Triangle Center for Evolutionary Medicine

Sleep is essential to cognitive function and health in humans, yet the ultimate reasons for sleep-i.e. 'why' sleep evolved-remain mysterious. We integrate findings from human sleep studies, the ethnographic record, and the ecology and evolution of mammalian sleep to better understand sleep along the human lineage and in the modern world. Compared to other primates, sleep in great apes has undergone substantial evolutionary change, with all great apes building a sleeping platform or 'nest'. Further evolutionary change characterizes human sleep, with humans having the shortest sleep duration, yet the highest proportion of rapid eye movement sleep among primates. These changes likely reflect that our ancestors experienced fitness benefits from being active for a greater portion of the 24-h cycle than other primates, potentially related to advantages arising from learning, socializing and defending against predators and hostile conspecifics. Perspectives from evolutionary medicine have implications for understanding sleep disorders; we consider these perspectives in the context of insomnia, narcolepsy, seasonal affective disorder, circadian rhythm disorders and sleep apnea. We also identify how human sleep today differs from sleep through most of human evolution, and the implications of these changes for global health and health disparities. More generally, our review highlights the importance of phylogenetic comparisons in understanding human health, including well-known links between sleep, cognitive performance and health in humans.

The adaptive landscape of the ancestral human environments selected for a suite of genetic, behavioural and physiological traits, many of which persist in contemporary human populations. The transition to modernity [1] rapidly reshaped these environments, yet the slower rate of biological evolution limits phenotypic change. This results in evolutionary mismatch, defined here as the phenomenon by which previously adaptive alleles are no longer favoured in a new environment (Fig. 1). This definition operates across space and time, while other uses of mismatch are applied over the life course [2, 3]. The ancestral environment (i) favours a certain combination of alleles (darker colours). Transitions to modernity produce shifts in the allelic combination that is best suited to the new environment (ii-iv). Mismatch occurs when ancestral alleles (star) persist in new settings where the environment, but not yet genetics, has changed. Due to variation in food availability and quality, the ancestral environment favoured efficient energy extraction and storage [4, 5]. These once-adaptive traits become mismatched to industrialized settings with an overabundance of easily accessible, calorie-dense foods. This surplus, coupled with the relatively low energy output required by the modern lifestyle [5], promotes an energy imbalance that contributes to weight gain. Today, obesity is rampant across populations in developed countries and rapidly increasing in developing nations transitioning to the industrialized lifestyle [6]. Humans evolved in environments rich with biodiversity, including helminthic worms that co-evolved to regulate our immune systems [7]. Modern medicine and hygiene largely eradicated these helminths from industrialized settings, and their absence is now implicated in a suite of hyper-inflammatory conditions, including multiple sclerosis and irritable bowel disease [7, 8]. Helminthic therapy, which reunites the human body with part of its ancestral biota, has been suggested as a treatment for the immune system’s inappropriate response to a mismatched environment.

The transmission of infectious disease through a population is often modeled assuming that interactions occur randomly in groups, with all individuals potentially interacting with all other individuals at an equal rate. However, it is well known that pairs of individuals vary in their degree of contact. Here, we propose a measure to account for such heterogeneity: effective network size (ENS), which refers to the size of a maximally complete network (i.e., unstructured, where all individuals interact with all others equally) that corresponds to the outbreak characteristics of a given heterogeneous, structured network. We simulated susceptible-infected (SI) and susceptible-infected-recovered (SIR) models on maximally complete networks to produce idealized outbreak duration distributions for a disease on a network of a given size. We also simulated the transmission of these same diseases on random structured networks and then used the resulting outbreak duration distributions to predict the ENS for the group or population. We provide the methods to reproduce these analyses in a public R package, "enss." Outbreak durations of simulations on randomly structured networks were more variable than those on complete networks, but tended to have similar mean durations of disease spread. We then applied our novel metric to empirical primate networks taken from the literature and compared the information represented by our ENSs to that by other established social network metrics. In AICc model comparison frameworks, group size and mean distance proved to be the metrics most consistently associated with ENS for SI simulations, while group size, centralization, and modularity were most consistently associated with ENS for SIR simulations. In all cases, ENS was shown to be associated with at least two other independent metrics, supporting its use as a novel metric. Overall, our study provides a proof of concept for simulation-based approaches toward constructing metrics of ENS, while also revealing the conditions under which this approach is most promising.

Racial health disparities are a pervasive feature of modern experience and structural racism is increasingly recognized as a public health crisis. Yet evolutionary medicine has not adequately addressed the racialization of health and disease, particularly the systematic embedding of social biases in biological processes leading to disparate health outcomes delineated by socially defined race. In contrast to the sheer dominance of medical publications which still assume genetic 'race' and omit mention of its social construction, we present an alternative biological framework of racialized health. We explore the unifying evolutionary-ecological principle of niche construction as it offers critical insights on internal and external biological and behavioral feedback processes environments at every level of the organization. We Integrate insights of niche construction theory in the context of human evolutionary and social history and phenotype-genotype modification, exposing the extent to which racism is an evolutionary mismatch underlying inequitable disparities in disease. We then apply ecological models of niche exclusion and exploitation to institutional and interpersonal racial constructions of population and individual health and demonstrate how discriminatory processes of health and harm apply to evolutionarily relevant disease classes and life-history processes in which socially defined race is poorly understood and evaluated. Ultimately, we call for evolutionary and biomedical scholars to recognize the salience of racism as a pathogenic process biasing health outcomes studied across disciplines and to redress the neglect of focus on research and application related to this crucial issue.

The global impact of the COVID-19 pandemic has disproportionately affected some communities and populations more than others. We propose that an interdisciplinary framework of 'One Health Disparities' advances understanding of the social and systemic issues that drive COVID-19 in vulnerable populations. One Health Disparities integrates the social environment with One Health perspectives on the interconnectedness of human, animal, and environmental health. To apply this framework, we consider One Health Disparities that emerge in three key components of disease transmission: exposure, susceptibility, and disease expression. Exposure disparities arise through variation in contact with COVID-19's causative agent, SARS-CoV-2. Disparities in susceptibility and disease expression also exist; these are driven by biological and social factors, such as diabetes and obesity, and through variation in access to healthcare. We close by considering how One Health Disparities informs understanding of spillback into new animal reservoirs, and what this might mean for further human health disparities. LAY SUMMARY: One Health focuses on interconnections between human, animal, and environmental health. We propose that social environments are also important to One Health and help illuminate disparities in the coronavirus pandemic, including its origins, transmission and susceptibility among humans, and spillback to other species. We call this framework One Health Disparities.

PURPOSE: Aspects of medical education and clinical practice continue to reflect the antiquated notion that race is a biologically valid distinction among individuals rather than a social construct. The authors analyzed the use of race and ethnicity in a popular pediatrics textbook to determine if these concepts were being used consistently and correctly. METHOD: In May 2021, using the search function on the American Academy of Pediatrics (AAP) eBooks platform, the authors searched for 29 race- or ethnicity-related terms (e.g., African, Asian, Black, race) in the AAP Textbook of Pediatric Care, 2nd Edition , which was published in 2016. One researcher extracted direct quotes containing at least one of these search terms. Three researchers independently coded each quote as problematic or nonproblematic with respect to the use of the search terms, excluding examples in which the terms were used in irrelevant contexts (e.g., black box warning). The researchers then identified themes based on the quotes that used race and ethnicity problematically. RESULTS: The search produced 2,167 total results across the search terms, 806 of which were relevant to race or ethnicity and were analyzed. Problematic quotes: (1) used race or ethnicity as a surrogate for social variables, (2) conflated terminology (e.g., conflated socially defined race with genetic ancestry), (3) overgeneralized or made claims based on limited data, (4) lacked clinical relevance, (5) lacked inclusivity, (6) promoted racial stereotypes, or (7) made contradicting claims about race. CONCLUSIONS: The use of race and ethnicity in the AAP Textbook of Pediatric Care, 2nd Edition was not always appropriate, as demonstrated by examples that reified race as a biological fact and thereby promoted structural racism. Critical evaluation of the use of race and ethnicity in all current medical textbooks and future revisions is warranted.

BACKGROUND AND OBJECTIVES: Research in evolutionary medicine provides many examples of how evolution has shaped human susceptibility to disease. Traits undergoing rapid evolutionary change may result in associated costs or reduce the energy available to other traits. We hypothesize that humans have experienced more such changes than other primates as a result of major evolutionary change along the human lineage. We investigated 41 physiological traits across 50 primate species to identify traits that have undergone marked evolutionary change along the human lineage. METHODOLOGY: We analysed the data using two Bayesian phylogenetic comparative methods. One approach models trait covariation in non-human primates and predicts human phenotypes to identify whether humans are evolutionary outliers. The other approach models adaptive shifts under an Ornstein-Uhlenbeck model of evolution to assess whether inferred shifts are more common on the human branch than on other primate lineages. RESULTS: We identified four traits with strong evidence for an evolutionary increase on the human lineage (amylase, haematocrit, phosphorus and monocytes) and one trait with strong evidence for decrease (neutrophilic bands). Humans exhibited more cases of distinct evolutionary change than other primates. CONCLUSIONS AND IMPLICATIONS: Human physiology has undergone increased evolutionary change compared to other primates. Long distance running may have contributed to increases in haematocrit and mean corpuscular haemoglobin concentration, while dietary changes are likely related to increases in amylase. In accordance with the pathogen load hypothesis, human monocyte levels were increased, but many other immune-related measures were not. Determining the mechanisms underlying conspicuous evolutionary change in these traits may provide new insights into human disease.

Many recent studies have examined the impact of predicted changes in temperature and precipitation patterns on infectious diseases under different greenhouse gas emissions scenarios. But these emissions scenarios symbolize more than altered temperature and precipitation regimes; they also represent differing levels of change in energy, transportation, and food production at a global scale to reduce the effects of climate change. The ways humans respond to climate change, either through adaptation or mitigation, have underappreciated, yet hugely impactful effects on infectious disease transmission, often in complex and sometimes nonintuitive ways. Thus, in addition to investigating the direct effects of climate changes on infectious diseases, it is critical to consider how human preventative measures and adaptations to climate change will alter the environments and hosts that support pathogens. Here, we consider the ways that human responses to climate change will likely impact disease risk in both positive and negative ways. We evaluate the evidence for these impacts based on the available data, and identify research directions needed to address climate change while minimizing externalities associated with infectious disease, especially for vulnerable communities. We identify several different human adaptations to climate change that are likely to affect infectious disease risk independently of the effects of climate change itself. We categorize these changes into adaptation strategies to secure access to water, food, and shelter, and mitigation strategies to decrease greenhouse gas emissions. We recognize that adaptation strategies are more likely to have infectious disease consequences for under-resourced communities, and call attention to the need for socio-ecological studies to connect human behavioral responses to climate change and their impacts on infectious disease. Understanding these effects is crucial as climate change intensifies and the global community builds momentum to slow these changes and reduce their impacts on human health, economic productivity, and political stability.

Purpose of Review: Preparing for pandemics requires a degree of interdisciplinary work that is challenging under the current paradigm. This review summarizes the challenges faced by the field of pandemic science and proposes how to address them. Recent Findings: The structure of current siloed systems of research organizations hinders effective interdisciplinary pandemic research. Moreover, effective pandemic preparedness requires stakeholders in public policy and health to interact and integrate new findings rapidly, relying on a robust, responsive, and productive research domain. Neither of these requirements are well supported under the current system. Summary: We propose a new paradigm for pandemic preparedness wherein interdisciplinary research and close collaboration with public policy and health practitioners can improve our ability to prevent, detect, and treat pandemics through tighter integration among domains, rapid and accurate integration, and translation of science to public policy, outreach and education, and improved venues and incentives for sustainable and robust interdisciplinary work.

Charles L Nunn; COVID-19 and Evolution, Medicine, and Public Health, Evolution, Medicine, and Public Health, , eoad002, https://doi.org/10.1093/emph/eoad002

One hundred years ago, a pandemic of unprecedented size and scope afflicted the human population. This pandemic was caused by an H1N1 influenza virus of avian origin. Over the course of 1918–1919, this virus infected approximately one-third of the nearly 2 billion people living on Earth at the time, resulting in at least 50 million deaths. The pandemic caused massive economic disruptions, severely strained many of the public health infrastructures that were designed to contain disease, and spread to the farthest and most isolated corners of the globe, often with especially deadly consequences in remote areas. The disease caused by this virus had several unusual characteristics that remain incompletely understood, including high mortality in previously healthy, young adults (i.e., 20–40 years of age). Questions also remain about the geographic origin of the pandemic, and the underlying drivers that led to emergence from avian hosts. The 1918 influenza pandemic remains one of the most feared epidemics in world history, and a rallying cry for more effective preparedness for future outbreaks of influenza and other viruses. It is well worth reflecting on this pandemic, including with an evolutionary lens. In this special collection of papers, we present new evolutionary perspectives on the history of the 1918 influenza pandemic. Our collection includes a review by Dr. Margaret Humphreys that weaves together historical and evolutionary perspectives, providing a broad overview of the pandemic for those interested in evolutionary medicine. Dr. Michael Worobey and colleagues provide new perspectives on the geographic origins and timing of the first cases of the 1918 influenza pandemic, including insights from phylogenetic analyses and the causes of young adult mortality. In the time since the 1918 pandemic, a greater appreciation for the cross-species spread of viruses has emerged. To provide some of these new insights from a One Health perspective, Dr. Emily Bailey and her colleagues review new knowledge on influenza viruses. Lastly, as a provocative and forward-looking Commentary, Dr. David Fedson provides new insights to the causes of young adult mortality and proposes how this knowledge can be used to reduce mortality in future pandemics. He also outlines approaches for future testing of these proposals. In addition to these four papers, we have other papers that are in the works for this collection over the next year, and we welcome additional submissions. As Editor-in-Chief of Evolution, Medicine and Public Health, I am excited to help orchestrate this highly interdisciplinary collection of papers. I would like to see other topical collections emerge on the pages of the journal, especially those that present different viewpoints based on rigorous science that move evolutionary medicine research forward. If you have ideas for other collections—including sets of papers from organized symposia—please contact me about the possibilities for publishing those papers at EMPH. Conflict of interest: None declared.

Ecological and evolutionary perspectives are essential for understanding human health. Consider, for example, the Ebola virus, which is thought to erupt from bat populations through contact among humans, bats, and other wildlife. In the ongoing outbreak in West Africa, the index case was a 2-year-old boy who may have played in and around a tree that was home to a colony of bats (Saéz et al. 2015). Thus, interactions between humans and wildlife in a highly disturbed ecological habitat probably served as the spark that ignited this epidemic that has killed more than 20,000 people (Baize et al. 2014). Every transmission of the Ebola virus to a new host represents an opportunity for natural selection and therefore for evolution of the virus. Some strains have longer chains of transmission, with more mutations, enabling viruses to discover more fit phenotypes. Phylogenetic analyses revealed the great extent of evolutionary change that occurred early in this latest epidemic, with 73 nonsynonymous substitutions among 78 infected individuals just from Sierra Leone (Gire et al. 2014).