Evolution, Medicine, and Public Health最新文献

{"title":"Lower testosterone levels are associated with higher risk of death in men.","authors":"Michael P Muehlenbein,&nbsp;Jeffrey Gassen,&nbsp;Eric C Shattuck,&nbsp;Corey S Sparks","doi":"10.1093/emph/eoac044","DOIUrl":"https://doi.org/10.1093/emph/eoac044","url":null,"abstract":"<p><strong>Background and objectives: </strong>Testosterone plays an important role in regulating male development, reproduction and health. Declining levels across the lifespan may reflect, or even contribute to, chronic disease and mortality in men.</p><p><strong>Methodology: </strong>Relationships between testosterone levels and male mortality were analyzed using data from multiple samples of the cross-sectional National Health and Nutrition Examination Survey (<i>n</i> = 10 225). Target outcomes included known deaths from heart disease, malignant neoplasms, chronic lower respiratory diseases, cerebrovascular diseases, Alzheimer's disease, diabetes mellitus, influenza and pneumonia, kidney diseases, and accidents or unintentional injuries.</p><p><strong>Results: </strong>Results of discrete-time hazard models revealed that lower levels of testosterone were related to higher mortality for the majority of disease categories in either an age-dependent or age-independent fashion. Analysis of all-cause mortality-which included deaths from any known disease-also revealed greater general risk for those with lower testosterone levels. For most disease categories, the hazard associated with low testosterone was especially evident at older ages when mortality from that particular ailment was already elevated. Notably, testosterone levels were not related to mortality risk for deaths unrelated to chronic disease (i.e. accidents and injuries).</p><p><strong>Conclusions and implications: </strong>While the causal direction of relationships between testosterone and mortality risk remains unclear, these results may reflect the decline in testosterone that accompanies many disease states. Accordingly, the relationship between testosterone and male mortality may be indirect; ill individuals are expected to have both lower testosterone and higher mortality risk.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"30-40"},"PeriodicalIF":3.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9938530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9192307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disgusting odors trigger the oral immune system.","authors":"Stephanie Anja Juran,&nbsp;Arnaud Tognetti,&nbsp;Johan N Lundström,&nbsp;Lalit Kumar,&nbsp;Richard J Stevenson,&nbsp;Mats Lekander,&nbsp;Mats J Olsson","doi":"10.1093/emph/eoac042","DOIUrl":"https://doi.org/10.1093/emph/eoac042","url":null,"abstract":"<p><p>Recent research has characterized the behavioral defense against disease. In particular the detection of sickness cues, the adaptive reactions (e.g. avoidance) to these cues and the mediating role of disgust have been the focus. A presumably important but less investigated part of a behavioral defense is the immune system response of the observer of sickness cues. Odors are intimately connected to disease and disgust, and research has shown how olfaction conveys sickness cues in both animals and humans. This study aims to test whether odorous sickness cues (i.e. disgusting odors) can trigger a preparatory immune response in humans. We show that subjective and objective disgust measures, as well as TNFα levels in saliva increased immediately after exposure to disgusting odors in a sample of 36 individuals. Altogether, these results suggest a collaboration between behavioral mechanisms of pathogen avoidance in olfaction, mediated by the emotion of disgust, and mechanisms of pathogen elimination facilitated by inflammatory mediators. Disgusting stimuli are associated with an increased risk of infection. We here test whether disgusting odors, can trigger an immune response in the oral cavity. The results indicate an increase level of TNFα in the saliva. This supports that disease cues can trigger a preparatory response in the oral cavity.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"8-17"},"PeriodicalIF":3.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9912705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10793536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COVID-19 and <i>Evolution, Medicine, and Public Health</i>.","authors":"Charles L Nunn","doi":"10.1093/emph/eoad002","DOIUrl":"https://doi.org/10.1093/emph/eoad002","url":null,"abstract":"According to the World Health Organization, 6.7 million people have died from COVID19 as of the start of 2023. These deaths are tragic with many societal ramifications. For example, more than 10 million children have lost caregivers globally through 1 May 2022 [1], while many others have suffered dramatic losses in educational attainment [2]. At times, the pandemic has overwhelmed healthcare services that have resulted in additional non-COVID death and suffering. COVID-19 has also caused sharp declines in mental health, particularly among children and adolescents [3, 4]. Mental disorders, such as depression and anxiety, are often debilitating and long-lasting, thus contributing greatly to years lived with disability. Some bright spots have also occurred, including the marked reduction in deaths due to influenza in the first year of the pandemic due to masking and social isolation and the rapid rollout of vaccines using new technologies such as mRNA vaccines, which offer great promise in battling other infectious diseases. One lesson from the pandemic is the importance of interdisciplinary approaches for addressing complex problems. We cannot control a viral pandemic with just virology. We need epidemiologists, engineers, sociologists, political scientists, historians, medical doctors, economists, statisticians, anthropologists, mathematicians and geographers (among others!) to comprehend the interconnections of human behavior, disease transmission, government interventions, global transport and trade, and the production and distribution of vaccines and treatments. Evolutionary biology is another field that has been crucial for making sense of the COVID-19 pandemic. Examples of evolutionary biology’s importance are many, including identifying selective pressures that lead to the rise of new variants of concern, understanding human responses to disease in relation to past evolutionary pressures from other infectious diseases, and investigating the breadth of hosts that coronaviruses infect and the ecological context of their spillover among hosts. In many cases, these evolutionary perspectives are also crucial to mitigation efforts. For example, phylogenetic approaches can reveal the origins of a new human pathogen from other species, helping guide surveillance efforts in wildlife or domesticated animals, while also revealing transmission pathways among human populations. In the early months of the pandemic, for example, many of us spent hours on NextStrain (https:// nextstrain.org/) examining the most up-to-date phylogenies of SARS-CoV-2 to help make sense of its global movement. We can see the breadth of these evolutionary perspectives on COVID-19 in the pages of Evolution, Medicine, and Public Health (EMPH). So far, EMPH has published 24 scientific articles EDITORIAL BY INVITATION ONLY","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"41-43"},"PeriodicalIF":3.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9993055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9642505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-pharmaceutical interventions and the emergence of pathogen variants.","authors":"Ben Ashby, Cameron A Smith, Robin N Thompson","doi":"10.1093/emph/eoac043","DOIUrl":"10.1093/emph/eoac043","url":null,"abstract":"<p><p>Non-pharmaceutical interventions (NPIs), such as social distancing and contact tracing, are important public health measures that can reduce pathogen transmission. In addition to playing a crucial role in suppressing transmission, NPIs influence pathogen evolution by mediating mutation supply, restricting the availability of susceptible hosts, and altering the strength of selection for novel variants. Yet it is unclear how NPIs might affect the emergence of novel variants that are able to escape pre-existing immunity (partially or fully), are more transmissible or cause greater mortality. We analyse a stochastic two-strain epidemiological model to determine how the strength and timing of NPIs affect the emergence of variants with similar or contrasting life-history characteristics to the wild type. We show that, while stronger and timelier NPIs generally reduce the likelihood of variant emergence, it is possible for more transmissible variants with high cross-immunity to have a greater probability of emerging at intermediate levels of NPIs. This is because intermediate levels of NPIs allow an epidemic of the wild type that is neither too small (facilitating high mutation supply), nor too large (leaving a large pool of susceptible hosts), to prevent a novel variant from becoming established in the host population. However, since one cannot predict the characteristics of a variant, the best strategy to prevent emergence is likely to be an implementation of strong, timely NPIs.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"80-89"},"PeriodicalIF":3.3,"publicationDate":"2022-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10052376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9234396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sound reasons for unsound sleep: Comparative support for the sentinel hypothesis in industrial and nonindustrial groups.","authors":"Leela McKinnon, Eric C Shattuck, David R Samson","doi":"10.1093/emph/eoac039","DOIUrl":"10.1093/emph/eoac039","url":null,"abstract":"<p><strong>Background and objectives: </strong>Sleep is a vulnerable state in which individuals are more susceptible to threat, which may have led to evolved mechanisms for increasing safety. The sentinel hypothesis proposes that brief awakenings during sleep may be a strategy for detecting and responding to environmental threats. Observations of sleep segmentation and group sentinelization in hunter-gatherer and small-scale communities support this hypothesis, but to date it has not been tested in comparisons with industrial populations characterized by more secure sleep environments.</p><p><strong>Methodology: </strong>Here, we compare wake after sleep onset (WASO), a quantitative measure of nighttime awakenings, between two nonindustrial and two industrial populations: Hadza hunter-gatherers (<i>n</i> = 33), Malagasy small-scale agriculturalists (<i>n</i> = 38), and Hispanic (<i>n</i> = 1,531) and non-Hispanic White (NHW) (<i>n</i> = 347) Americans. We compared nighttime awakenings between these groups using actigraphically-measured sleep data. We fit linear models to assess whether WASO varies across groups, controlling for sex and age.</p><p><strong>Results: </strong>We found that WASO varies significantly by group membership and is highest in Hadza (2.44 h) and Malagasy (1.93 h) and lowest in non-Hispanic Whites (0.69 h). Hispanics demonstrate intermediate WASO (0.86 h), which is significantly more than NHW participants. After performing supplementary analysis within the Hispanic sample, we found that WASO is significantly and positively associated with increased perception of neighborhood violence.</p><p><strong>Conclusions and implications: </strong>Consistent with principles central to evolutionary medicine, we propose that evolved mechanisms to increase vigilance during sleep may now be mismatched with relatively safer environments, and in part responsible for driving poor sleep health.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"53-66"},"PeriodicalIF":3.3,"publicationDate":"2022-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10024786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9215093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antigenic evolution of SARS-CoV-2 in immunocompromised hosts.","authors":"Cameron A Smith, Ben Ashby","doi":"10.1093/emph/eoac037","DOIUrl":"10.1093/emph/eoac037","url":null,"abstract":"<p><strong>Objectives/aims: </strong>Prolonged infections of immunocompromised individuals have been proposed as a crucial source of new variants of SARS-CoV-2 during the COVID-19 pandemic. In principle, sustained within-host antigenic evolution in immunocompromised hosts could allow novel immune escape variants to emerge more rapidly, but little is known about how and when immunocompromised hosts play a critical role in pathogen evolution.</p><p><strong>Materials and methods: </strong>Here, we use a simple mathematical model to understand the effects of immunocompromised hosts on the emergence of immune escape variants in the presence and absence of epistasis.</p><p><strong>Conclusions: </strong>We show that when the pathogen does not have to cross a fitness valley for immune escape to occur (no epistasis), immunocompromised individuals have no qualitative effect on antigenic evolution (although they may accelerate immune escape if within-host evolutionary dynamics are faster in immunocompromised individuals). But if a fitness valley exists between immune escape variants at the between-host level (epistasis), then persistent infections of immunocompromised individuals allow mutations to accumulate, therefore, facilitating rather than simply speeding up antigenic evolution. Our results suggest that better genomic surveillance of infected immunocompromised individuals and better global health equality, including improving access to vaccines and treatments for individuals who are immunocompromised (especially in lower- and middle-income countries), may be crucial to preventing the emergence of future immune escape variants of SARS-CoV-2.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"90-100"},"PeriodicalIF":3.3,"publicationDate":"2022-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10061940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9240283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolution of higher mesenchymal CD44 expression in the human lineage: A gene linked to cancer malignancy.","authors":"Xinghong Ma,&nbsp;Anasuya Dighe,&nbsp;Jamie Maziarz,&nbsp;Edwin Neumann,&nbsp;Eric Erkenbrack,&nbsp;Yuan-Yuan Hei,&nbsp;Yansheng Liu,&nbsp;Yasir Suhail,&nbsp;Irene Pak,&nbsp;Andre Levchenko,&nbsp;Günter P Wagner","doi":"10.1093/emph/eoac036","DOIUrl":"https://doi.org/10.1093/emph/eoac036","url":null,"abstract":"<p><p>CD44 is an extracellular matrix receptor implicated in cancer progression. CD44 increases the invasibility of skin (SF) and endometrial stromal fibroblasts (ESF) by cancer and trophoblast cells. We reasoned that the evolution of CD44 expression can affect both, the fetal-maternal interaction through CD44 in ESF as well as vulnerability to malignant cancer through expression in SF. We studied the evolution of <i>CD44</i> expression in mammalian SF and ESF and demonstrate that in the human lineage evolved higher <i>CD44</i> expression. Isoform expression in cattle and human is very similar suggesting that differences in invasibility are not due to the nature of expressed isoforms. We then asked whether the concerted gene expression increase in both cell types is due to shared regulatory mechanisms or due to cell type-specific factors. Reporter gene experiments with cells and <i>cis</i>-regulatory elements from human and cattle show that the difference of <i>CD44</i> expression is due to <i>cis</i> effects as well as cell type-specific <i>trans</i> effects. These results suggest that the concerted expression increase is likely due to selection acting on both cell types because the evolutionary change in cell type-specific factors requires selection on cell type-specific functions. This scenario implies that the malignancy enhancing effects of elevated CD44 expression in humans likely evolved as a side-effect of positive selection on a yet unidentified other function of CD44. A possible candidate is the anti-fibrotic effect of CD44 but there are no reliable data showing that humans and primates are less fibrotic than other mammals.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":" ","pages":"447-462"},"PeriodicalIF":3.7,"publicationDate":"2022-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9487634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33477224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early life adversity, reproductive history and breast cancer risk.","authors":"Amy M Boddy, Shawn Rupp, Zhe Yu, Heidi Hanson, Athena Aktipis, Ken Smith","doi":"10.1093/emph/eoac034","DOIUrl":"10.1093/emph/eoac034","url":null,"abstract":"<p><strong>Background and objectives: </strong>Individuals who experience early life adversity are at an increased risk for chronic disease later in life. Less is known about how early life factors are associated with cancer susceptibility. Here, we use a life history framework to test whether early life adversity increases the risk of breast cancer. We predict that early life adversity can shift investment in somatic maintenance and accelerate the timing of reproduction, which may mediate or interact with the risk of breast cancer.</p><p><strong>Methodology: </strong>We use population-wide data from the Utah Population Database (UPDB) and Utah Cancer Registry, leading to 24 957 cases of women diagnosed with breast cancer spanning 20 years (1990-2010) and 124 785 age-matched controls. We generated a cumulative early life adversity summation score to evaluate the interaction (moderation) and mediation between early life adversity, reproductive history and their association with breast cancer risk.</p><p><strong>Results: </strong>Our analyses led to three key findings: (i) more early life adversity, when considered as a main effect, accelerates the time to first birth and death, (ii) early age at first birth and high parity decreases the risk of breast cancer and (iii) we find no association between early adversity and breast cancer risk either as a main effect or in its interaction with reproductive history.</p><p><strong>Conclusion and implications: </strong>Early adversity elevates the risk of overall mortality through mechanisms other than breast cancer risk. This suggests early life factors can generate different effects on health. Future work should incorporate more complex view of life history patterns, including multiple life stages, when making predictions about cancer susceptibility.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"10 1","pages":"429-438"},"PeriodicalIF":3.7,"publicationDate":"2022-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9464099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9953211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Socioeconomic impacts on Andean adolescents' growth: Variation between households, between communities and over time.","authors":"Mecca E Burris,&nbsp;Esperanza Caceres,&nbsp;Emily M Chester,&nbsp;Kathryn A Hicks,&nbsp;Thomas W McDade,&nbsp;Lynn Sikkink,&nbsp;Hilde Spielvogel,&nbsp;Jonathan Thornburg,&nbsp;Virginia J Vitzthum","doi":"10.1093/emph/eoac033","DOIUrl":"https://doi.org/10.1093/emph/eoac033","url":null,"abstract":"<p><strong>Background/objectives: </strong>We evaluated potential socioeconomic contributors to variation in Andean adolescents' growth between households within a peri-urban community undergoing rapid demographic and economic change, between different community types (rural, peri-urban, urban) and over time. Because growth monitoring is widely used for assessing community needs and progress, we compared the prevalences of stunting, underweight, and overweight estimated by three different growth references.</p><p><strong>Methods: </strong>Anthropometrics of 101 El Alto, Bolivia, adolescents (Alteños), 11.0-14.9 years old in 2003, were compared between households (economic status assessed by parental occupations); to one urban and two rural samples collected in 1983/1998/1977, respectively; and to the WHO growth reference, a representative sample of Bolivian children (MESA), and a region-wide sample of high-altitude Peruvian children (Puno).</p><p><strong>Results: </strong>Female Alteños' growth was positively associated with household and maternal income indices. Alteños' height averaged ∼0.8SD/∼0.6SD/∼2SDs greater than adolescents' height in urban and rural communities measured in 1983/1998/1977, respectively. Overweight prevalence was comparable to the WHO, and lower than MESA and Puno, references. Stunting was 8.5/2.5/0.5 times WHO/MESA/Puno samples, respectively.</p><p><strong>Conclusions/implications: </strong>Both peri-urban conditions and temporal trends contributed to gains in Alteños' growth. Rural out-migration can alleviate migrants' poverty, partly because of more diverse economic options in urbanized communities, especially for women. Nonetheless, Alteños averaged below WHO and MESA height and weight medians. Evolved biological adaptations to environmental challenges, and the consequent variability in growth trajectories, favor using multiple growth references. Growth monitoring should be informed by community- and household-level studies to detect and understand local factors causing or alleviating health disparities.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":" ","pages":"409-428"},"PeriodicalIF":3.7,"publicationDate":"2022-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9454678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33460122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selfish evolution of placental hormones.","authors":"Grace Keegan,&nbsp;Manus M Patten","doi":"10.1093/emph/eoac031","DOIUrl":"https://doi.org/10.1093/emph/eoac031","url":null,"abstract":"<p><p>We hypothesize that some placental hormones-specifically those that arise by tandem duplication of genes for maternal hormones-may behave as gestational drivers, selfish genetic elements that encourage the spontaneous abortion of offspring that fail to inherit them. Such drivers are quite simple to evolve, requiring just three things: a decrease in expression or activity of some essential maternal hormone during pregnancy; a compensatory increase in expression or activity of the homologous hormone by the placenta; and genetic linkage between the two effects. Gestational drive may therefore be a common selection pressure experienced by any of the various hormones of mammalian pregnancy that have arisen by tandem gene duplication. We examine the evolution of chorionic gonadotropin in the human lineage in light of this hypothesis. Finally, we postulate that some of the difficulties of human pregnancy may be a consequence of the action of selfish genes.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":" ","pages":"391-397"},"PeriodicalIF":3.7,"publicationDate":"2022-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9426663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40341508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}