implicitly induced by assumptions about conflict structure and frequency. Then, a number of simplifying assumptions made in the construction of these models are pointed out which currently limit their explanatory power. Next, relevant empirical evidence from several disciplines which could guide future theoretical extensions is reviewed. Finally, selected alternative accounts of evolutionary links between intergroup conflict and intragroup cooperation are briefly discussed which could be integrated with parochial altruism in the future.     

Human altruism: economic, neural, and evolutionary perspectives

Human cooperation represents a spectacular outlier in the animal world. Unlike other creatures, humans frequently cooperate with genetically unrelated strangers, often in large groups, with people they will never meet again, and when reputation gains are small or absent. Experimental evidence and evolutionary models suggest that strong reciprocity, the behavioral propensity for altruistic punishment and altruistic rewarding, is of key importance for human cooperation. Here, we review both evidence documenting altruistic punishment and altruistic cooperation and recent brain imaging studies that combine the powerful tools of behavioral game theory with neuroimaging techniques. These studies show that mutual cooperation and the punishment of defectors activate reward related neural circuits, suggesting that evolution has endowed humans with proximate mechanisms that render altruistic behavior psychologically rewarding.     

Asynchronous spatial evolutionary games

Over the past 50 years, much attention has been given to the Prisoner's Dilemma as a metaphor for problems surrounding the evolution and maintenance of cooperative and altruistic behavior. The bulk of this work has dealt with the successfulness and robustness of various strategies. Nowak and May (1992) considered an alternative approach to studying evolutionary games. They assumed that players were distributed across a two-dimensional (2D) lattice, interactions between players occurred locally, rather than at long range as in the well mixed situation. The resulting spatial evolutionary games display dynamics not seen in their well-mixed counterparts. An assumption underlying much of the work on spatial evolutionary games is that the state of all players is updated in unison or in synchrony. Using the framework outlined in Nowak and May (1992), we examine the effect of various asynchronous updating schemes on the dynamics of spatial evolutionary games. There are potential implications for the dynamics of a wide variety of spatially extended systems in biology, physics and chemistry.     

On the spatial spread of rabies among foxes

We present a simple model for the spatial spread of rabies among foxes and use it to quantify its progress in England if rabies were introduced. The model is based on the known ecology of fox behaviour and on the assumption that the main vector for the spread of the disease is the rabid fox. Known data and facts are used to determine real parameter values involved in the model. We calculate the speed of propagation of the epizootic front, the threshold for the existence of an epidemic, the period and distance apart of the subsequent cyclical epidemics which follow the main front, and finally we quantify a means for control of the spatial spread of the disease. By way of illustration we use the model to determine the progress of rabies up through the southern part of England if it were introduced near Southampton. Estimates for the current fox density in England were used in the simulations. These suggest that the disease would reach Manchester within about 3.5 years, moving at speeds as high as 100 km per year in the central region. The model further indicates that although it might seem that the disease had disappeared after the wave had passed it would reappear in the south of England after just over 6 years and at periodic times after that. We consider the possibility of stopping the spread of the disease by creating a rabies 'break' ahead of the front through vaccination to reduce the population to a level below the threshold for an epidemic to exist. Based on parameter values relevant to England, we estimate its minimum width to be about 15 km. The model suggests that vaccination has considerable advantages over severe culling.     

The effect of the spatial configuration of habitat fragmentation on invasive spread

To address how the spatial configuration of habitat fragmentation influences the persistence and the rate of spread of an invasive species, we consider three simple periodically fragmented environments, a lattice-like corridor environment, an island-like environment and a striped environment. By numerically analyzing Fisher’s equation with a spatially varying diffusion coefficient and the intrinsic growth rate, we find the following. (1) When the scale of fragmentation is sufficiently large, the minimum favorable area needed for successful invasion reduces in the following order: lattice-like corridor, striped and island-like environments. (2) When the scale of fragmentation and the fraction of favorable area are sufficiently large, the spreading speeds along contiguous favorable habitats in the lattice-like corridor and striped environments are faster than the speeds across isolated favorable habitats in the island-like environment and the striped environment. (3) When the periodicity of fragmentation is relaxed by stochastically shifting the boundaries between favorable and unfavorable habitats, the average speed increases with increases in the irregularity of fragmentation.     

The spatial spread and final size of the deterministic non-reducible n-type epidemic

A model has been formulated in [6] to describe the spatial spread of an epidemic involving n types of individual, and the possible wave solutions at different speeds were investigated. The final size and pandemic theorems are now established for such an epidemic. The results are relevant to the measles, host-vector, carrier-borne epidemics, rabies and diseases involving an intermediate host. Diseases in which some of the population is vaccinated, and models that divide the population into several strata are also covered.     

The typological versus the evolutionary approach in skeletal population studies

An examination of ideal and extreme type constructs indicates that ideal types do not serve as testable hypotheses in a theoretical system. Extreme types, on the other hand, can be empirically valid. In physical anthropological studies of human skeletal populations, ideal typology must be replaced with population thinking if we hope to arrive at a meaningful understanding of the biological attributes of prehistoric populations.     

Predation may defeat spatial spread of infection

A model of a phytoplankton-zooplankton prey-predator system with viral infection of phytoplankton is investigated. Virus particles (V) are taken into account by an explicit equation. Phytoplankton is split into a susceptible (S) and an infected (I) class. A lytic infection is considered, thus, infected phytoplankton cells stop reproducing as soon as the infection starts and die at an increased mortality rate. Zooplankton (Z) is grazing on both susceptible and infected phytoplankton following a Holling-type II functional response. After the local dynamics of the V-S-I-Z system is analysed, numerical solutions of a stochastic reaction-diffusion model of the four species are presented. These show a spatial competition between zooplankton and viruses, although these two species are not explicitly coupled by the model equations.     

Predation may defeat spatial spread of infection

A model of a phytoplankton–zooplankton prey-predator system with viral infection of phytoplankton is investigated. Virus particles (V) are taken into account by an explicit equation. Phytoplankton is split into a susceptible (S) and an infected (I) class. A lytic infection is considered, thus, infected phytoplankton cells stop reproducing as soon as the infection starts and die at an increased mortality rate. Zooplankton (Z) is grazing on both susceptible and infected phytoplankton following a Holling-type II functional response. After the local dynamics of the V?S?I?Z system is analysed, numerical solutions of a stochastic reaction–diffusion model of the four species are presented. These show a spatial competition between zooplankton and viruses, although these two species are not explicitly coupled by the model equations.     

A model for the spatial spread of an epidemic

Summary We set up a deterministic model for the spatial spread of an epidemic. Essentially, the model consists of a nonlinear integral equation which has an unique solution. We show that this solution has a temporally asymptotic limit which describes the final state of the epidemic and is the minimal solution of another nonlinear integral equation. We outline the asymptotic behaviour of this minimal solution at a great distance from the epidemic's origin and generalize D. G. Kendall's pandemic threshold theorem (1957).     

The role of deer in facilitating the spatial spread of the pathogen Borrelia burgdorferi

Borrelia burgdorferi is a vector-bourne zoonosis which propagates in wild populations of rodents and deer. The latter are incompetent for the pathogen but are required for the life cycle of hard-backed ticks which act as a vector for the pathogen. Increasing the diversity of hosts has previously suggested the presence of a ‘dilution effect’ in which such an increase reduces successful pathogen transmission as it increases the chance that a tick will encounter an incompetent host. This paper will produce a model which shows that whilst a dilution effect is possible for a system in which deer are the only incompetent host, this effect is not likely to be strong. Extending the population dynamics to include movement of deer into regions previously only inhabited by competent hosts, we find that, although ticks come in with the deer, there is a significant time lag before Borrelia appears.     

The spatial spread and final size of models for the deterministic host-vector epidemic

A disease is considered which is transferred between two populations, termed hosts and vectors. The disease is transmitted solely from infected vector to uninfected host and from infected host to uninfected vector. Two models are formulated in which infectious individuals are introduced at time t = 0 into the populations of susceptibles, thus triggering an epidemic through those populations. Conditions are established for a major epidemic to occur, and the final size of the epidemic is obtained for these models when no spatial aspect is considered. When a spatial aspect is included in the models, again the condition for a major epidemic is obtained. The pandemic theorem is proved rigorously, giving a lower bound for the proportion of each population, at each point, who eventually suffer the epidemic. The behavior a long way from the initial focus of infection is also rigorously obtained.     

On the spatial spread of the grey squirrel in Britain

We present a diffusion-competition model to describe the interaction between the externally introduced grey squirrel and the indigenous red squirrel in Britain. We estimate the model parameters from field data. Solution of the model predicts waves of grey squirrel invasion with speed of invasion typical of that observed in the field. Numerical solution of the model on a two-dimensional domain gives population distributions qualitatively similar to those observed. We suggest that competition alone could account for the observed displacement of the red squirrel by the grey in large regions of Britain. The solutions are qualitatively similar to those for a single species spreading in the absence of competition. The quantitative difference is because competition slows down the speed of advance of the invading species.     

The evolutionary consequence of the individualistic response to climate change

The Quaternary fossil record has abundant evidence for ecologically nonanalogue communities made up of combinations of modern taxa not seen in sympatry today. A brief review of the literature detailing these nonanalogue communities is given with a discussion of their various proposed causes. The individualistic, Gleasonian, response of species to climate and environmental change is favoured by many. The degree to which communities are nonanalogue appears to increase with greater time depth, and this progressive process is a necessary outcome of the individualistic response of species to climate change through time. In addition, it is noted that populations within species, as well as the species as a whole, respond individualistically. This paper proposes that many elements of nonanalogue communities are extinct populations, which may explain their environmentally anomalous combinations. These extinct populations are, by definition, lineages without descendents. It is further proposed that the differential extinction of populations, as a result of continuous ecological reassembly, could amount to a significant evolutionary phenomenon.