Evolution, Medicine, and Public Health最新文献

Background and objectives: Epigenetic estimators based on DNA methylation levels have emerged as promising biomarkers of human aging. These estimators exhibit natural variations across human groups, but data about indigenous populations remain underrepresented in research. This study aims to investigate differences in epigenetic estimators between two distinct human populations, both residing in the Gran Chaco region of Argentina, the Native-American Wichí, and admixed Criollos who are descendants of intermarriages between Native Americans and the first European colonizers, using a population genetic approach.

Methodology: We analyzed 24 Wichí (mean age: 39.2 ± 12.9 yo) and 24 Criollos (mean age: 41.1 ± 14.0 yo) for DNA methylation levels using the Infinium MethylationEPIC (Illumina) to calculate 16 epigenetic estimators. Additionally, we examined genome-wide genetic variation using the HumanOmniExpress BeadChip (Illumina) to gain insights into the genetic history of these populations.

Results: Our results indicate that Native-American Wichí are epigenetically older compared to Criollos according to five epigenetic estimators. Analyses within the Criollos population reveal that global ancestry does not influence the differences observed, while local (chromosomal) ancestry shows positive associations between specific SNPs located in genomic regions over-represented by Native-American ancestry and measures of epigenetic age acceleration (AgeAccelHannum). Furthermore, we demonstrate that differences in population ecologies also contribute to observed epigenetic differences.

Conclusions and implications: Overall, our study suggests that while the genomic history may partially account for the observed epigenetic differences, non-genetic factors, such as lifestyle and ecological factors, play a substantial role in the variability of epigenetic estimators, thereby contributing to variations in human epigenetic aging.

Danger requires a strong rapid response. Speedy triggers are prone to false signals. False alarms can be costly, requiring strong negative regulators to oppose the initial triggers. Strongly opposed forces can easily be perturbed, leading to imbalance and disease. For example, immunity and fear response balance strong rapid triggers against widespread slow negative regulators. Diseases of immunity and behavior arise from imbalance. A different opposition of forces occurs in mammalian growth, which balances strong paternally expressed accelerators against maternally expressed suppressors. Diseases of overgrowth or undergrowth arise from imbalance. Other examples of opposing forces and disease include control of dopamine expression and male versus female favored traits.

Background and objectives: Brown adipose tissue (BAT) plays key roles in mammalian physiology, most notably with regard to thermoregulation in infants and juveniles. Previous studies have suggested that intragenomic conflict, in the form of genomic imprinting, mediates BAT thermogenesis, because it represents a public good for groups of siblings, or a mother with her offspring, who huddle together to conserve warmth. By this hypothesis, maternally expressed imprinted genes should promote BAT, while paternally expressed genes should repress it.

Methodology: We systematically searched the literature using two curated lists of genes imprinted in humans and/or mice, in association with evidence regarding effects of perturbation to imprinted gene expression on BAT development or activity.

Results: Overall, enhanced BAT was associated with relatively higher expression of maternally expressed imprinted genes, and relatively lower expression of paternally expressed imprinted genes; this pattern was found for 16 of the 19 genes with sufficient information for robust ascertainment (Binomial test, P < 0.005, 2-tailed).

Conclusions and implications: These results support the kinship theory of imprinting and indicate that future studies of BAT, and its roles in human health and disease, may usefully focus on effects of imprinted genes and associated genomic conflicts.

Background and objectives: It has been argued that sex and disease-related traits should influence how observers respond to sensory sickness cues. In fact, there is evidence that humans can detect sensory cues related to infection in others, but lack of power from earlier studies prevents any firm conclusion regarding whether perception of sickness cues is associated with sex and disease-related personality traits. Here, we tested whether women (relative to men), individuals with poorer self-reported health, and who are more sensitive to disgust, vulnerable to disease, and concerned about their health, overestimate the presence of, and/or are better at detecting sickness cues.

Methodology: In a large online study, 343 women and 340 men were instructed to identify the sick faces from a series of sick and healthy photographs of volunteers with an induced acute experimental inflammation. Participants also completed several disease-related questionnaires.

Results: While both men and women could discriminate between sick and healthy individuals above chance level, exploratory analyses revealed that women outperformed men in accuracy and speed of discrimination. Furthermore, we demonstrated that higher disgust sensitivity to body odors is associated with a more liberal decision criterion for categorizing faces as sick.

Conclusion: Our findings give strong support for the human ability to discriminate between sick and healthy individuals based on early facial cues of sickness and suggest that women are significantly, although only slightly, better at this task. If this finding is replicated, future studies should determine whether women's better performance is related to increased avoidance of sick individuals.

Background and objectives: Non-communicable disease risk and the epidemic of cardiometabolic diseases continue to grow across the expanding industrialized world. Probing the relationships between evolved human physiology and modern socioecological conditions is central to understanding this health crisis. Therefore, we investigated the relationships between increased market access, shifting subsistence patterns and cardiometabolic health indicators within Daasanach semi-nomadic pastoralists who vary in their engagement in traditional lifestyle and emerging market behaviors.

Methodology: We conducted cross-sectional socioecological, demographic and lifestyle stressor surveys along with health, biomarker and nutrition examinations among 225 (51.6% female) Daasanach adults in 2019-2020. We used linear mixed-effects models to test how differing levels of engagement in market integration and traditional subsistence activities related to blood pressure (BP), body composition and blood chemistry.

Results: We found that systolic and diastolic BP, as well as the probability of having high BP (hypertension), were negatively associated with distance to market, a proxy for market integration. Additionally, body composition varied significantly by socioeconomic status (SES), with significant positive associations between BMI and body fat and higher SES among adults.

Conclusions and implications: While evidence for evolutionary mismatch and health variation have been found across a number of populations affected by an urban/rural divide, these results demonstrate the effects of market integration and sedentarization on cardiometabolic health associated with the early stages of lifestyle changes. Our findings provide evidence for the changes in health when small-scale populations begin the processes of sedentarization and market integration that result from myriad market pressures.

Sex and reproductive status of the host have a major impact on the immune response against infection. Our aim was to understand their impact on host tolerance or resistance in the systemic Mycobacterium marinum infection of Drosophila melanogaster. We measured host survival and bacillary load at time of death, as well as expression by quantitative real-time polymerase chain reaction of immune genes (diptericin and drosomycin). We also assessed the impact of metabolic and hormonal regulation in the protection against infection by measuring expression of upd3, impl2 and ecR. Our data showed increased resistance in actively mating flies and in mated females, while reducing their tolerance to infection. Data suggests that Toll and immune deficiency (Imd) pathways determine tolerance and resistance, respectively, while higher basal levels of ecR favours the stimulation of the Imd pathway. A dual role has been found for upd3 expression, linked to increased/decreased mycobacterial load at the beginning and later in infection, respectively. Finally, impl2 expression has been related to increased resistance in non-actively mating males. These results allow further assessment on the differences between sexes and highlights the role of the reproductive status in D. melanogaster to face infections, demonstrating their importance to determine resistance and tolerance against M. marinum infection.

Background and objectives: Universities throughout the USA increasingly offer undergraduate courses in evolutionary medicine (EvMed), which creates a need for pedagogical resources. Several resources offer course content (e.g. textbooks) and a previous study identified EvMed core principles to help instructors set learning goals. However, assessment tools are not yet available. In this study, we address this need by developing an assessment that measures students' ability to apply EvMed core principles to various health-related scenarios.

Methodology: The EvMed Assessment (EMA) consists of questions containing a short description of a health-related scenario followed by several likely/unlikely items. We evaluated the assessment's validity and reliability using a variety of qualitative (expert reviews and student interviews) and quantitative (Cronbach's α and classical test theory) methods. We iteratively revised the assessment through several rounds of validation. We then administered the assessment to undergraduates in EvMed and Evolution courses at multiple institutions.

Results: We used results from the pilot to create the EMA final draft. After conducting quantitative validation, we deleted items that failed to meet performance criteria and revised items that exhibited borderline performance. The final version of the EMA consists of six core questions containing 25 items, and five supplemental questions containing 20 items.

Conclusions and implications: The EMA is a pedagogical tool supported by a wide range of validation evidence. Instructors can use it as a pre/post measure of student learning in an EvMed course to inform curriculum revision, or as a test bank to draw upon when developing in-class assessments, quizzes or exams.

Background and objectives: While the primary goals of medical treatment are typically to shorten illness or relieve symptoms, we explore the idea that an important additional goal for some patients is to communicate their needs. Drawing on signalling theory, we argue that undergoing treatments can help patients legitimize their illness and thereby enable access to crucial support during convalescence.

Methods and results: Four pre-registered within-subjects experiments (n = 874) show that participants are more inclined to provide care to people who undergo treatment, especially when that treatment is painful. Results show this incentivizes the use of antibiotic treatments for viral infections as well as drug treatments for mental illness. A cross-sectional study of 194 chronic pain patients shows that those who experience stigma and doubt over the legitimacy of their illness are more likely to accept aversive treatments. Furthermore, two experiments (n = 653) indicate that subtle manipulations of one's sense of social support may increase willingness to accept treatment.

Conclusions and implications: These results indicate that people make decisions to provide care in part based on the presence or absence of treatment and furthermore that patients' treatment decision-making is informed by the social consequences of their choices. Signalling theory may help explain the surprising longevity of some ineffective and costly medical procedures.

Background and objectives: The Developmental Origins of Health and Disease hypothesis posits that early life adversity is associated with poor adult health outcomes. Epidemiological evidence has supported this framework by linking low birthweight with adult health and mortality, but the mechanisms remain unclear. Accelerated epigenetic aging may be a pathway to connect early life experiences with adult health outcomes, based on associations of accelerated epigenetic aging with increased morbidity and mortality.

Methodology: Sixty-seven mother-infant dyads were recruited in the eastern Democratic Republic of Congo. Birthweight data were collected at birth, and blood samples were collected at birth and follow-up visits up to age 3. DNA methylation data were generated with the Illumina MethylationEPIC array and used to estimate epigenetic age. A multilevel model was used to test for associations between birthweight and epigenetic age acceleration.

Results: Chronological age was highly correlated with epigenetic age from birth to age 3 (r = 0.95, p < 2.2 × 10^-16). Variation in epigenetic age acceleration increased over time. Birthweight, dichotomized around 2500 g, predicted epigenetic age acceleration over the first 3 years of life (b = -0.39, p = 0.005).

Conclusions and implications: Our longitudinal analysis provides the first evidence for accelerated epigenetic aging that emerges between birth and age 3 and associates with low birthweight. These results suggest that early life experiences, such as low birthweight, may shape the trajectory of epigenetic aging in early childhood. Furthermore, accelerated epigenetic aging may be a pathway that links low birthweight and poor adult health outcomes.

Background and objectives: There is significant evidence from large-scale, industrial and post-industrial societies that greater income and wealth inequality is negatively associated with both population health and increasing health inequalities. However, whether such relationships are inevitable and should be expected to impact the health of small-scale societies as they become more market-integrated is less clear.

Methodology: Here, using mixed-effect models, we explore the relationship between health, wealth, wealth inequality and health inequalities in a small-scale foraging population from the Philippines, the Agta.

Results: Across 11 camps, we find small to moderate degrees of wealth inequality (maximal Gini Coefficient 0.44) which is highest in the most permanent camps, where individuals engage more heavily in the formal market. However, in both adults (n = 161) and children (n = 215), we find little evidence that either wealth or wealth inequality associates with ill health, except for one measure of nutritional condition-red blood cell count.

Conclusions and implications: We interpret these results in the light of high levels of cooperation among the Agta which may buffer against the detrimental effects of wealth inequality documented in industrial and post-industrial societies. We observe little intergenerational wealth transmission, highlighting the fluid nature of wealth, and thus wealth inequality, particularly in mobile communities. The deterioration of nutritional status, as indicated by red blood cell counts, requires further investigation before concluding the Agta's extensive cooperation networks may be beginning to breakdown in the face of increasing inequality.