Subjects -> ESTATE, HOUSING AND URBAN PLANNING (Total: 304 journals)
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HOME ECONOMICS (9 journals)

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Community, Work & Family     Hybrid Journal   (Followers: 23)
Evolution, Medicine, and Public Health     Open Access   (Followers: 8)
Family and Consumer Sciences Research Journal     Hybrid Journal   (Followers: 1)
Field Actions Science Reports     Open Access  
Food, Culture and Society: An International Journal of Multidisciplinary Research     Full-text available via subscription   (Followers: 13)
Instyle     Full-text available via subscription  
International Journal of Home Economics     Full-text available via subscription   (Followers: 2)
Nutrition & Food Science     Hybrid Journal   (Followers: 8)
Review of Economics of the Household     Hybrid Journal   (Followers: 5)
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Evolution, Medicine, and Public Health
Number of Followers: 8  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2050-6201
Published by Oxford University Press Homepage  [419 journals]
  • Cesarean section and breastfeeding outcomes in an Indigenous Qom community
           with high breastfeeding support

    • Authors: Martin M; Keith M, Olmedo S, et al.
      Pages: 36 - 46
      Abstract: AbstractBackground and objectivesCesarean section may lead to suboptimal breastfeeding outcomes, though evidence has been mixed. Factors, such as premature birth, birth weight and maternal age may independently increase risk of cesarean and hinder breastfeeding initiation, while maternal preferences, support and sociostructural barriers may influence breastfeeding practices beyond the immediate postpartum period.MethodologyWe assessed impacts of cesarean section and gestational factors on breastfeeding duration among Indigenous Qom mothers in Argentina who have strong traditional breastfeeding support. We modeled transitions from exclusive breastfeeding to complementary feeding and from complementary feeding to full weaning in a Bayesian time-to-event framework with birth mode and gestational covariates (n = 89 infants).ResultsEstimated median time to full weaning was 30 months. Cesarean-delivered babies were weaned an average of 5 months later adjusting for gestational age, maternal parity and infant sex. No factors were associated with time-to-complementary feeding, and time-to-complementary feeding was not associated with time-to-full weaning.Conclusions and implicationsAmong Indigenous Qom mothers in Argentina, cesarean section was not associated with suboptimal breastfeeding outcomes. Although some Qom mothers do experience early breastfeeding problems, particularly following first birth, problems are not more frequent following cesarean delivery. Traditional postpartum kin and community support during prolonged postpartum periods may be instrumental in helping mothers to overcome early breastfeeding problems due to cesarean or other risk factors.
      PubDate: Tue, 04 Jan 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoab045
      Issue No: Vol. 10, No. 1 (2022)
  • Immune cell type and DNA methylation vary with reproductive status in
           women: possible pathways for costs of reproduction

    • Authors: Ryan C; Jones M, Edgar R, et al.
      Pages: 47 - 58
      Abstract: AbstractBackgroundConsistent with evolutionarily theorized costs of reproduction (CoR), reproductive history in women is associated with life expectancy and susceptibility to certain cancers, autoimmune disorders and metabolic disease. Immunological changes originating during reproduction may help explain some of these relationships.MethodologyTo explore the potential role of the immune system in female CoR, we characterized leukocyte composition and regulatory processes using DNA methylation (DNAm) in a cross-sectional cohort of young (20–22 years old) women differing in reproductive status.ResultsCompared to nulliparity, pregnancy was characterized by differential methylation at 828 sites, 96% of which were hypomethylated and enriched for genes associated with T-cell activation, innate immunity, pre-eclampsia and neoplasia. Breastfeeding was associated with differential methylation at 1107 sites (71% hypermethylated), enriched for genes involved in metabolism, immune self-recognition and neurogenesis. There were no significant differences in DNAm between nulliparous and parous women. However, compared to nullipara, pregnant women had lower proportions of B, CD4T, CD8T and natural killer (NK) cells, and higher proportions of granulocytes and monocytes. Monocyte counts were lower and NK counts higher among breastfeeding women, and remained so among parous women.ImplicationsOur findings point to widespread differences in DNAm during pregnancy and lactation. These effects appear largely transient, but may accumulate with gravidity become detectable as women age. Nulliparous and parous women differed in leukocyte composition, consistent with more persistent effects of reproduction on cell type. These findings support transient (leukocyte DNAm) and persistent (cell composition) changes associated with reproduction in women, illuminating potential pathways contributing to CoR.Lay Summary: Evolutionary theory and epidemiology support costs of reproduction (CoR) to women’s health that may involve changes in immune function. We report differences in immune cell composition and gene regulation during pregnancy and breastfeeding. While many of these differences appear transient, immune cell composition may remain, suggesting mechanisms for female CoR.
      PubDate: Wed, 02 Feb 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac003
      Issue No: Vol. 10, No. 1 (2022)
  • Optimal non-pharmaceutical intervention policy for Covid-19 epidemic via
           neuroevolution algorithm

    • Authors: Saeidpour A; Rohani P.
      Pages: 59 - 70
      Abstract: AbstractBackgroundNational responses to the Covid-19 pandemic varied markedly across countries, from business-as-usual to complete shutdowns. Policies aimed at disrupting the viral transmission cycle and preventing the overwhelming of healthcare systems inevitably exact an economic toll.MethodologyWe developed an intervention policy model that comprised the relative human, implementation and healthcare costs of non-pharmaceutical epidemic interventions and identified the optimal strategy using a neuroevolution algorithm. The proposed model finds the minimum required reduction in transmission rates to maintain the burden on the healthcare system below the maximum capacity.ResultsWe find that such a policy renders a sharp increase in the control strength during the early stages of the epidemic, followed by a steady increase in the subsequent ten weeks as the epidemic approaches its peak, and finally the control strength is gradually decreased as the population moves towards herd immunity. We have also shown how such a model can provide an efficient adaptive intervention policy at different stages of the epidemic without having access to the entire history of its progression in the population.Conclusions and implicationsThis work emphasizes the importance of imposing intervention measures early and provides insights into adaptive intervention policies to minimize the economic impacts of the epidemic without putting an extra burden on the healthcare system.Lay SummaryWe developed an intervention policy model that comprised the relative human, implementation and healthcare costs of non-pharmaceutical epidemic interventions and identified the optimal strategy using a neuroevolution algorithm. Our work emphasizes the importance of imposing intervention measures early and provides insights into adaptive intervention policies to minimize the economic impacts of the epidemic without putting an extra burden on the healthcare system.
      PubDate: Fri, 28 Jan 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac002
      Issue No: Vol. 10, No. 1 (2022)
  • Serial passage in an insect host indicates genetic stability of the human
           probiotic Escherichia coli Nissle 1917

    • Authors: Schröder N; Korša A, Wami H, et al.
      Pages: 71 - 86
      Abstract: AbstractBackground and objectivesThe probiotic Escherichia coli strain Nissle 1917 (EcN) has been shown to effectively prevent and alleviate intestinal diseases. Despite the widespread medical application of EcN, we still lack basic knowledge about persistence and evolution of EcN outside the human body. Such knowledge is important also for public health aspects, as in contrast to abiotic therapeutics, probiotics are living organisms that have the potential to evolve. This study made use of experimental evolution of EcN in an insect host, the red flour beetle Tribolium castaneum, and its flour environment.MethodologyUsing a serial passage approach, we orally introduced EcN to larvae of T.castaneum as a new host, and also propagated it in the flour environment. After eight propagation cycles, we analyzed phenotypic attributes of the passaged replicate EcN lines, their effects on the host in the context of immunity and infection with the entomopathogen Bacillus thuringiensis, and potential genomic changes using WGS of three of the evolved lines.ResultsWe observed weak phenotypic differences between the ancestral EcN and both, beetle and flour passaged EcN lines, in motility and growth at 30°C, but neither any genetic changes, nor the expected increased persistence of the beetle-passaged lines. One of these lines displayed distinct morphological and physiological characteristics.Conclusions and implicationsOur findings suggest that EcN remains rather stable during serial passage in an insect. Weak phenotypic changes in growth and motility combined with a lack of genetic changes indicate a certain degree of phenotypic plasticity of EcN.Lay SummaryFor studying adaptation of the human probiotic Escherichia coli strain Nissle 1917, we introduced it to a novel insect host system and its environment using a serial passage approach. After passage, we observed weak phenotypic changes in growth and motility but no mutations or changes in persistence inside the host.
      PubDate: Fri, 11 Feb 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac001
      Issue No: Vol. 10, No. 1 (2022)
  • The evolution of the human healthcare system and implications for
           understanding our responses to COVID-19

    • Authors: Kessler S; Aunger R.
      Pages: 87 - 107
      Abstract: AbstractThe COVID-19 pandemic has revealed an urgent need for a comprehensive, multidisciplinary understanding of how healthcare systems respond successfully to infectious pathogens—and how they fail. This study contributes a novel perspective that focuses on the selective pressures that shape healthcare systems over evolutionary time. We use a comparative approach to trace the evolution of care-giving and disease control behaviours across species and then map their integration into the contemporary human healthcare system. Self-care and pro-health environmental modification are ubiquitous across animals, while derived behaviours like care for kin, for strangers, and group-level organizational responses have evolved via different selection pressures. We then apply this framework to our behavioural responses to COVID-19 and demonstrate that three types of conflicts are occurring: (1) conflicting selection pressures on individuals, (2) evolutionary mismatches between the context in which our healthcare behaviours evolved and our globalized world of today and (3) evolutionary displacements in which older forms of care are currently dispensed through more derived forms. We discuss the significance of understanding how healthcare systems evolve and change for thinking about the role of healthcare systems in society during and after the time of COVID-19—and for us as a species as we continue to face selection from infectious diseases.
      PubDate: Sat, 12 Feb 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac004
      Issue No: Vol. 10, No. 1 (2022)
  • A growth areaA review of the value of clinical studies of child growth for

    • Authors: Decrausaz S; Cameron M.
      Pages: 108 - 122
      Abstract: AbstractStudies of living children demonstrate that early life stress impacts linear growth outcomes. Stresses affecting linear growth may also impact later life health outcomes, including increased cardiometabolic disease risk. Palaeopathologists also assess the growth of children recovered from bioarchaeological contexts. Early life stresses are inferred to affect linear growth outcomes, and measurements of skeletal linear dimensions alongside other bioarchaeological information may indicate the types of challenges faced by past groups. In clinical settings, the impacts of stress on growing children are typically measured by examining height. Palaeopathologists are limited to examining bone dimensions directly and must grapple with incomplete pictures of childhood experiences that may affect growth. Palaeopathologists may use clinical growth studies to inform observations among past children; however, there may be issues with this approach. Here, we review the relationship between contemporary and palaeopathological studies of child and adolescent growth. We identify approaches to help bridge the gap between palaeopathological and biomedical growth studies. We advocate for: the creation of bone-specific growth reference information using medical imaging and greater examination of limb proportions; the inclusion of children from different global regions and life circumstances in contemporary bone growth studies; and greater collaboration and dialogue between palaeopathologists and clinicians as new studies are designed to assess linear growth past and present. We advocate for building stronger bridges between these fields to improve interpretations of growth patterns across human history and to potentially improve interventions for children living and growing today.
      PubDate: Tue, 08 Feb 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac005
      Issue No: Vol. 10, No. 1 (2022)
  • Roles for non-human primate-associated phage diversity in improving
           medicine and public health

    • Authors: Gogarten J.
      Pages: 123 - 129
      Abstract: AbstractMammals harbor trillions of microorganisms and understanding the ecological and evolutionary processes structuring these ecosystems may provide insights relevant to public health and medicine. Comparative studies with our closest living relatives, non-human primates, have provided first insights into their rich bacteriophage communities. Here, I discuss how this phage diversity can be useful for combatting antibiotic-resistant infections and understanding disease emergence risk. For example, some primate-associated phages show a pattern suggesting a long-term co-divergence with their primate superhosts—co-diverging phages may be more likely to exhibit a narrow host range and thus less useful for phage therapy. Captive primates lose their natural phageome, which is replaced by human-associated phages making phages an exciting tool for studying rates of microorganism transmission at human–wildlife interfaces. This commentary tackles avenues for selecting phages for therapeutic interventions based on their ecological and evolutionary history, while discussing frameworks to allow primate-associated phages to be incorporated into the arsenal of clinicians.
      PubDate: Fri, 18 Feb 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac006
      Issue No: Vol. 10, No. 1 (2022)
  • Strength is negatively associated with depression and accounts for some of
           the sex differenceA replication and extension

    • Authors: Smith C; Rosenström T, Hagen E.
      Pages: 130 - 141
      Abstract: AbstractBackgroundDepression occurs about twice as often in women as in men, a disparity that remains poorly understood. In a previous publication, Hagen and Rosenström predicted and found that grip strength, a highly sexually dimorphic index of physical formidability, mediated much of the effect of sex on depression. Striking results like this are more likely to be published than null results, potentially biasing the scientific record. It is therefore critical to replicate and extend them.MethodologyUsing new data from the 2013–14 cycle of the National Health and Nutrition Examination Survey, a nationally representative sample of US households (n = 3650), we replicated models of the effect of sex and grip strength on depression reported in Hagen and Rosenström, along with additional potential confounds and a new detailed symptom-level exploration.ResultsOverall, the effects from the original paper were reproduced although with smaller effect sizes. Grip strength mediated 38% of the effect of sex on depression, compared to 63% in Hagen and Rosenström. These results were extended with findings that grip strength had a stronger association with some depression symptoms, like suicidality, low interest and low mood than with other symptoms, like appetite changes.ConclusionsGrip strength is negatively associated with depression, especially its cognitive–affective symptoms, controlling for numerous possible confounds. Although many factors influence depression, few of these reliably occur cross-culturally in a sex-stratified manner and so are unlikely to explain the well-established, cross-cultural sex difference in depression. The sex difference in upper body strength occurs in all populations and is therefore a candidate evolutionary explanation for some of the sex difference in depression.Lay summary: Why are women at twice the risk of developing depression as men' Depression typically occurs during social conflicts, such as physical or sexual abuse. Physically strong individuals can often single-handedly resolve conflicts in their favor, whereas physically weaker individuals often need help from others. We argue that depression is a credible cry for help. Because men generally have greater strength than women, we argue that men may be more likely to resolve conflicts using physical formidability and women to signal others for help. We find that higher grip strength is associated with lower depression, particularly symptoms like feeling down or thoughts of suicide and that strength accounts for part of the sex difference in rates of depression.
      PubDate: Tue, 22 Feb 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac007
      Issue No: Vol. 10, No. 1 (2022)
  • Mutation rate of SARS-CoV-2 and emergence of mutators during experimental

    • Authors: Amicone M; Borges V, Alves M, et al.
      Pages: 142 - 155
      Abstract: AbstractBackground and objectivesTo understand how organisms evolve, it is fundamental to study how mutations emerge and establish. Here, we estimated the rate of mutation accumulation of SARS-CoV-2 in vitro and investigated the repeatability of its evolution when facing a new cell type but no immune or drug pressures.MethodologyWe performed experimental evolution with two strains of SARS-CoV-2, one carrying the originally described spike protein (CoV-2-D) and another carrying the D614G mutation that has spread worldwide (CoV-2-G). After 15 passages in Vero cells and whole genome sequencing, we characterized the spectrum and rate of the emerging mutations and looked for evidences of selection across the genomes of both strains.ResultsFrom the frequencies of the mutations accumulated, and excluding the genes with signals of selection, we estimate a spontaneous mutation rate of 1.3 × 10−6 ± 0.2 × 10−6 per-base per-infection cycle (mean across both lineages of SARS-CoV-2 ± 2SEM). We further show that mutation accumulation is larger in the CoV-2-D lineage and heterogeneous along the genome, consistent with the action of positive selection on the spike protein, which accumulated five times more mutations than the corresponding genomic average. We also observe the emergence of mutators in the CoV-2-G background, likely linked to mutations in the RNA-dependent RNA polymerase and/or in the error-correcting exonuclease protein.Conclusions and implicationsThese results provide valuable information on how spontaneous mutations emerge in SARS-CoV-2 and on how selection can shape its genome toward adaptation to new environments.Lay Summary: Each time a virus replicates inside a cell, errors (mutations) occur. Here, via laboratory propagation in cells originally isolated from the kidney epithelium of African green monkeys, we estimated the rate at which the SARS-CoV-2 virus mutates—an important parameter for understanding how it can evolve within and across humans. We also confirm the potential of its Spike protein to adapt to a new environment and report the emergence of mutators—viral populations where mutations occur at a significantly faster rate.
      PubDate: Tue, 29 Mar 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac010
      Issue No: Vol. 10, No. 1 (2022)
  • Greater chronic morbidity is associated with greater fatigue in six
           countriesA case of evolutionary mismatch'

    • Authors: Schrock J; Sugiyama L, Naidoo N, et al.
      Pages: 156 - 169
      Abstract: AbstractBackground and objectivesHuman susceptibility to chronic non-communicable disease may be explained, in part, by mismatches between our evolved biology and contemporary environmental conditions. Disease-induced fatigue may function to reduce physical activity during acute infection, thereby making more energy available to mount an effective immune response. However, fatigue in the context of chronic disease may be maladaptive because long-term reductions in physical activity increase risks of disease progression and the acquisition of additional morbidities. Here, we test whether cumulative chronic morbidity is associated with subjective fatigue.MethodologyWe constructed a cumulative chronic morbidity score using self-reported diagnoses and algorithm-based assessments, and a subjective fatigue score based on four questionnaire items using cross-sectional survey data from the Study on global AGEing and adult health, which features large samples of adults from six countries (China, Ghana, India, Mexico, Russia and South Africa).ResultsIn a mixed-effects linear model with participants nested in countries (N = 32 455), greater cumulative chronic morbidity is associated with greater subjective fatigue (β = 0.34, SE = 0.005, P < 2e−16). This association replicates within each country and is robust to adjustment for key sociodemographic and physical covariates (sex, age, household wealth, physical function score, habitual physical activity, BMI and BMI2).Conclusions and implicationsFatigue is a common but perhaps maladaptive neuropsychological response to chronic morbidity. Disease-induced fatigue may mediate a self-perpetuating cycle, in which chronic morbidity reduces physical activity, and less physical activity increases cumulative chronic morbidity. Longitudinal research is needed to test whether chronic morbidity, fatigue and physical activity form a cyclical feedback loop.Lay Summary: Fatigue during acute illness may promote recovery, but persistent fatigue in the context of chronic disease may make matters worse. We present evidence from six countries that more chronic disease is associated with more fatigue. This fatigue may reduce physical activity, which increases risks of acquiring additional chronic health problems.
      PubDate: Mon, 11 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac011
      Issue No: Vol. 10, No. 1 (2022)
  • A novel perspective suggesting high sustained energy expenditure may be
           net protective against cancer

    • Authors: Biro P; Thomas F, Ujvari B, et al.
      Pages: 170 - 176
      Abstract: AbstractEnergy expenditure (EE) is generally viewed as tumorigenic, due to production of reactive oxygen species (ROS) that can damage cells and DNA. On this basis, individuals within a species that sustain high EE should be more likely to develop cancer. Here, we argue the opposite, that high EE may be net protective effect against cancer, despite high ROS production. This is possible because individuals that sustain high EE have a greater energetic capacity (=greater energy acquisition, expenditure and ability to up-regulate output), and can therefore allocate energy to multiple cancer-fighting mechanisms with minimal energetic trade-offs. Our review finds that individuals sustaining high EE have greater antioxidant production, lower oxidative stress, greater immune function and lower cancer incidence. Our hypothesis and literature review suggest that EE may indeed be net protective against cancer, and that individual variation in energetic capacity may be a key mechanism to understand the highly individual nature of cancer risk in contemporary human populations and laboratory animals.Lay summary The process of expending energy generates reactive oxygen species that can lead to oxidative stress, cell and DNA damage, and the accumulation of this damage is thought to be a major contributor to many ageing related diseases that include cancer. Here, we challenge this view, proposing how and why high energy expenditure (EE) may actually be net protective against cancer, and provide literature support for our hypothesis. We find individuals with high sustained EE have greater energetic capacity and thus can invest more in repair to counter oxidative stress, and more in immune function, both of which reduce cancer risk. Our hypothesis provides a novel mechanism to understand the highly individual nature of cancer, why taller individuals are more at risk, why physically active individuals have lower cancer risk, and why regular exercise can reduce cancer risk.
      PubDate: Wed, 13 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac012
      Issue No: Vol. 10, No. 1 (2022)
  • Kyle Harper, Plagues upon the Earth: Disease and the Course of Human
           History. John Mokyr, series ed. The Princeton Economic History of the
           Western World

    • Authors: Humphreys M.
      Pages: 177 - 178
      Abstract: HarperKyle, Plagues upon the Earth Princeton: Disease and the Course of Human History. MokyrJohn, series ed. The Princeton Economic History of the Western World.Princeton University Press, Princeton and Oxford, 2021, $35.00/£28.00, ISBN 9780691192123, pp.
      PubDate: Mon, 18 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac014
      Issue No: Vol. 10, No. 1 (2022)
  • Modeling the evolution of SARS-CoV-2 under non-pharmaceutical
           interventions and testing

    • Authors: Gurevich Y; Ram Y, Hadany L.
      Pages: 179 - 188
      Abstract: AbstractBackground and objectivesSocial and behavioral non-pharmaceutical interventions (NPIs), such as mask-wearing, social distancing and travel restrictions, as well as diagnostic tests, have been broadly implemented in response to the COVID-19 pandemic. Epidemiological models and data analysis affirm that wide adoption of NPIs helps to control the pandemic. However, SARS-CoV-2 has extensively demonstrated its ability to evolve. Therefore, it is crucial to examine how NPIs may affect the evolution of the virus. Such evolution could have important effects on the spread and impact of the pandemic.MethodologyWe used evo-epidemiological models to examine the effect of NPIs and testing on two evolutionary trajectories for SARS-CoV-2: attenuation and test evasion.ResultsOur results show that when stronger measures are taken, selection may act to reduce disease severity. Additionally, the timely application of NPIs could significantly affect the competition between viral strains, favoring the milder strain. Furthermore, a higher testing rate can select for a test-evasive viral strain, even if that strain is less infectious than the detectable competing strain. Importantly, if a less detectable strain evolves, epidemiological metrics such as confirmed daily cases may distort our assessment of the pandemic.Conclusions and implicationsOur results highlight the important implications NPIs can have on the evolution of SARS-CoV-2.Lay SummaryWe used evo-epidemiological models to examine the effect of non-pharmaceutical interventions and testing on two evolutionary trajectories for SARS-CoV-2: attenuation and test evasion. Our results show that when stronger measures are taken, selection may act to reduce disease severity.
      PubDate: Mon, 18 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac013
      Issue No: Vol. 10, No. 1 (2022)
  • Migration and descent, adaptations to altitude and tuberculosis in Nepalis
           and Tibetans

    • Authors: Corbett S; Cho J, Ulbricht E, et al.
      Pages: 189 - 201
      Abstract: AbstractBackgroundHigh rates of tuberculosis (TB) in migrants from Tibet and Nepal have been documented for over 120 years and were previously ascribed to poor living conditions in the places of settlement. Adaptations to altitude involving genes in the Hypoxia-Inducible Factor pathway are present in 90–95% of Tibetans and in Nepalis these allele frequencies increase by 17% with each 1000 m increase in altitude.MethodsWe calculated the incidence of TB by country of origin in immigrants from South and East Asia in New South Wales (NSW), Australia between 2004 and 2018, and compared disease severity, site of infection, evidence of local transmission and prevalence of latent TB, among these groups.ResultsThe incidence of active TB was consistently higher among 30 000 Nepalese and 1000 Tibetans than among all other immigrants to NSW. Nepal was the only country of origin where TB incidence in immigrants was not significantly lower than the reported TB incidence in the country of origin.Conclusions and implicationsHigh rates of TB among Nepalese and Tibetan immigrants in Australia are unlikely to be attributable to pre-existing disease or local acquisition. Phenotypic effects of high-altitude adaptations may include a dampening of inflammatory responses to hypoxia, an effect unmasked by descent to a normoxic environment. A corollary of these findings may be that hypoxia-induced inflammation limits TB progression, reconfirming previous explanations for the apparent efficacy of high-altitude sanatoria. If vindicated by subsequent research, these provisional findings could open new avenues into preventive and host-directed interventions for tuberculosis.Lay SummaryThe incidence of tuberculosis among Nepalese immigrants to Australia and other people of Tibetan heritage who migrate to lower altitudes is very high. In these screened populations, pre-existing active TB or locally acquired infection are unlikely explanations. We suggest that adaptations to altitude combined with descent to higher oxygen levels in air at sea level may be contributing factors.
      PubDate: Tue, 08 Mar 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac008
      Issue No: Vol. 10, No. 1 (2022)
  • Which ‘imperfect vaccines’ encourage the evolution of higher

    • Authors: Bull J; Antia R.
      Pages: 202 - 213
      Abstract: AbstractBackground and objectivesTheory suggests that some types of vaccines against infectious pathogens may lead to the evolution of variants that cause increased harm, particularly when they infect unvaccinated individuals. This theory was supported by the observation that the use of an imperfect vaccine to control Marek’s disease virus in chickens resulted in the virus evolving to be more lethal to unvaccinated birds. This raises the concern that the use of some other vaccines may lead to similar pernicious outcomes. We examine that theory with a focus on considering the regimes in which such outcomes are expected.MethodologyWe evaluate the plausibility of assumptions in the original theory. The previous theory rested heavily on a particular form of transmission–mortality–recovery trade-off and invoked other assumptions about the pathways of evolution. We review alternatives to mortality in limiting transmission and consider evolutionary pathways that were omitted in the original theory.ResultsThe regime where the pernicious evolutionary outcome occurs is narrowed by our analysis but remains possible in various scenarios. We propose a more nuanced consideration of alternative models for the within-host dynamics of infections and for factors that limit virulence. Our analysis suggests imperfect vaccines against many pathogens will not lead to the evolution of pathogens with increased virulence in unvaccinated individuals.Conclusions and implicationsEvolution of greater pathogen mortality driven by vaccination remains difficult to predict, but the scope for such outcomes appears limited. Incorporation of mechanistic details into the framework, especially regarding immunity, may be requisite for prediction accuracy.Lay SummaryA virus of chickens appears to have evolved high mortality in response to a vaccine that merely prevented disease symptoms. Theory has predicted this type of evolution in response to a variety of vaccines and other interventions such as drug treatment. Under what circumstances is this pernicious result likely to occur' Analysis of the theory in light of recent changes in our understanding of viral biology raises doubts that medicine-driven, pernicious evolution is likely to be common. But we are far from a mechanistic understanding of the interaction between pathogen and host that can predict when vaccines and other medical interventions will lead to the unwanted evolution of more virulent pathogens. So, while the regime where a pernicious result obtains may be limited, caution remains warranted in designing many types of interventions.
      PubDate: Tue, 26 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac015
      Issue No: Vol. 10, No. 1 (2022)
  • An evolutionary explanation for antibiotics’ association with
           increased colon cancer risk

    • Authors: Voskarides K.
      Pages: 214 - 220
      Abstract: Abstract More than 10 studies have confirmed the association of antibiotic overuse with colorectal cancer. The exact cause is unknown, but most authors hypothesize that disturbance of colon microbiota is the main culprit. In this commentary, an evolutionary explanation is proposed. It is well known that antibiotics can induce antibiotic resistance in bacteria through selection of mutators—DNA mismatch repair deficient (dMMR) strains. Mutators have an increased survival potential due to their high mutagenesis rate. Antibiotics can also cause stress in human cells. Selection of dMMR colon cells may be advantageous under this stress, mimicking selection of bacterial mutators. Concomitantly, mismatch repair deficiency is a common cause of cancer, this may explain the increased cancer risk after multiple cycles of oral antibiotics. This proposed rationale is described in detail, along with supporting evidence from the peer-reviewed literature and suggestions for testing hypothesis validity. Treatment schemes could be re-evaluated, considering toxicity and somatic selection mechanisms.Lay SummaryThe association of antibiotics with colon cancer is well established but of unknown cause. Under an evolutionary framework, antibiotics may select for stress-resistant cancerous cells that lack mechanisms for DNA mismatch repair (MMR). This mimics the selection of antibiotic resistant ‘mutators’—MMR-deficient micro-organisms—highly adaptive due to their increased mutagenesis rate.
      PubDate: Fri, 29 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac018
      Issue No: Vol. 10, No. 1 (2022)
  • Exome sequencing of hepatocellular carcinoma in lemurs identifies
           potential cancer driversA pilot study

    • Authors: Gunady E; Ware K, Hoskinson Plumlee S, et al.
      Pages: 221 - 230
      Abstract: AbstractBackground and objectivesHepatocellular carcinoma occurs frequently in prosimians, but the cause of these liver cancers in this group is unknown. Characterizing the genetic changes associated with hepatocellular carcinoma in prosimians may point to possible causes, treatments and methods of prevention, aiding conservation efforts that are particularly crucial to the survival of endangered lemurs. Although genomic studies of cancer in non-human primates have been hampered by a lack of tools, recent studies have demonstrated the efficacy of using human exome capture reagents across primates.MethodologyIn this proof-of-principle study, we applied human exome capture reagents to tumor–normal pairs from five lemurs with hepatocellular carcinoma to characterize the mutational landscape of this disease in lemurs.ResultsSeveral genes implicated in human hepatocellular carcinoma, including ARID1A, TP53 and CTNNB1, were mutated in multiple lemurs, and analysis of cancer driver genes mutated in these samples identified enrichment of genes involved with TP53 degradation and regulation. In addition to these similarities with human hepatocellular carcinoma, we also noted unique features, including six genes that contain mutations in all five lemurs. Interestingly, these genes are infrequently mutated in human hepatocellular carcinoma, suggesting potential differences in the etiology and/or progression of this cancer in lemurs and humans.Conclusions and implicationsCollectively, this pilot study suggests that human exome capture reagents are a promising tool for genomic studies of cancer in lemurs and other non-human primates.Lay SummaryHepatocellular carcinoma occurs frequently in prosimians, but the cause of these liver cancers is unknown. In this proof-of-principle study, we applied human DNA sequencing tools to tumor–normal pairs from five lemurs with hepatocellular carcinoma and compared the lemur mutation profiles to those of human hepatocellular carcinomas.
      PubDate: Fri, 29 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac016
      Issue No: Vol. 10, No. 1 (2022)
  • Different predictors of intimate partner and natal family violence against

    • Authors: Campbell O; Mace R.
      Pages: 231 - 242
      Abstract: AbstractBackgroundViolence against women is often studied in the context of violence from intimate partners. However, women receive violence from a wider range of individuals—such as their natal kin—including their siblings, parents, uncles and cousins. Applying insights from evolutionary theory, we examine whether cousin marriage, which has been hypothesized to both reduce the risk of partner violence but increase the risk of natal family violence, associates differently with each type of violence. Second, we test whether common risk factors for partner violence, such as wealth, associate similarly with natal violence.MethodologyWe analyse over 16 000 Jordanian women from three cohorts of the Jordan Demographic Health Surveys. Predictor variables include type of cousin marriage (patrilateral or matrilateral), education, wealth, number of children, urban living and polygyny. Outcome variables include whether a woman’s husband or her natal family has ever been physically violent towards her.ResultsBeing married to a patrilateral cousin but not a matrilateral cousin is associated with a reduced risk of reporting intimate partner violence (IPV). By contrast being married to a matrilateral cousin but not a patrilateral one is associated with a reduced risk of reporting natal family violence. As expected, wealth is negatively associated with reporting partner violence, but we find no association with reports of natal family violence. Finally, individuals with more children are more likely to report IPV.Conclusions and implicationsFindings indicate the importance of distinguishing between types of cousin marriage and highlight substantial differences in risk factors for intimate partner compared to natal family violence.Lay SummarySociodemographic risk factors, such as wealth, may associate differently with intimate partner and natal family violence. Results suggest that whether cousin marriage is protective of violence may depend on the type of cousin and secondly, that violence can have fitness relevant outcomes.
      PubDate: Mon, 02 May 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac019
      Issue No: Vol. 10, No. 1 (2022)
  • Squatting, pelvic morphology and a reconsideration of childbirth

    • Authors: Gorman J; Roberts C, Newsham S, et al.
      Pages: 243 - 255
      Abstract: Abstract Childbirth is commonly viewed as difficult in human females, encompassed by the ‘Obstetrical Dilemma’ (OD) described by early palaeoanthropologists as an evolved trade-off between a narrow pelvis necessitated by bipedalism and a large-brained fetal head. The OD has been challenged on several grounds. We add to these challenges by suggesting humans likely squatted regularly during routine tasks prior to the advent of farming societies and use of seats. We suggest that habitual squatting, together with taller stature and better nutrition of ancestral hunter-gatherers compared with later Neolithic and industrial counterparts, obviated an OD. Instead, difficulties with parturition may have arisen much later in our history, accompanying permanent settlements, poorer nutrition, greater infectious disease loads and negligible squatting in daily life. We discuss bioarchaeological and contemporary data that support these viewpoints, suggest ways in which this hypothesis might be tested further and consider its implications for obstetrical practice.Lay SummaryHuman childbirth is viewed as universally difficult. Evidence from physical therapies/engineering and studies of living and ancestral humans illustrates habitual squatting widens the pelvis and could improve childbirth outcomes. Obstetrical difficulties emerged late in prehistory accompanying settled agriculture, poorer nutrition and less squatting. Specific physical exercises could improve obstetrical practice.
      PubDate: Tue, 26 Apr 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac017
      Issue No: Vol. 10, No. 1 (2022)
  • Bet-hedging in innate and adaptive immune systems

    • Authors: Tate A; Van Cleve J.
      Pages: 256 - 265
      Abstract: AbstractImmune system evolution is shaped by the fitness costs and trade-offs associated with mounting an immune response. Costs that arise mainly as a function of the magnitude of investment, including energetic and immunopathological costs, are well-represented in studies of immune system evolution. Less well considered, however, are the costs of immune cell plasticity and specialization. Hosts in nature encounter a large diversity of microbes and parasites that require different and sometimes conflicting immune mechanisms for defense, but it takes precious time to recognize and correctly integrate signals for an effective polarized response. In this perspective, we propose that bet-hedging can be a viable alternative to plasticity in immune cell effector function, discuss conditions under which bet-hedging is likely to be an advantageous strategy for different arms of the immune system, and present cases from both innate and adaptive immune systems that suggest bet-hedging at play.
      PubDate: Tue, 24 May 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac021
      Issue No: Vol. 10, No. 1 (2022)
  • Evolved resistance to a novel cationic peptide antibiotic requires high
           mutation supply

    • Authors: Santos-Lopez A; Fritz M, Lombardo J, et al.
      Pages: 266 - 276
      Abstract: AbstractBackground and ObjectivesA key strategy for resolving the antibiotic resistance crisis is the development of new drugs with antimicrobial properties. The engineered cationic antimicrobial peptide WLBU2 (also known as PLG0206) is a promising broad-spectrum antimicrobial compound that has completed Phase I clinical studies. It has activity against Gram-negative and Gram-positive bacteria including infections associated with biofilm. No definitive mechanisms of resistance to WLBU2 have been identified.MethodologyHere, we used experimental evolution under different levels of mutation supply and whole genome sequencing (WGS) to detect the genetic pathways and probable mechanisms of resistance to this peptide. We propagated populations of wild-type and hypermutator Pseudomonas aeruginosa in the presence of WLBU2 and performed WGS of evolved populations and clones.ResultsPopulations that survived WLBU2 treatment acquired a minimum of two mutations, making the acquisition of resistance more difficult than for most antibiotics, which can be tolerated by mutation of a single target. Major targets of resistance to WLBU2 included the orfN and pmrB genes, previously described to confer resistance to other cationic peptides. More surprisingly, mutations that increase aggregation such as the wsp pathway were also selected despite the ability of WLBU2 to kill cells growing in a biofilm.Conclusions and implicationsThe results show how experimental evolution and WGS can identify genetic targets and actions of new antimicrobial compounds and predict pathways to resistance of new antibiotics in clinical practice.
      PubDate: Mon, 30 May 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac022
      Issue No: Vol. 10, No. 1 (2022)
  • Multiple sclerosis and the microbiotaProgress in understanding the
           contribution of the gut microbiome to disease

    • Authors: Engelenburg H; Lucassen P, Sarafian J, et al.
      Pages: 277 - 294
      Abstract: AbstractMultiple sclerosis (MS), a neurological autoimmune disorder, has recently been linked to neuro-inflammatory influences from the gut. In this review, we address the idea that evolutionary mismatches could affect the pathogenesis of MS via the gut microbiota. The evolution of symbiosis as well as the recent introduction of evolutionary mismatches is considered, and evidence regarding the impact of diet on the MS-associated microbiota is evaluated. Distinctive microbial community compositions associated with the gut microbiota of MS patients are difficult to identify, and substantial study-to-study variation and even larger variations between individual profiles of MS patients are observed. Furthermore, although some dietary changes impact the progression of MS, MS-associated features of microbiota were found to be not necessarily associated with diet per se. In addition, immune function in MS patients potentially drives changes in microbial composition directly, in at least some individuals. Finally, assessment of evolutionary histories of animals with their gut symbionts suggests that the impact of evolutionary mismatch on the microbiota is less concerning than mismatches affecting helminths and protists. These observations suggest that the benefits of an anti-inflammatory diet for patients with MS may not be mediated by the microbiota per se. Furthermore, any alteration of the microbiota found in association with MS may be an effect rather than a cause. This conclusion is consistent with other studies indicating that a loss of complex eukaryotic symbionts, including helminths and protists, is a pivotal evolutionary mismatch that potentiates the increased prevalence of autoimmunity within a population.
      PubDate: Mon, 13 Jun 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac009
      Issue No: Vol. 10, No. 1 (2022)
  • Tradeoffs in milk immunity affect infant infectious disease risk

    • Pages: 295 - 304
      Abstract: AbstractBackground and objectivesThe human immune system has evolved to balance protection against infection with control of immune-mediated damage and tolerance of commensal microbes. Such tradeoffs between protection and harm almost certainly extend to the immune system of milk.MethodologyAmong breastfeeding mother–infant dyads in Kilimanjaro, Tanzania, we characterized in vitro proinflammatory milk immune responses to Salmonella enterica (an infectious agent) and Escherichia coli (a benign target) as the increase in interleukin-6 after 24 h of incubation with each bacterium. We characterized incident infectious diseases among infants through passive monitoring. We used Cox proportional hazards models to describe associations between milk immune activity and infant infectious disease.ResultsAmong infants, risk for respiratory infections declined with increasing milk in vitro proinflammatory response to S. enterica (hazard ratio [HR]: 0.68; 95% confidence interval [CI]: 0.54, 0.86; P: 0.001), while risk for gastrointestinal infections increased with increasing milk in vitro proinflammatory response to E. coli (HR: 1.44; 95% CI: 1.05, 1.99; P: 0.022). Milk proinflammatory responses to S. enterica and E. coli were positively correlated (Spearman’s rho: 0.60; P: 0.000).Conclusions and implicationsThese findings demonstrate a tradeoff in milk immune activity: the benefits of appropriate proinflammatory activity come at the hazard of misdirected proinflammatory activity. This tradeoff is likely to affect infant health in complex ways, depending on prevailing infectious disease conditions. How mother–infant dyads optimize proinflammatory milk immune activity should be a central question in future ecological–evolutionary studies of the immune system of milk.
      PubDate: Mon, 13 Jun 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac020
      Issue No: Vol. 10, No. 1 (2022)
  • Phylogenetic prioritization of HIV-1 transmission clusters with viral
           lineage-level diversification rates

    • Pages: 305 - 315
      Abstract: AbstractBackground and objectivesPublic health officials faced with a large number of transmission clusters require a rapid, scalable and unbiased way to prioritize distribution of limited resources to maximize benefits. We hypothesize that transmission cluster prioritization based on phylogenetically derived lineage-level diversification rates will perform as well as or better than commonly used growth-based prioritization measures, without need for historical data or subjective interpretation.Methodology9822 HIV pol sequences collected during routine drug resistance genotyping were used alongside simulated sequence data to infer sets of phylogenetic transmission clusters via patristic distance threshold. Prioritized clusters inferred from empirical data were compared to those prioritized by the current public health protocols. Prioritization of simulated clusters was evaluated based on correlation of a given prioritization measure with future cluster growth, as well as the number of direct downstream transmissions from cluster members.ResultsEmpirical data suggest diversification rate-based measures perform comparably to growth-based measures in recreating public heath prioritization choices. However, unbiased simulated data reveals phylogenetic diversification rate-based measures perform better in predicting future cluster growth relative to growth-based measures, particularly long-term growth. Diversification rate-based measures also display advantages over growth-based measures in highlighting groups with greater future transmission events compared to random groups of the same size. Furthermore, diversification rate measures were notably more robust to effects of decreased sampling proportion.Conclusions and implicationsOur findings indicate diversification rate-based measures frequently outperform growth-based measures in predicting future cluster growth and offer several additional advantages beneficial to optimizing the public health prioritization process.
      PubDate: Fri, 22 Jul 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac026
      Issue No: Vol. 10, No. 1 (2022)
  • Implications of leg length for metabolic health and fitness

    • Pages: 316 - 324
      Abstract: AbstractBackground and objectivesSeveral studies have linked longer legs with favorable adult metabolic health outcomes and greater offspring birth weight. A recent Mendelian randomization study suggested a causal link between height and cardiometabolic risk; however, the underlying reasons remain poorly understood.MethodologyUsing a cross-sectional design, we tested in a convenience sample of 70 healthy young women whether birth weight and tibia length as markers of early-life conditions associated more strongly with metabolically beneficial traits like organ size and skeletal muscle mass (SMM) than a statistically derived height-residual variable indexing later, more canalized growth.ResultsConsistent with the ‘developmental origins of health and disease’ hypothesis, we found relatively strong associations of tibia length—but not birth weight—with adult organ size, brain size, SMM and resting energy expenditure measured by magnetic resonance imaging (MRI), dual-energy X-ray absorptiometry and indirect calorimetry, respectively.Conclusions and implicationsBuilding on prior work, these results suggest that leg length is a sensitive marker of traits directly impacting metabolic and reproductive health. Alongside findings in the same sample relating tibia length and height-residual to MRI-measured pelvic dimensions, we suggest there may exist a degree of coordination in the development of long bone, lean mass and pelvic traits, possibly centered on early, pre-pubertal growth periods. Such phenotypic coordination has important implications for fitness, serving to benefit both adult health and the health of offspring in subsequent generations.
      PubDate: Thu, 21 Jul 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac023
      Issue No: Vol. 10, No. 1 (2022)
  • Associations of age at marriage and first pregnancy with maternal
           nutritional status in Nepal

    • Pages: 325 - 338
      Abstract: AbstractBackground and objectivesWomen’s nutritional status is important for their health and reproductive fitness. In a population where early marriage is common, we investigated how women’s nutritional status is associated with their age at marriage (marking a geographical transfer between households), and at first pregnancy.MethodologyWe used data from a cluster-randomized control trial from lowland Nepal (n = 4071). Outcomes including body mass index (BMI) were measured in early pregnancy and trial endpoint, after delivery. We fitted mixed-effects linear and logistic regression models to estimate associations of age at marriage and age at pregnancy with outcomes, and with odds of chronic energy deficiency (CED, BMI <18.5 kg/m2), at both timepoints.ResultsBMI in early pregnancy averaged 20.9 kg/m2, with CED prevalence of 12.5%. In 750 women measured twice, BMI declined 1.2 (95% confidence interval 1.1, 1.3) kg/m2 between early pregnancy and endpoint, when CED prevalence was 35.5%. Early pregnancy was associated in dose-response manner with poorer nutritional status. Early marriage was independently associated with poorer nutritional status among those pregnant ≤15 years, but with better nutritional status among those pregnant ≥19 years.Conclusions and implicationsThe primary determinant of nutritional status was age at pregnancy, but this association also varied by marriage age. Our results suggest that natal households may marry their daughters earlier if food insecure, but that their nutritional status can improve in the marital household if pregnancy is delayed. Marriage age therefore determines which household funds adolescent weight gain, with implications for Darwinian fitness of the members of both households.
      PubDate: Mon, 25 Jul 2022 00:00:00 GMT
      DOI: 10.1093/emph/eoac025
      Issue No: Vol. 10, No. 1 (2022)
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