Evolution, Medicine, and Public Health

Fever is a widespread and adaptive defence response that enhances immune performance through an increase in body temperature above normal values. In ectotherms, fever is expressed behaviourally through the selection of warmer microhabitats following infection, yet its magnitude and determinants vary widely across species and environments. Here, we performed a phylogenetically informed meta-analysis of behavioural fever in amphibians and reptiles to test whether its expression was shaped by climatic thermal variability, pathogen identity, and taxonomy. Specifically, we tested the hypotheses that (i) species from thermally variable environments would exhibit stronger behavioural fever than species from thermally stable environments, consistent with the climate variability hypothesis, and that (ii) reptiles would exhibit stronger fever responses than amphibians due to lower hydrothermal constraints. Across 47 studies encompassing 103 effect sizes, we found that behavioural fever is widespread but highly context-dependent. We found that evidence for behavioural fever was strongest in species from more thermally variable habitats, regardless of body size and phylogeny, suggesting that access to thermally heterogeneous landscapes and enhanced behavioural plasticity amplify the capacity to sustain febrile responses. Contrary to our hypothesis, amphibians exhibited stronger fever responses than reptiles, possibly reflecting differences in baseline thermoregulatory demands and environmental opportunity, or as a consequence of methodological artefacts. The expression of behavioural fever also varied with pathogen identity, with bacterial infections eliciting larger body temperature increases than fungal or viral challenges, although pathogen representation was uneven across studies. Together, our results support the idea that the capacity to express behavioural fever depends on access to thermally heterogeneous landscapes, and may vary according to pathogen biology. Ultimately, our study emphasises that temperature is not a background condition for host-pathogen interactions, but an active and environmentally contingent component of ectotherm immune defence in amphibians and reptiles.

Background In a retrospective online survey, we assessed the extent to which people with symptomatic hypermobility are at risk of Long COVID with a high degree of post-exertional symptom exacerbation, a form of Long COVID similar to myalgic encephalomyelitis. Methods Participants were 1,816 adults with prior COVID-19 infection; 19.4% reported Long COVID, defined as symptoms persisting [≥]3 months. Survey measures identified Long COVID with high post-exertional symptom exacerbation, generalized joint hypermobility (GJH), extreme hypermobility, and a pre-COVID orthostatic/neurocognitive symptom burden (ONS profile). Logistic regression assessed whether ONS profile and hypermobility, together defined as symptomatic hypermobility, were associated with increased risk of Long COVID with post-exertional symptom exacerbation. Results In the full sample, both extreme hypermobility (OR 3.15, 95 % CI 2.00-4.95) and an ONS profile pre-COVID (OR 3.29, 95% CI 2.34-4.61) were strongly predictive of Long COVID with high post-exertional symptom exacerbation. These effects were cumulative, leading to an OR of 9.46 (95% CI 4.93-18.17) for people with both conditions. People who both had an ONS profile pre-COVID and had generalized joint hypermobility also had a higher risk of Long COVID with high post-exertional symptom exacerbation (OR 5.54, 95% CI 3.51-8.75). Conclusions In this dataset, people with symptomatic hypermobility were at high risk of Long COVID with high levels of post-exertional symptom exacerbation. Further research is needed to understand the biological mechanisms of viral-onset illness to promote more effective and targeted treatments tailored to the disease pathways shared by groups of individuals with common vulnerabilities.

The multinational Andes virus outbreak linked to the MV Hondius has exposed contacts across several countries, but the absence of further confirmed cases remains difficult to interpret given the long incubation period. We estimate the probability that secondary clusters may emerge using a stratified branching-process model parameterized with country-level tracing and isolation indicators. The risk of sustained spread is low, but secondary clusters remain plausible under imperfect isolation or pre-symptomatic transmission. These results support coordinated contact tracing and effective isolation while exposed contacts remain within the risk window.

There is growing recognition that host behavioral responses to disease risk are critical factors driving disease dynamics, but understanding how behavioral responses influence dynamics remains a major challenge. Coupled behavioral and epidemiological models commonly assume that hosts use population prevalence as an indicator of disease risk. However, real-world estimates of prevalence come from data aggregated over coarse spatial scales, while transmission occurs through fine-scale contacts. Fine-scale changes in movement behavior represent an important type of risk response because individuals must use proxies for infection risk, such as host density or environmental factors, whose relationship with actual transmission risk may vary across contexts. In this study, we examine the consequences of using diierent risk proxies to inform fine-scale movement and determine when and if relying on imperfect proxies can cause risk-averse behaviors to increase, rather than decrease, disease transmission relative to no behavioral change. We examine the effect of three risk proxies - local prevalence, local host density, and local transmission coefficient (i.e., "place") - in the context of "simple trips", where individuals may respond to disease risk by altering rates of travel from home to "away" locations and back. In one case, individuals stay home more frequently (an absolute risk response) and in the other case, individuals shift their travel to less risky, away locations (a relative risk response). Absolute responses were far more effective in reducing prevalence than relative responses, which were detrimental in some parameter regimes. Detrimental responses occurred when information used to perceive risk was mismatched with the mode of transmission (either density-dependent or frequency-dependent), such that individuals either failed to use pertinent information or used irrelevant information. Imperfect information thus plays a critical role in determining whether behavioral response reduces or elevates disease risk.

Biological phase changes provoked by stress, such as vitrification or gel-sol transitions, enable many organisms, including extremotolerant tardigrades, to enter quiescent states and survive extreme environmental conditions. Protein-driven phase transitions are hypothesized to produce large-scale changes in intracellular viscosity, allowing tardigrades to survive extreme stresses such as desiccation. We report that the tardigrade Hypsibius exemplaris undergoes both large-scale and local increases in intracellular viscosity following exposure to anoxic and hyperosmotic stress. Such dramatic shifts in cellular viscosity would be expected to enhance cellular resilience to physical force. Indeed, we found that tardigrades can survive, behave normally, and reproduce after exposure to the highest simulated hypergravity (HG) achievable in an ultracentrifuge (one million times Earths gravity). In contrast, Caenorhabditis elegans, a similarly sized animal, does not survive these extreme forces owing to loss of cellular integrity. Remarkably, tardigrades frozen during exposure to extreme hypergravitational force show minimal disruption of fine cellular ultrastructure and little evidence of stratification of cellular components whose density varies by nearly a factor of two. Further, exposure to anoxia, hyperosmotic stress, and HG all result in a large increase in reactive oxygen species (ROS), which is required for survival under these extreme environments. Inhibition of NADPH oxidase (NOX) suppresses survival both to HG and hyperosmotic stress. Our findings suggest that intracellular viscosity changes in response to multiple extreme stresses may underlie the resilience of these animals to extraordinary physical stress, and that survival in or recovery from these states relies on ROS signaling via NADPH oxidase. Significance StatementTardigrades are renowned for surviving conditions that are lethal to nearly all other life forms. We reveal two mechanisms that support this resilience: intracellular viscosity changes and NADPH oxidase-mediated ROS signaling. Through direct assessment of the effects of altered cellular material properties, found that tardigrades are resilient to forces up to one million times Earths gravity, establishing them as the most hypergravity-resistant animal currently known.

Maximum lifespan varies more than 100-fold across vertebrates, yet within each species aging emerges as a coordinated syndrome spanning metabolism, immunity, endocrine signaling, cognition, and regeneration. We propose the Metabolic Scope Theory of Aging (MSTA), which treats longevity as the time required to exhaust mitochondrial bioenergetic reserve rather than as a consequence of resting metabolic rate alone. The framework decomposes lifespan into three physical axes: Scope, the reserve capacity that buffers cumulative damage; Stability, the resistance of mtDNA-linked OXPHOS architecture to erosion; and Pace, the temperature-dependent kinetics of lesion accumulation. Using body mass as a Scope proxy, mtDNA GC content as a Stability proxy, and body temperature as Pace, the resulting Scope-Stability-Pace relation, lnMLS = lnBM + {beta} GC% -{gamma} Tb + c, explains [~]69% of mammalian maximum-lifespan variance across 379 species. Cross-class comparisons reinforce the same constraint structure: birds offset high thermal Pace through elevated mtDNA Stability, and the SSP temperature coefficient derived from mammals matches the temperature dependence of lifespan observed in ectotherms. The framework further connects comparative lifespan scaling to Gompertz-like mortality acceleration through progressive reserve erosion and threshold crossing. Mechanistically, MSTA models cumulative mtDNA-linked damage as rising impedance within OXPHOS. Increasing internal resistance drives mitochondria toward a high-redox-pressure, low-current regime that preserves basal ATP while restricting NAD+ regeneration, CoQ acceptor availability, and {Delta}p-dependent work. The earliest failure is therefore not energetic collapse but loss of regenerative scope: NAD+-gated TCA flux, aspartate and nucleotide synthesis, one-carbon metabolism, and redox-buffered repair become progressively harder to sustain, and diverse age- related pathologies emerge as tissue-specific projections of this shared upstream constraint. MSTA separates a reversible, operational impedance (redox poise, membrane potential, endocrine tone) from a fixed, informational one (accumulated mtDNA damage) that sets the hard ceiling on lifespan. Because the informational layer cannot be reversed by regulatory means, the framework predicts that until therapies can directly restore mitochondrial conductance, interventions will be most effective when they relieve redox pressure or bypass constrained biosynthetic gates.

Hosts defend themselves against parasites through resistance (reducing parasite burden) and tolerance (reducing the fitness cost of infection without affecting parasites). This distinction has important evolutionary implications: resistance is predicted to maintain polymorphism while tolerance tends to fix, and only resistance is expected to provoke parasite counter-adaptation. The reaction-norm framework, which infers tolerance from the slope of host fitness regressed on parasite burden, assumes that a shallow slope reflects parasite-independent host protection. We test this assumption using a within-host model in two variants: microparasites (Model 1, with within-host replication) and macroparasites (Model 2, without). Sublethal immunity impairs the host-exploitation rate of the parasite, reducing both growth and per-parasite virulence without killing them. We show that this generates systematic slope differences among host genotypes that the framework interprets as variation in tolerance. Furthermore, the ranking of slopes across genotypes reverses between linear and sigmoidal damage functions: under linear damage, the strongest immune responder appears most tolerant; under sigmoidal damage, the weakest responder does. Decomposition of the damage reduction shows that virulence reduction accounts for the majority of the effect across both model variants. Thus, the reaction-norm slope cannot determine whether host fitness is maintained by parasite-independent tissue protection or by sublethal impairment of parasites.

Theory predicts that virulence evolves as a consequence of selection to optimize transmission, generating a trade off in which increased exploitation enhances transmission but shortens the infectious period. Despite its central role in evolutionary epidemiology, empirical support for this virulence-transmission trade off remains limited, has focused largely on microparasites, and often overlooks variation in host immunity which can fundamentally alter links between virulence and transmission. Here, we provide a rare empirical test of virulence-transmission dynamics in a macroparasite with a complex life cycle. Using a field survey of the helminth parasite, Schistocephalus solidus, and its second intermediate host, threespine stickleback (Gasterosteus aculeatus), we quantify how host immune variation shapes relationships among parasite burden (a proxy for virulence) and transmission potential to definitive hosts, piscivorous birds. Importantly, host populations in the focal lakes span a gradient of evolved immune strategies, from low to high fibrosis, a strong anti-growth resistance mechanism. We find that variation in immune timing across host populations constrains the window in which parasites can reach transmissible stages. Subsequent changes in parasite burden scale up to alter transmission potential and reveal a nonlinear relationship consistent with a virulence-transmission trade off. Transmission potential is highest at intermediate parasite burdens, which also corresponds to intermediate immune responses. Together, this work links within-host processes to population-level epidemiological outcomes and demonstrates how host immune variation can shape virulence-transmission relationships. Incorporating immune heterogeneity may therefore help reconcile the mixed empirical support for trade off theory.

Segregated variation between populations is a fundamental evolutionary process leading to parasite specialization, yet the resulting impacts on infection heterogeneity within populations are theoretically and empirically understudied. We asked whether the distribution of host susceptibility to infection within populations carries the signatures of geographic structure from pathogen local adaptation, maladaptation, or generalism in a nuclear polyhedrosis virus that infects the Gulf Fritillary butterfly Dione vanillae. For this virus, there is genetic support for two geographically distinct groups within San Diego County, based on whole genome sequencing of 16 virus isolates. Reciprocal laboratory infections showed evidence of two contrasting viral life history strategies: a generalist phenotype that consistently infected variable hosts and a specialist that performed slightly better in its local host population. As predicted by our theoretical model, the more consistent infection displayed by the generalist across populations corresponded to lower heterogeneity in susceptibility within populations, modeled as gamma distribution. Furthermore, the generalist phenotype was collected over a wider geographic range despite having a tenfold-lower mean infection rate than the specialist, suggesting that a strategy of more consistent infection provides key fitness advantages across diverse host populations. Intriguingly, when there is variation in host susceptibility, interpretations of pathogen local adaptation are dose-dependent. Measuring infectivity across multiple doses enables estimation of the whole distribution of susceptibility, which provides more reliable identification of pathogen specialization to its local host. Our work demonstrates how trait distributions and not only their mean values can carry quantifiable signatures of eco-evolutionary processes in interspecific interactions.

The ecological and evolutionary dynamics of populations, including viral populations, are known to be jointly shaped by deterministic and stochastic processes. While the impact of stochastic processes has been rigorously explored for viral dynamics at the level of the host population, most dynamic models for acutely-infecting respiratory viral pathogens at the within-host scale remain deterministic in their formulation. While this may be reasonable for identifying key processes shaping their within-host viral population dynamics, recent studies indicate that stochastic processes need to be invoked for understanding patterns of within-host viral evolution. Specifically, several studies have shown that viral allele frequencies can change dramatically over the time course of days in acute infections. Here, we use stochastic dynamic models to explore the role of environmental noise in shaping observed patterns of virus evolution in acute respiratory virus infections. We summarize ways in which environmental stochasticity can be biologically realized in these acute viral infections and describe within-host models that can be implemented to jointly yield viral population dynamics and evolutionary dynamics. We further develop a statistical approach to estimate the extent of environmental noise from observed within-host allele frequency changes. We test this approach on simulated data and apply it to existing influenza A virus and SARS-CoV-2 within-host data. With these applications, we show that environmental stochasticity can parsimoniously reproduce key features of empirically observed allele frequency changes without needing to invoke demographic stochasticity or to adopt Wright-Fisher model formulations with a constant effective population size. Finally, we show that purifying selection and positive selection can both still contribute to within-host viral evolution in the context of a noisy environment, providing theoretical support for studies that have found purifying and positive selection in acutely-infecting respiratory virus populations.

O_LIRapid and ongoing anthropogenic habitat modification has the potential to alter the species composition, abundance and activity of biting insect communities, which are important disease vectors. The resulting changes in the network of interactions between biting insects and their hosts have implications for the transmission of vector-borne pathogens. C_LIO_LIWe used DNA metabarcoding of Diptera blood meals to document bipartite networks of interactions between biting flies (Diptera) and their hosts (including humans, domesticated and wild animals) across a gradient of anthropogenic habitat modification (village, agricultural and near-natural habitat) surrounding two rural villages in Ghana. C_LIO_LIWe collected 7,095 biting Diptera (of 42 species) from 30 collection sites, and generated sequencing data from 75 blood meals (from 29 species). These blood meals contained DNA from 18 vertebrate host species, dominated by humans and their livestock. C_LIO_LIHabitats with lower levels of anthropogenic modification had higher richness of biting Diptera and their host species. Species diversity and evenness did not differ significantly among habitats. Less modified habitats had higher network specificity, but connectance was highest in heavily modified habitats. C_LIO_LIHumans were highly embedded within biting Diptera-host networks, detected in 68% of blood meals. The networks reveal several potential disease transmission pathways linking competent vectors with susceptible hosts. The presence of mixed blood meals containing DNA of both human and wild animal origin highlights the potential for transmission of established and emerging zoonotic disease via bridge vectors. The high betweenness-centrality within interaction networks of the important disease vector Culex watti, combined with its high abundance across all levels of anthropogenic landscape modification, suggest that it may be a connector species, linking and facilitating disease transmission between spatially distinct communities. C_LIO_LISynthesis and applications: Our results are of epidemiological interest, as they identify the exposure of humans to pathogen transmission cycles across a gradient of anthropogenic habitat modification through the movement of opportunistic bridge vectors. We discuss the implications for the transmission of emerging and established zoonotic disease and for the targeting and implementation of initiatives to reduce disease exposure and transmission. C_LI

BackgroundNovel HIV prevention interventions such as long-acting pre-exposure prophylaxis (PrEP) could substantially reduce HIV transmission in Africa. However, efficient implementation in high-prevalence settings where incidence has declined requires an understanding of the contemporary dynamics driving new infections. MethodsWe identified incident HIV cases from a longitudinal, population-based cohort in Uganda. We individually matched cases to HIV-negative controls; traced and enrolled reported sexual partners; and enrolled female sex workers (FSWs) from reported venues. Conditional logistic regression, transmission modeling, and phylogenetics were used to characterize transmission networks. FindingsFrom 2021-2024, 38,899 HIV tests among 22,255 people identified 187 people with incident infections (47.6% male); 164 (88%) were enrolled and matched to 164 HIV-negative controls. Overall, 593 non-sex-worker partners (371 enrolled,62.6%), 146 FSW partners (21 enrolled,14.4%), and 28 venues (208 FSWs enrolled) were reported. Incident infection was most strongly predicted by partnership with a FSW (odds ratio:15.5; 95%CI:3.7-64.8), identified in 43.0% of male cases versus 6.3% of controls. Men with FSW partners had larger sexual networks than men without (median:6 vs 2 partners), and 91.2% of men with FSW partners also had non-sex-worker partners. Transmission modeling attributed 34.4% (95%CI:31.5-36.8%) of all male infections and 80.0% (95%CI:73.2-84.4%) of infections among male clients to sex with FSWs. Oral PrEP use among HIV-negative partners of incident cases was low (8.9% in women; 2.1% in men). InterpretationMen with FSW partners accounted for a substantial share of incident HIV infections and had markedly higher odds of infection than men without such partnerships. Together with the high potential for onward transmission within male client networks, these findings suggest that inclusion of male clients in long-acting HIV prevention strategies could be highly efficient and impactful. FundingNational Institutes of Health, United States; Gates Foundation; National Health and Medical Research Council, Australia

Viruses exhibit diverse genome architectures and replication strategies that shape their evolutionary trajectories and taxonomic diversification. Here, we test whether the complexity of viral genetic information processing predicts large-scale patterns of viral diversity. We define a propagation index that quantifies a minimal number of steps required for viral genome expression and replication across the Baltimore classes. Using ICTV taxonomy data (1971-2024), we identify a strong consistent linear relationship between the propagation index and viral diversification at both the family and genus levels. This statistically significant association is also observed for DNA and RNA viruses independently. Notably, the correlation persists across decades of ICTV releases despite substantial expansion and restructuring of viral taxonomy. Viruses with simpler propagation strategies consistently exhibit greater diversification, suggesting that genome processing complexity constrains macroevolutionary potential. These findings establish a quantitative link between propagation architecture and viral diversification and provide a predictive framework for understanding large-scale patterns of virus evolution.

In many animal species, individuals acquire knowledge from others that enhances their survival and reproduction. However, among the many available cultural exemplars, not all provide reliable information. Consequently, individuals tend to choose their exemplars selectively. One widespread pattern is a preference for older individuals, who may have accumulated valuable knowledge through life. Yet empirical studies also show that individuals frequently learn from age peers, suggesting that copying elders is not universally optimal. The ecological and social conditions that favor learning from elders rather than peers, therefore, remain unclear. Here, we investigate the evolutionary drivers of age-biased exemplar choice in age-structured populations where individuals accumulate knowledge over their lifespan. We develop a model that captures the coevolution of exemplar age choice and age-specific investments in social learning, individual learning, and the use of acquired knowledge for energy extraction. We show that selection promotes a progressive shift from social to individual learning and from learning to energy extraction with age. Exemplar age choice, in turn, evolves through a trade-off between targeting knowledgeable individuals and accessible ones. This trade-off leads young learners to learn preferentially from relatively young exemplars, who are common and still able to provide substantial amounts of novel knowledge, given learners limited knowledge at early ages. As individuals age, encountering exemplars with substantially novel knowledge becomes increasingly difficult. Consequently, as they age, individuals are expected to shift toward learning from older individuals, who possess more knowledge. Population, environment, and knowledge characteristics can shift this balance, generating a wide range of strategies from learning primarily from peers to consistently targeting the oldest individuals. In particular, learning from age peers is favored in populations with strong within-cohort interaction structure, high mortality, or high encounter rates, in unstable environments with rapid knowledge loss, and when knowledge is easily acquired or transmitted.

Parasites can alter host populations in fundamentally different ways depending on whether exposure results in infection. Yet, most epidemiological and evolutionary inference focuses on established infections, leaving the fitness consequences of parasite exposure comparatively understudied. This gap is consequential because hosts are frequently exposed to diverse parasite genotypes, and these encounters can impose substantial fitness costs even when infection does not occur. Theory predicts that hosts may mitigate these costs when interacting with commonly encountered parasite genotypes, such that exposure to sympatric parasites incurs lower fitness consequences than exposure to novel, allopatric parasites. Here, we examine the fitness consequences of exposure and infection in the first intermediate host of the trophically transmitted tapeworm Schistocephalus solidus, a cyclopoid copepod that serves as the first host in a three-host life cycle. Using sympatric (Vancouver Island, Canada) and allopatric (Norway) host-parasite combinations, we found a striking reciprocal asymmetry. Sympatric parasites were significantly more infective, yet exposure to sympatric parasites imposed weaker fitness costs when infection did not establish. In contrast, allopatric parasites were less infective, but exposed females produced fewer eggs and had lower hatching success than both controls and females exposed to sympatric parasites, indicating substantial genotype-dependent costs of exposure. Moreover, we found that infection was highly virulent across all genotypes: a single parasite caused near-complete reproductive suppression and reduced host survival across all host-parasite pairings, confirming S. solidus as a castrating parasite in copepods. Together, these results demonstrate that exposure, not just infection, acts as a critical ecological filter with potentially large and underappreciated consequences for host population dynamics and parasite transmission.

Reproductive seasonality offsets the energetic costs of reproduction by synchronizing births with peak resources and is traditionally expected to increase with latitude and environmental seasonality. However, life-history and behavioural strategies may also buffer energetic shortages and reduce dependency on environmental cycles. Here, we propose and test an integrative framework integrating climatic, life-history and behavioural factors using high-resolution measures of reproductive seasonality for 132 wild primate populations from 94 species. As expected, reproductive seasonality declines at lower latitudes, in less seasonal and in less predictable environments, even after controlling for productivity. It also decreases in species that spread reproductive costs by extending developmental periods, or when a higher infant mortality urges females to resume fertility shortly after loss. Unexpectedly, reproductive seasonality increases with environmental productivity and is not reduced by cognitive (foraging innovations), social (allomaternal care), or ecological (dietary breadth) buffering. Broader diets even enhance seasonality. These findings suggest that reproductive seasonality emerges from opportunity more than from constraints in productive environments, where females exploit abundant resources to accelerate their reproductive pace. Together, our results shed light on the diverse selective pressures shaping primate reproductive seasonality, including climate, life-history pace, and infanticide risk, and help to explain why humans reproduce year-round.

Viral populations can experience a dramatic reduction in population size and genetic diversity during transmission between donor and recipient hosts. Transmission bottlenecks can therefore decrease the evolutionary potential of viral populations, slowing adaptation by increasing the strength of genetic drift and decreasing the strength of selection. Recent barcoded influenza experiments in guinea pigs showed that recipient animals receive a diverse viral inoculum but lose most of that diversity within one to two days. The resulting bottleneck therefore arises not at physical transfer but during early viral growth in the recipient. We develop a branching-process framework to quantify how much of this loss follows from stochasticity in early growth alone. Each transmitted lineage is treated as an independent stochastic process governed by measurable viral parameters. We recover these parameters from viral growth rates estimated from observed viral load. A residual filter for each animal then captures any additional loss imposed by the recipient host. Applied to twenty-four recipient animals, the model reveals two distinct groups. For roughly half of the animals, the stochastic extinction during early growth already accounts for the observed loss. For the remaining animals, the additional host filter is severe. Only about one in a hundred free virions pass through. This decomposition offers a quantitative entry point for future work on immune contributions to transmission bottlenecks.

Stable variation in public-good production can generate biological division of labor. Two key drivers are the size of interacting groups and the degree of assortment (relatedness) among individuals with similar investment levels. Here we extend adaptive-dynamic models of continuous public-goods investment by allowing assortment in group formation. We show that increasing group size typically enlarges the range of benefit and cost curvatures that permit evolutionary branching, whereas assortment tends to shrink this range and prevents branching under complete relatedness. For a broad class of models, branching requires diminishing marginal public benefits and diminishing marginal private costs, with costs decreasing faster than benefits. Finally, we analyze post-branching dynamics for one and two public goods, and find that assortment can stabilize the resulting two-type division of labor. Together, these results show how group size, assortment, and payoff curvature jointly determine when heterogeneity in public-goods production can evolve.

There are some disputed hypotheses for the recurrent observations of insular gigantism and dwarfism, like the island rule: small organisms would become larger on islands, while large organisms would become smaller. But, why is the latter? In addition, not all the observations fit this rule. Here I propose a causal model. Following the Island Biogeography Theory (IBT), insular aspects influence the census N. Observations suggest that variation in N is associated with variation in effective population size (Ne). The body size of insular colonisers might change, following Damuths law, as Ne can decrease at a differential rate from the island area A, resulting in a distinctive effective density [Formula]. Interestingly, a prediction of the drift-barrier hypothesis is that Ne is affecting mutation rates. Consequently, body mass, genome size and {micro} may be predicted to some extent by island area, as they are influenced by De and Ne. Falsification of the latter hypothesis is feasible by determining changes in genomic features of insular species. We now have the opportunity to interrogate the extensive data available. Here I ask: (i) How is decreasing island area predicting average body sizes? (ii) To which levels does this prediction apply (species, cells, genomes)? (iii) How well does the model fare on predicting {micro} over paradigmatic case studies? The resolution of these questions may provide a more reliable diagnosis of the evolutionary causes for somatic size variation. Significance statementNaturalists have long reported that insular species tend to become unusually large or small compared to their mainland relatives. Despite the familiarity of this "island rule", there is still no broad mechanistic explanation for why these changes occur so consistently across different groups of organisms. This work proposes that an important neutral factor can be the change in effective density of isolated populations. By combining the expectations of Damuths law, the IBT model, and the nearly-neutral theory it offers unified predictions on how sudden constraints in island area can influence not only the evolution of body size, but also the direction of changes in genome size and evolutionary rates.

Reproductive strategies vary widely among vertebrates, yet the selective drivers of life history trait evolution remain unresolved. Viviparity is typically associated with a slower life history syndrome of larger bodies, increased lifespans, and reduced fecundity. However, viviparity is often coupled to increased matrotrophic investment, which according to the Disposable Soma Theory (DST) should reduce longevity. Conversely, the Selfish Mother Hypothesis (SMH) suggests that matrotrophic mothers withhold nutrients for the sake of their own future survival and reproduction. These opposing frameworks imply conflicting life history outcomes, and it remains unclear whether such dynamics operate primarily among individuals of the same species or shape higher-level clade-wide divergence. Here, we used a phylogenetically controlled comparative analysis of chondrichthyan (n = 162) and mammalian (n = 620) species to show that both the convergent origin and quantitative degree of matrotrophy is associated with reduced longevity across two major vertebrate clades. Our results decouple parity mode and nutrient provisioning to show that matrotrophy reduces maternal longevity, which counteracts the slower life history strategy of viviparity. We provide evolutionary support for the DST, and not the SMH, in reproductive strategy diversification. Using a simple stochastic simulation, we propose a unified Sacrificial Mother framework, in which increased matrotrophic investment specifically reduces maternal longevity through the accumulation of somatic costs. Our work identifies the somatic costs of viviparous matrotrophy as a fundamental, but previously unrecognised, evolutionary trade-off against individual embryonic fitness which shapes the diversification of vertebrate life history strategies beyond resource allocation in intraspecific individuals.