Authors:Basile A; Renner M, Hidaka B, et al. Abstract: An evolutionary perspective provides a unifying explanation for the modifiable risk factors and lifestyle-based interventions for the leading causes of morbidity and mortality globally. Non-communicable diseases develop from an evolutionary mismatch between the prior environment and modern patterns of behavior; however, it is unclear whether an evolutionary mismatch narrative could promote positive behavior change in patients. We hypothesize that educating patients about evolutionary mismatch could augment efforts to improve healthful behavior. Specifically, explaining the ‘why’ behind what is being recommended could promote health literacy and adherence. Furthermore, we offer suggestions of how clinicians could educate patients about evolutionary mismatch for key-lifestyle factors, diet and physical activity, as well as several specific modern diseases. We also consider how to sidestep patients’ skepticism of evolutionary theory. Here, we lay the groundwork for research on how educating patients with an evolutionary mismatch narrative could impact health behaviors and improve outcomes. PubDate: Wed, 24 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab010 Issue No:Vol. 9, No. 1 (2021)
Authors:Gunst A; Sundén M, Korja R, et al. Pages: 11 - 23 Abstract: Background and objectivesAs the mother–offspring relationship is central to human reproduction, postpartum depression symptoms are difficult to explain in evolutionary terms. We proposed that postpartum depression might arise as a result of evolutionary mother–offspring conflict over maternal investment, and investigated the association between postpartum depression symptoms, infant night waking, maternal sleep disturbance and breastfeeding frequency.MethodologyWe conducted a cross-sectional analysis using survey responses at 6 months postpartum from 1598 Finnish mothers. We hypothesized that infant night waking at 6 months postpartum would be associated with postpartum depression symptoms, and that this association would be mediated by maternal sleep disturbance and a higher breastfeeding frequency.ResultsInfant night waking was moderately associated with postpartum depression symptoms, and this association was mediated by maternal sleep disturbance (R2=0.09). Contrary to our prediction, we found that increased breastfeeding was associated with less postpartum depression symptoms.Conclusions and implicationsWe conclude that postpartum depression symptoms might partly be the result of increased maternal fatigue stemming from high offspring demands on maternal investment, but that this is not due to the metabolic strain from increased breastfeeding. Studying postpartum depression from the mother–offspring conflict perspective can potentially improve our understanding of the involved behavioral processes of both mother and offspring, and allow interventions designed to benefit the well-being of both parties.Lay Summary: We proposed that postpartum depression is due to an evolutionary conflict between mother and infant, where the infant tires the mother to delay the arrival of a sibling. We found a link between infant night waking and postpartum depression, mediated by the mother’s sleep, but not by breastfeeding frequency. PubDate: Sat, 02 Jan 2021 00:00:00 GMT DOI: 10.1093/emph/eoaa049 Issue No:Vol. 9, No. 1 (2021)
Authors:Thomas M; Ewunkem A, Boyd S, et al. Pages: 53 - 67 Abstract: BackgroundThere has been an increased usage of metallic antimicrobial materials to control pathogenic and multi-drug resistant bacteria. Yet, there is a corresponding need to know if this usage leads to genetic adaptations that could produce more harmful strains.MethodologyExperimental evolution was used to adapt Escherichia coli K-12 MG1655 to excess iron (II) with subsequent genomic analysis. Phenotypic assays and gene expression studies were conducted to demonstrate pleiotropic effects associated with this adaptation and to elucidate potential cellular responses.ResultsAfter 200 days of adaptation, populations cultured in excess iron (II), showed a significant increase in 24-h optical densities compared to controls. Furthermore, these populations showed increased resistance toward other metals [iron (III) and gallium (III)] and to traditional antibiotics (bacitracin, rifampin, chloramphenicol and sulfanilamide). Genomic analysis identified selective sweeps in three genes; fecA, ptsP and ilvG unique to the iron (II) resistant populations, and gene expression studies demonstrated that their cellular response may be to downregulate genes involved in iron transport (cirA and fecA) while increasing the oxidative stress response (oxyR, soxS and soxR) prior to FeSO4 exposure.Conclusions and implicationsTogether, this indicates that the selected populations can quickly adapt to stressful levels of iron (II). This study is unique in that it demonstrates that E. coli can adapt to environments that contain excess levels of an essential micronutrient while also demonstrating the genomic foundations of the response and the pleiotropic consequences. The fact that adaptation to excess iron also causes increases in general antibiotic resistance is a serious concern.Lay summary: The evolution of iron resistance in E. coli leads to multi-drug and general metal resistance through the acquisition of mutations in three genes (fecA, ptsP and ilvG) while also initiating cellular defenses as part of their normal growth process. PubDate: Mon, 18 Jan 2021 00:00:00 GMT DOI: 10.1093/emph/eoaa051 Issue No:Vol. 9, No. 1 (2021)
Authors:Solis A; Nunn C. Pages: 70 - 77 Abstract: 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 summaryOne 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. PubDate: Sat, 13 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab003 Issue No:Vol. 9, No. 1 (2021)
Authors:Kelsey M. Pages: 78 - 82 Abstract: Long interspersed nuclear element-1 (LINE-1 or L1) is the only autonomously active retrotransposon in humans. While L1 has been implicated in several pathologies and the aging process, I present a model which challenges an understanding of L1 as predominantly antagonistic to human health. I hypothesize that L1 serves as a reporter in an early cancer alert system: a tripwire strung throughout the genome poised to trigger p53 and a type I interferon (IFN-1) response when the epigenetic landscape portends cancer. Cell proliferation and a shift to aerobic glycolysis cause dramatic changes in the epigenome which are permissive to L1’s escape from suppression. L1 has several properties which make it particularly apt to fulfill this hypothesized sentinel function. Being present in many copies spread throughout the genome allows it to monitor many regions for epigenetic instability and renders it robust to deactivation by mutation. This proposed cancer alert system would alter the cancer cell fitness landscape discouraging the use of growth-favoring aerobic glycolysis by threatening the activation of tumor-suppressive mechanisms. It also imposes costs on a strategy of non-specific global transcriptional derepression aimed at activating oncogenes. Erroneous activations of this system are predicted to increase the rate of aging, suggesting this represents a case of antagonistic pleiotropy trading prolonged youth for cancer prevention. More research is needed to assess this model.Lay summary: During carcinogenesis the epigenome is remodeled by the Warburg effect and cellular proliferation. These processes globally relax chromatin. This epigenetic environment is permissive to the retrotransposon long interspersed nuclear element-1’s (LINE-1 or L1) escape from suppression. I hypothesize and present evidence for the notion that L1 has been co-opted to serve as a reporter in an early cancer alert system, poised to trigger tumor suppressive mechanisms when the epigenetic landscape portends cancer. This hypothesis describes a potentially major means by which transformation is thwarted early on. PubDate: Sun, 14 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab004 Issue No:Vol. 9, No. 1 (2021)
Authors:Alcock J; Masters A. Pages: 83 - 92 Abstract: Lay SummaryMany treatments for COVID-19 are aimed at calming a cytokine storm, a dangerous immune overreaction to the infection. Treating cytokine storms has been tried for decades in sepsis and other viral illnesses, but these treatments most often do not work. We explain why cytokine storms should be rare, and what special evolutionary circumstances can cause them to occur. PubDate: Thu, 04 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab005 Issue No:Vol. 9, No. 1 (2021)
Authors:Woods P; Alcock J. Pages: 118 - 119 Abstract: Lay summary: High Altitude Pulmonary Edema (HAPE) is a potentially fatal disease of altitude, in which the lungs can become filled with fluid. In this article we explore the mechanisms causing this condition and how it can be viewed as a condition of a mismatch between current environment and evolutionary experience. PubDate: Wed, 06 Jan 2021 00:00:00 GMT DOI: 10.1093/emph/eoaa052 Issue No:Vol. 9, No. 1 (2021)
Authors:Parker W; Sarafian J, Broverman S, et al. Pages: 120 - 130 Abstract: Suboptimal understanding of concepts related to hygiene by the general public, clinicians and researchers is a persistent problem in health and medicine. Although hygiene is necessary to slow or prevent deadly pandemics of infectious disease such as coronavirus disease 2019 (COVID-19), hygiene can have unwanted effects. In particular, some aspects of hygiene cause a loss of biodiversity from the human body, characterized by the almost complete removal of intestinal worms (helminths) and protists. Research spanning more than half a century documents that this loss of biodiversity results in an increased propensity for autoimmune disease, allergic disorders, probably neuropsychiatric problems and adverse reactions to infectious agents. The differences in immune function between communities with and communities without helminths have become so pronounced that the reduced lethality of severe acute respiratory syndrome coronavirus 2 in low-income countries compared to high-income countries was predicted early in the COVID-19 pandemic. This prediction, based on the maladaptive immune responses observed in many cases of COVID-19 in high-income countries, is now supported by emerging data from low-income countries. Herein, hygiene is subdivided into components involving personal choice versus components instituted by community wide systems such as sewage treatment facilities and water treatment plants. The different effects of personal hygiene and systems hygiene are described, and appropriate measures to alleviate the adverse effects of hygiene without losing the benefits of hygiene are discussed. Finally, text boxes are provided to function as stand-alone, public-domain handouts with the goal of informing the public about hygiene and suggesting solutions for biomedical researchers and policy makers.Lay Summary: Hygiene related to sewer systems and other technology can have adverse effects on immune function, and is distinct from personal hygiene practices such as hand washing and social distancing. Dealing with the drawbacks of hygiene must be undertaken without compromising the protection from infectious disease imposed by hygiene. PubDate: Fri, 12 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab006 Issue No:Vol. 9, No. 1 (2021)
Authors:Sauer S; Beinart D, Finn S, et al. Pages: 131 - 138 Abstract: Background and objectivesAn individual’s risk of breast cancer is profoundly affected by evolutionary mismatch. Mismatches in Western society known to increase the risk of breast cancer include a sedentary lifestyle and reproductive factors. Biota alteration, characterized by a loss of biodiversity from the ecosystem of the human body as a result of Western society, is a mismatch known to increase the risk of a variety of inflammation-related diseases, including colitis-associated colon cancer. However, the effect of biota alteration on breast cancer has not been evaluated.MethodologyIn this study, we utilized the C3(1)-TAg mouse model of breast cancer to evaluate the role of biota alteration in the development of breast cancer. This model has been used to recapitulate the role of exercise and pregnancy in reducing the risk of breast cancer. C3(1)-TAg mice were treated with Hymenolepis diminuta, a benign helminth that has been shown to reverse the effects of biota alteration in animal models.ResultsNo effect of the helminth H. diminuta was observed. Neither the latency nor tumor growth was affected by the therapy, and no significant effects on tumor transcriptome were observed based on RNAseq analysis.Conclusions and implicationsThese findings suggest that biota alteration, although known to affect a variety of Western-associated diseases, might not be a significant factor in the high rate of breast cancer observed in Western societies.Lay summaryAn almost complete loss of intestinal worms in high-income countries has led to increases in allergic disorders, autoimmune conditions, and perhaps colon cancer. However, in this study, results using laboratory mice suggest that loss of intestinal worms might not be associated with breast cancer. PubDate: Fri, 12 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab007 Issue No:Vol. 9, No. 1 (2021)
Authors:Amoroso C; Nunn C. Pages: 139 - 148 Abstract: Background and objectivesIn absolute terms, humans are extremely highly parasitized compared to other primates. This may reflect that humans are outliers in traits correlated with parasite richness: population density, geographic range area, and study effort. The high degree of parasitism could also reflect amplified disease risk associated with agriculture and urbanization. Alternatively, controlling for other variables, cultural and psychological adaptations could have reduced parasitism in humans over evolutionary time.MethodologyWe predicted the number of parasites that would infect a nonhuman primate with human phenotypic characteristics and phylogenetic position, and then compared observed parasitism of humans in eight geopolitical countries to the predicted distributions. The analyses incorporated study effort, phylogeny, and drivers of parasitism in 33 primate species.ResultsAnalyses of individual countries were not supportive of either hypothesis. When analyzed collectively, however, human populations showed consistently lower than expected richness of protozoa and helminths, but higher richness of viruses. Thus, human evolutionary innovations and new parasite exposures may have impacted groups of parasites in different ways, with support for both hypotheses in the overall analysis.Conclusions and implicationsThe high level of parasitism observed in humans only applies to viruses, and was not extreme in any of our tests of individual countries. In contrast, we find consistent reductions in protozoa and helminths across countries, suggesting reduced parasitism by these groups during human evolution. We propose that hygienic and technological advances might have extinguished fecal-orally or indirectly transmitted parasites like helminths, whereas higher human densities and host-shifting potential of viruses have supported increased virus richness.Lay SummaryVastly more parasite species infect humans than any other primate host. Controlling for factors that influence parasite richness, such as the intensity of study effort and body mass, we find that humans may have more viruses, but fewer helminths and protozoa, than expected based on evolutionary analyses of parasitism in other primates. PubDate: Tue, 23 Feb 2021 00:00:00 GMT DOI: 10.1093/emph/eoab009 Issue No:Vol. 9, No. 1 (2021)
Authors:Smith N; Sievert L, Muttukrishna S, et al. Pages: 164 - 173 Abstract: Background and objectivesLow levels of vitamin D among dark-skinned migrants to northern latitudes and increased risks for associated pathologies illustrate an evolutionary mismatch between an environment of high ultraviolet (UV) radiation to which such migrants are adapted and the low UV environment to which they migrate. Recently, low levels of vitamin D have also been associated with higher risks for contracting COVID-19. South Asians in the UK have higher risk for low vitamin D levels. In this study, we assessed vitamin D status of British-Bangladeshi migrants compared with white British residents and Bangladeshis still living in Bangladesh (‘sedentees’).MethodologyThe cross-sectional study compared serum vitamin D levels among 149 women aged 35–59, comprising British-Bangladeshi migrants (n = 50), white British neighbors (n = 54) and Bangladeshi sedentees (n = 45). Analyses comprised multivariate models to assess serum levels of 25-hydroxyvitamin D (25(OH)D), and associations with anthropometric, lifestyle, health and migration factors.ResultsVitamin D levels in Bangladeshi migrants were very low: mean 25(OH)D = 32.2 nmol/L ± 13.0, with 29% of migrants classified as deficient (<25 nmol/L) and 94% deficient or insufficient (≤50 nmol/L). Mean levels of vitamin D were significantly lower among British-Bangladeshis compared with Bangladeshi sedentees (50.9 nmol/L ± 13.3, P < 0.001) and were also lower than in white British women (55.3 nmol/L ± 20.9). Lower levels of vitamin D were associated with increased body mass index and low iron status.Conclusions and implicationsWe conclude that lower exposure to sunlight in the UK reduces vitamin D levels in Bangladeshi migrants. Recommending supplements could prevent potentially adverse health outcomes associated with vitamin D deficiency.Lay SummaryVitamin D deficiency is one example of mismatch between an evolved trait and novel environments. Here we compare vitamin D status of dark-skinned British-Bangladeshi migrants in the UK to Bangladeshis in Bangladesh and white British individuals. Migrants had lower levels of vitamin D and are at risk for associated pathologies. PubDate: Mon, 25 Jan 2021 00:00:00 GMT DOI: 10.1093/emph/eoab001 Issue No:Vol. 9, No. 1 (2021)
Authors:Dinsdale N; Nepomnaschy P, Crespi B. Pages: 174 - 191 Abstract: We provide the first analysis and synthesis of the evolutionary and mechanistic bases for risk of endometriosis in humans, structured around Niko Tinbergen's four questions about phenotypes: phylogenetic history, development, mechanism and adaptive significance. Endometriosis, which is characterized by the proliferation of endometrial tissue outside of the uterus, has its phylogenetic roots in the evolution of three causally linked traits: (1) highly invasive placentation, (2) spontaneous rather than implantation-driven endometrial decidualization and (3) frequent extensive estrogen-driven endometrial proliferation and inflammation, followed by heavy menstrual bleeding. Endometriosis is potentiated by these traits and appears to be driven, proximately, by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that in extreme cases can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known from previous work to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis. The hypothesis that endometriosis risk is driven by low prenatal testosterone, and involves extreme expression of some reproductive phenotypes, is supported by a suite of evidence from genetics, development, endocrinology, morphology and life history. The hypothesis also provides insights into why these two diametric, fitness-reducing disorders are maintained at such high frequencies in human populations. Finally, the hypotheses described and evaluated here lead to numerous testable predictions and have direct implications for the treatment and study of endometriosis.Lay summary: Endometriosis is caused by endometrial tissue outside of the uterus. We explain why and how humans are vulnerable to this disease, and new perspectives on understanding and treating it. Endometriosis shows evidence of being caused in part by relatively low testosterone during fetal development, that ‘programs’ female reproductive development. By contrast, polycystic ovary syndrome is associated with relatively high testosterone in prenatal development. These two disorders can thus be seen as ‘opposite’ to one another in their major causes and correlates. Important new insights regarding diagnosis, study and treatment of endometriosis follow from these considerations. PubDate: Fri, 12 Mar 2021 00:00:00 GMT DOI: 10.1093/emph/eoab008 Issue No:Vol. 9, No. 1 (2021)
Authors:Yuksel M; Remien C, Karki B, et al. Pages: 1 - 10 Abstract: Background and objectivesGenetic engineering and similar technologies offer promising new approaches to controlling human diseases by blocking transmission from vectors. However, in spatially structured populations, imperfect coverage of the vector will leave pockets in which the parasite may persist. Movement by humans may disrupt this local persistence and facilitate eradication when these pockets are small, spreading parasite reproduction outside unprotected areas and into areas that block its reproduction. Here, we consider the sensitivity of this process to biological details: do simple generalities emerge that may facilitate interventions'MethodologyWe develop formal mathematical models of this process similar to standard Ross–Macdonald models, but (i) specifying spatial structure of two patches, with vector transmission blocked in one patch but not in the other, (ii) allowing temporary human movement (travel instead of migration) and (iii) considering two different modes of mosquito biting.ResultsWe find that there is no invariant effect of disrupting spatial structure with travel. For both biting models, travel out of the unprotected patch has different consequences than travel by visitors into the patch, but the effects are reversed between the two biting models.Conclusions and implicationsOverall, the effect of human travel on the maintenance of vector-borne diseases in structured habitats must be considered in light of the actual biology of mosquito abundances, biting dynamics and human movement patterns.Lay summary: Genetic interventions against pathogens transmitted by insect vectors are promising methods of controlling infectious diseases. These interventions may be imperfect, leaving pockets where the parasite persists. How will human movement between protected and unprotected areas affect persistence' Mathematical models developed here show that the answer is ecology-dependent, depending on vector biting behavior. PubDate: Sun, 27 Dec 2020 00:00:00 GMT DOI: 10.1093/emph/eoaa035 Issue No:Vol. 9, No. 1 (2020)
Authors:Wrotek S; LeGrand E, Dzialuk A, et al. Pages: 26 - 35 Abstract: Although fever is one of the main presenting symptoms of COVID-19 infection, little public attention has been given to fever as an evolved defense. Fever, the regulated increase in the body temperature, is part of the evolved systemic reaction to infection known as the acute phase response. The heat of fever augments the performance of immune cells, induces stress on pathogens and infected cells directly, and combines with other stressors to provide a nonspecific immune defense. Observational trials in humans suggest a survival benefit from fever, and randomized trials published before COVID-19 do not support fever reduction in patients with infection. Like public health measures that seem burdensome and excessive, fevers involve costly trade-offs but they can prevent infection from getting out of control. For infections with novel SARS-CoV-2, the precautionary principle applies: unless evidence suggests otherwise, we advise that fever should be allowed to run its course. PubDate: Mon, 23 Nov 2020 00:00:00 GMT DOI: 10.1093/emph/eoaa044 Issue No:Vol. 9, No. 1 (2020)
Authors:Dishakjian V; Fessler D, Sparks A. Pages: 36 - 52 Abstract: Background and objectivesLife History Theory (LHT) describes trade-offs that organisms make with regard to three investment pathways: growth, maintenance and reproduction. In light of the reparative functions of sleep, we examine sleep behaviors and corresponding attitudes as proximate manifestations of an individual’s underlying relative prioritization of short-term reproduction versus long-term maintenance.MethodologyWe collected survey data from 568 participants across two online studies having different participant pools. We use a mixture of segmented and hierarchical regression models, structural equation modeling and machine learning to infer relationships between sleep duration/quality, attitudes about sleep and biodemographic/psychometric measures of life history strategy (LHS).ResultsAn age-mediated U- or V-shaped relationship appears when LHS is plotted against habitual sleep duration, with the fastest strategies occupying the sections of the curve with the highest mortality risk: < 6.5 hr (short sleep) and > 8.5 hr (long sleep). LH ‘fastness’ is associated with increased sleepiness and worse overall sleep quality: delayed sleep onset latency, more wakefulness after sleep onset, higher sleep–wake instability and greater sleep duration variability. Hedonic valuations of sleep may mediate the effects of LHS on certain sleep parameters.Conclusions and implicationsThe costs of deprioritizing maintenance can be parameterized in the domain of sleep, where ‘life history fastness’ corresponds with sleep patterns associated with greater senescence and mortality. Individual differences in sleep having significant health implications can thus be understood as components of lifelong trajectories likely stemming from calibration to developmental circumstances. Relatedly, hedonic valuations of sleep may constitute useful avenues for non-pharmacological management of chronic sleep disorders.Lay Summary: Sleep is essential because it allows the body to repair and maintain itself. But time spent sleeping is time that cannot be spent doing other things. People differ in how much they prioritize immediate rewards, including sociosexual opportunities, versus long-term goals. In this research, we show that individual differences in sleep behaviors, and attitudes toward sleep, correspond with psychological and behavioral differences reflecting such differing priorities. Orientation toward sleep can thus be understood as part of the overall lifetime strategies that people pursue. PubDate: Wed, 02 Dec 2020 00:00:00 GMT DOI: 10.1093/emph/eoaa048 Issue No:Vol. 9, No. 1 (2020)
Authors:Keestra S; Högqvist Tabor V, Alvergne A. Pages: 93 - 112 Abstract: Lay SummaryThyroid hormone reference intervals—used to determine normal thyroid function —currently don’t take into account many significant factors that can cause variation in thyroid hormone levels. These factors include age, sex, ethnicity, season, time of day, iodine content in the diet, socioeconomic status, stress levels, body composition, immune status, menstrual cycle phase, and overall health status. This paper shows how early life experiences as well as short term stressors may affect variation in thyroid function. These are energetic challenges to which the thyroid physiology can respond to. Our investigation shows that much variation in thyroid function is natural. It may result from a complex interplay of evolutionary, genetic, developmental, and physiological factors in response to energetic challenges in the environment, beyond what is currently considered in biomedicine. A new research agenda for thyroid health should explore the way that diversity in thyroid function has evolved as a response to different contexts people live in—like focusing on how people’s metabolisms adapt to the energetic requirements of their environments. PubDate: Tue, 10 Nov 2020 00:00:00 GMT DOI: 10.1093/emph/eoaa043 Issue No:Vol. 9, No. 1 (2020)
Authors:Turke P. Pages: 113 - 117 Abstract: The severity of COVID-19 is age-related, with the advantage going to younger age-groups. Five reasons are presented. The first two are well-known, are being actively researched by the broader medical community, and therefore are discussed only briefly here. The third, fourth and fifth reasons derive from evolutionary life history theory, and potentially fill gaps in current understanding of why and how young and old age-groups respond differently to infection with SARS-CoV-2. Age of onset of generalized somatic aging and the timing of its progression are identified as important causes of these disparities, as are specific antagonistic pleiotropic tradeoffs in immune system function. Lay Summary: Covid-19 is less severe in younger age-groups than it is in older age-groups. Five advantages of youth are identified and explained in light of evolutionary life history theory, with a focus on the pattern of aging and specific tradeoffs between early and late immune system function. PubDate: Sat, 26 Dec 2020 00:00:00 GMT DOI: 10.1093/emph/eoaa050 Issue No:Vol. 9, No. 1 (2020)
Authors:Crespi B; Alcock J. Pages: 149 - 156 Abstract: Several recent studies have provided evidence that use of calcium channel blockers (CCBs), especially amlodipine and nifedipine, can reduce mortality from coronavirus disease 2019 (COVID-19). Moreover, hypocalcemia (a reduced level of serum ionized calcium) has been shown to be strongly positively associated with COVID-19 severity. Both effectiveness of CCBs as antiviral therapy, and positive associations of hypocalcemia with mortality, have been demonstrated for many other viruses as well. We evaluate these findings in the contexts of virus–host evolutionary conflicts over calcium metabolism, and hypocalcemia as either pathology, viral manipulation or host defence against pathogens. Considerable evidence supports the hypothesis that hypocalcemia represents a host defence. Indeed, hypocalcemia may exert antiviral effects in a similar manner as do CCBs, through interference with calcium metabolism in virus-infected cells. Prospective clinical studies that address the efficacy of CCBs and hypocalcemia should provide novel insights into the pathogenicity and treatment of COVID-19 and other viruses. PubDate: Mon, 23 Nov 2020 00:00:00 GMT DOI: 10.1093/emph/eoaa046 Issue No:Vol. 9, No. 1 (2020)
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