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"Nunn, Charles L."
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Sociality and health: impacts of sociality on disease susceptibility and transmission in animal and human societies
This paper introduces a theme issue presenting the latest developments in research on the impacts of sociality on health and fitness. The articles that follow cover research on societies ranging from insects to humans. Variation in measures of fitness (i.e. survival and reproduction) has been linked to various aspects of sociality in humans and animals alike, and variability in individual health and condition has been recognized as a key mediator of these relationships. Viewed from a broad evolutionary perspective, the evolutionary transitions from a solitary lifestyle to group living have resulted in several new health-related costs and benefits of sociality. Social transmission of parasites within groups represents a major cost of group living, but some behavioural mechanisms, such as grooming, have evolved repeatedly to reduce this cost. Group living also has created novel costs in terms of altered susceptibility to infectious and non-infectious disease as a result of the unavoidable physiological consequences of social competition and integration, which are partly alleviated by social buffering in some vertebrates. Here, we define the relevant aspects of sociality, summarize their health-related costs and benefits, and discuss possible fitness measures in different study systems. Given the pervasive effects of social factors on health and fitness, we propose a synthesis of existing conceptual approaches in disease ecology, ecological immunology and behavioural neurosciences by adding sociality as a key factor, with the goal to generate a broader framework for organismal integration of health-related research.
Journal Article
Stepwise Model Fitting and Statistical Inference: Turning Noise into Signal Pollution
Statistical inference based on stepwise model selection is applied regularly in ecological, evolutionary, and behavioral research. In addition to fundamental shortcomings with regard to finding the “best” model, stepwise procedures are known to suffer from a multiple‐testing problem, yet the method is still widely used. As an illustration of this problem, we present results of a simulation study of artificial data sets of uncorrelated variables, with two to 10 predictor variables and one dependent variable. We then compared results from stepwise regression with a regression model in which all predictor variables were entered simultaneously. These analyses clearly demonstrate that significance tests based on stepwise procedures lead to greatly inflated Type I error rates (i.e., the probability of erroneously rejecting a true null hypothesis). By using a simple simulation design, our study amplifies previous warnings about using stepwise procedures, and we follow others in recommending that biologists refrain from applying these methods.
Journal Article
Network-based diffusion analysis: a new method for detecting social learning
Social learning has been documented in a wide diversity of animals. In free-living animals, however, it has been difficult to discern whether animals learn socially by observing other group members or asocially by acquiring a new behaviour independently. We addressed this challenge by developing network-based diffusion analysis (NBDA), which analyses the spread of traits through animal groups and takes into account that social network structure directs social learning opportunities. NBDA fits agent-based models of social and asocial learning to the observed data using maximum-likelihood estimation. The underlying learning mechanism can then be identified using model selection based on the Akaike information criterion. We tested our method with artificially created learning data that are based on a real-world co-feeding network of macaques. NBDA is better able to discriminate between social and asocial learning in comparison with diffusion curve analysis, the main method that was previously applied in this context. NBDA thus offers a new, more reliable statistical test of learning mechanisms. In addition, it can be used to address a wide range of questions related to social learning, such as identifying behavioural strategies used by animals when deciding whom to copy.
Journal Article
Predictions of primate–parasite coextinction
Future biodiversity loss threatens the integrity of complex ecological associations, including among hosts and parasites. Almost half of primate species are threatened with extinction, and the loss of threatened hosts could negatively impact parasite associations and ecosystem functions. If endangered hosts are highly connected in host–parasite networks, then future host extinctions will also drive parasite extinctions, destabilizing ecological networks. If threatened hosts are not highly connected, however, then network structure should not be greatly affected by the loss of threatened hosts. Networks with high connectance, modularity, nestedness and robustness are more resilient to perturbations such as the loss of interactions than sparse, nonmodular and non-nested networks. We analysed the interaction network involving 213 primates and 763 parasites and removed threatened primates (114 species) to simulate the effects of extinction. Our analyses revealed that connections to 23% of primate parasites (176 species) may be lost if threatened primates go extinct. In addition, measures of network structure were affected, but in varying ways because threatened hosts have fewer parasite interactions than non-threatened hosts. These results reveal that host extinctions will perturb the host–parasite network and potentially lead to secondary extinctions of parasites. The ecological consequences of these extinctions remain unclear.
This article is part of the theme issue 'Infectious disease macroecology: parasite diversity and dynamics across the globe'.
Journal Article
Infectious disease and group size: more than just a numbers game
Increased risk of infectious disease is assumed to be a major cost of group living, yet empirical evidence for this effect is mixed. We studied whether larger social groups are more subdivided structurally. If so, the social subdivisions that form in larger groups may act as barriers to the spread of infection, weakening the association between group size and infectious disease. To investigate this ‘social bottleneck’ hypothesis, we examined the association between group size and four network structure metrics in 43 vertebrate and invertebrate species. We focused on metrics involving modularity, clustering, distance and centralization. In a meta-analysis of intraspecific variation in social networks, modularity showed positive associations with network size, with a weaker but still positive effect in cross-species analyses. Network distance also showed a positive association with group size when using intraspecific variation. We then used a theoretical model to explore the effects of subgrouping relative to other effects that influence disease spread in socially structured populations. Outbreaks reached higher prevalence when groups were larger, but subgrouping reduced prevalence. Subgrouping also acted as a ‘brake’ on disease spread between groups. We suggest research directions to understand the conditions under which larger groups become more subdivided, and to devise new metrics that account for subgrouping when investigating the links between sociality and infectious disease risk.
Journal Article
Community structure and the spread of infectious disease in primate social networks
Living in a large social group is thought to increase disease risk in wild animal populations, but comparative studies have provided mixed support for this prediction. Here, we take a social network perspective to investigate whether patterns of social contact within groups influence parasite risk. Specifically, increased modularity (i.e. sub-grouping) in larger groups could offset the increased disease risk associated with living in a large group. We simulated the spread of a contagious pathogen in random social networks to generate theoretically grounded predictions concerning the relationship between social network connectivity and the success of socially transmitted pathogens. Simulations yielded the prediction that community modularity (
Q
) negatively impacts parasite success. No clear predictions emerged for a second network metric we considered, the eigenvector centralization index (
C
), as the relationship between this measure and parasite success depended on the transmission probability of parasites. We then tested the prediction that
Q
reduces parasite success in a phylogenetic comparative analysis of social network modularity and parasite richness across 19 primate species. Using a Bayesian implementation of phylogenetic generalized least squares and controlling for sampling effort, we found that primates living in larger groups exhibited higher
Q,
and as predicted by our simulations, higher
Q
was associated with lower richness of socially transmitted parasites. This suggests that increased modularity mediates the elevated risk of parasitism associated with living in larger groups, which could contribute to the inconsistent findings of empirical studies on the association between group size and parasite risk. Our results indicate that social networks may play a role in mediating pressure from socially transmitted parasites, particularly in large groups where opportunities for transmitting communicable diseases are abundant. We propose that parasite pressure in gregarious primates may have favored the evolution of behaviors that increase social network modularity, especially in large social groups.
Journal Article
On sexual dimorphism in immune function
Sexual dimorphism in immune function is a common pattern in vertebrates and also in a number of invertebrates. Most often, females are more 'immunocompetent' than males. The underlying causes are explained by either the role of immunosuppressive substances, such as testosterone, or by fundamental differences in male and female life histories. Here, we investigate some of the main predictions of the immunocompetence handicap hypothesis (ICHH) in a comparative framework using mammals. We focus specifically on the prediction that measures of sexual competition across species explain the observed patterns of variation in sex-specific immunocompetence within species. Our results are not consistent with the ICHH, but we do find that female mammals tend to have higher white blood cell counts (WBC), with some further associations between cell counts and longevity in females. We also document positive covariance between sexual dimorphism in immunity, as measured by a subset of WBC, and dimorphism in the duration of effective breeding. This is consistent with the application of 'Bateman's principle' to immunity, with females maximizing fitness by lengthening lifespan through greater investment in immune defences. Moreover, we present a meta-analysis of insect immunity, as the lack of testosterone in insects provides a means to investigate Bateman's principle for immunity independently of the ICHH. Here, we also find a systematic female bias in the expression of one of the two components of insect immune function that we investigated (phenoloxidase). From these analyses, we conclude that the mechanistic explanations of the ICHH lack empirical support. Instead, fitness-related differences between the sexes are potentially sufficient to explain many natural patterns in immunocompetence.
Journal Article
Do Animals Living in Larger Groups Experience Greater Parasitism? A Meta-Analysis
Parasitism is widely viewed as the primary cost of sociality and a constraint on group size, yet studies report varied associations between group size and parasitism. Using the largest database of its kind, we performed a meta-analysis of 69 studies of the relationship between group size and parasite risk, as measured by parasitism and immune defenses. We predicted a positive correlation between group size and parasitism with organisms that show contagious and environmental transmission and a negative correlation for searching parasites, parasitoids, and possibly vector-borne parasites (on the basis of the encounter-dilution effect). Overall, we found a positive effect of group size (
) that varied in magnitude across transmission modes and measures of parasite risk, with only weak indications of publication bias. Among different groups of hosts, we found a stronger relationship between group size and parasite risk in birds than in mammals, which may be driven by ecological and social factors. A metaregression showed that effect sizes increased with maximum group size. Phylogenetic meta-analyses revealed no evidence for phylogenetic signal in the strength of the group size–parasitism relationship. We conclude that group size is a weak predictor of parasite risk except in species that live in large aggregations, such as colonial birds, in which effect sizes are larger.
Journal Article
Phylogenetic rate shifts in feeding time during the evolution of Homo
Unique among animals, humans eat a diet rich in cooked and nonthermally processed food. The ancestors of modern humans who invented food processing (including cooking) gained critical advantages in survival and fitness through increased caloric intake. However, the time and manner in which food processing became biologically significant are uncertain. Here, we assess the inferred evolutionary consequences of food processing in the human lineage by applying a Bayesian phylogenetic outlier test to a comparative dataset of feeding time in humans and nonhuman primates. We find that modern humans spend an order of magnitude less time feeding than predicted by phylogeny and body mass (4.7% vs. predicted 48% of daily activity). This result suggests that a substantial evolutionary rate change in feeding time occurred along the human branch after the human–chimpanzee split. Along this same branch, Homo erectus shows a marked reduction in molar size that is followed by a gradual, although erratic, decline in H. sapiens. We show that reduction in molar size in early Homo (H. habilis and H. rudolfensis) is explicable by phylogeny and body size alone. By contrast, the change in molar size to H. erectus, H. neanderthalensis, and H. sapiens cannot be explained by the rate of craniodental and body size evolution. Together, our results indicate that the behaviorally driven adaptations of food processing (reduced feeding time and molar size) originated after the evolution of Homo but before or concurrent with the evolution of H. erectus, which was around 1.9 Mya.
Journal Article