Evolution, Medicine, and Public Health最新文献

{"title":"No evidence that spice consumption is a cancer prevention mechanism in human populations.","authors":"Antoine M Dujon,&nbsp;Aurélie Tasiemski,&nbsp;Pascal Pujol,&nbsp;Anthony Turpin,&nbsp;Beata Ujvari,&nbsp;Frédéric Thomas","doi":"10.1093/emph/eoac040","DOIUrl":"https://doi.org/10.1093/emph/eoac040","url":null,"abstract":"<p><strong>Background: </strong>Why humans historically began to incorporate spices into their diets is still a matter of unresolved debate. For example, a recent study (Bromham et al. There is little evidence that spicy food in hot countries is an adaptation to reducing infection risk. <i>Nat Hum Behav</i> 2021;5:878-91.) did not support the most popular hypothesis that spice consumption was a practice favoured by selection in certain environments to reduce food poisoning, parasitic infections, and foodborne diseases.</p><p><strong>Methods: </strong>Because several spices are known to have anticancer effects, we explored the hypothesis that natural selection and/or cultural evolution may have favoured spice consumption as an adaptive prophylactic response to reduce the burden of cancer pathology. We used linear models to investigate the potential relationship between age-standardized gastrointestinal cancer rates and spice consumption in 36 countries.</p><p><strong>Results: </strong>Patterns of spice are not consistent with a cancer mitigation mechanism: the age-standardized rate of almost all gastrointestinal cancers was not related to spice consumption.</p><p><strong>Conclusions: </strong>Direction other than foodborne pathogens and cancers should be explored to understand the health reasons, if any, why our ancestors developed a taste for spices.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"45-52"},"PeriodicalIF":3.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10024787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9215096","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":"The evolution of antibiotic resistance in an incurable and ultimately fatal infection: A retrospective case study.","authors":"Robert J Woods,&nbsp;Camilo Barbosa,&nbsp;Laura Koepping,&nbsp;Juan A Raygoza,&nbsp;Michael Mwangi,&nbsp;Andrew F Read","doi":"10.1093/emph/eoad012","DOIUrl":"https://doi.org/10.1093/emph/eoad012","url":null,"abstract":"<p><strong>Background and objectives: </strong>The processes by which pathogens evolve within a host dictate the efficacy of treatment strategies designed to slow antibiotic resistance evolution and influence population-wide resistance levels. The aim of this study is to describe the underlying genetic and phenotypic changes leading to antibiotic resistance within a patient who died as resistance evolved to available antibiotics. We assess whether robust patterns of collateral sensitivity and response to combinations existed that might have been leveraged to improve therapy.</p><p><strong>Methodology: </strong>We used whole-genome sequencing of nine isolates taken from this patient over 279 days of a chronic infection with <i>Enterobacter hormaechei</i>, and systematically measured changes in resistance against five of the most relevant drugs considered for treatment.</p><p><strong>Results: </strong>The entirety of the genetic change is consistent with <i>de novo</i> mutations and plasmid loss events, without acquisition of foreign genetic material via horizontal gene transfer. The nine isolates fall into three genetically distinct lineages, with early evolutionary trajectories being supplanted by previously unobserved multi-step evolutionary trajectories. Importantly, although the population evolved resistance to all the antibiotics used to treat the infection, no single isolate was resistant to all antibiotics. Evidence of collateral sensitivity and response to combinations therapy revealed inconsistent patterns across this diversifying population.</p><p><strong>Conclusions: </strong>Translating antibiotic resistance management strategies from theoretical and laboratory data to clinical situations, such as this, will require managing diverse population with unpredictable resistance trajectories.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"11 1","pages":"163-173"},"PeriodicalIF":3.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10266578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9654994","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":"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":3.7,"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":"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":"Implications of leg length for metabolic health and fitness.","authors":"Meghan K Shirley, Owen J Arthurs, Kiran K Seunarine, Tim J Cole, Simon Eaton, Jane E Williams, Chris A Clark, Jonathan C K Wells","doi":"10.1093/emph/eoac023","DOIUrl":"10.1093/emph/eoac023","url":null,"abstract":"<p><strong>Background and objectives: </strong>Several 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.</p><p><strong>Methodology: </strong>Using 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.</p><p><strong>Results: </strong>Consistent 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.</p><p><strong>Conclusions and implications: </strong>Building 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.</p>","PeriodicalId":12156,"journal":{"name":"Evolution, Medicine, and Public Health","volume":"10 1","pages":"316-324"},"PeriodicalIF":3.7,"publicationDate":"2022-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10701439","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}