Evolution, Medicine, and Public Health最新文献

Background and objectives: The optimal iron hypothesis (OIH) posits that risk for infection is lowest at a mild level of iron deficiency. The extent to which this protection results from arms race dynamics in the evolution of iron acquisition and sequestration mechanisms is unclear. We evaluated the OIH with regard to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an emerging infectious agent.

Methodology: We tested 304 healthcare workers at baseline for iron deficiency (zinc protoporphyrin:heme), anemia (hemoglobin), and SARS-CoV-2 (salivary PCR), and followed them for ~3 months with biweekly SARS-CoV-2 tests. We fit logistic regression models based on Akaike Information Criterion.

Results: Adequate data were available for 199 participants. Iron replete (OR: 2.87, 95% CI: 0.85, 9.75) and anemia (OR: 2.48; 95% CI: 0.82, 7.85) were associated with higher risk for SARS-CoV-2 infection after control for covariates. Logistic regression and Cox proportional hazards models of the SARS-CoV-2 outcome were similar. Anemia (OR: 1.81; 95% CI: 0.88, 3.71) was associated with respiratory symptoms regardless of SARS-CoV-2 infection.

Conclusions and implications: These findings provide partial support for the OIH: SARS-CoV-2 infection risk was elevated at the high end of the range of iron availability; however, the elevated risk among those with anemia was not, as expected, specific to severe iron deficiency. Narrowly, for COVID-19 epidemiology, these findings accord with evidence that SARS-CoV-2's ability to establish infection is enhanced by access to iron. More broadly, these findings suggest that the OIH does not hinge on a long history of evolutionary arms race dynamics in access to host iron.

Background and objectives: Selective pressures on human childbirth have led to the evolution of cooperative birth practices, with birth attendants playing a crucial role in providing emotional support during labor.

Methodology: We leveraged COVID-19-related healthcare disruptions to investigate the impact of the evolutionary mismatch in the availability of emotional support persons on perceived birth stress among a US-based convenience sample (N = 1082).

Results: Individuals who stated during pregnancy that they desired support from their partner or a doula but who did not receive this support had significantly higher perceived childbirth stress (B = 12.5, P < .0001; and B = 5.2, P = .02, respectively, measured on a scale of 0-100). The absence of any support persons (B = 6.7, P < .001), the number of emotional support persons present (B = -5.8 for each additional support person, P = .01), and the feeling that the healthcare provider was busy or distracted during labor (B = 15, P < .001) was significantly associated with childbirth stress. Virtual support did not attenuate these effects.

Conclusions and implications: Not being able to have desired emotional support during labor was associated with significantly higher childbirth stress, even after adjusting for clinical childbirth complications. These effect sizes were substantial, comparable to the elevated stress associated with cesarean section delivery and other childbirth complications. These findings underscore the importance of preventing an evolutionary mismatch in emotional needs during labor by ensuring access to continuous support, even during public health emergencies.

Cancer research has historically focused on the somatic mutation theory, viewing cancer as a consequence of genetic mutations. However, this perspective has limitations in explaining phenomena like tumor reversion and cancer heterogeneity. This paper introduces an alternative approach: viewing cancer as a complex information-processing system shaped by its microenvironment. By integrating historical data on tumor reversion and insights into evolutionary dynamics, I propose a reframing of cancer biology. This process-oriented perspective highlights the role of cellular plasticity and adaptive behaviors, offering new pathways for therapeutic development.

Evolutionary perspectives on obesity have been dominated by genetic frameworks, but plastic responses are also central to its aetiology. While often considered a relatively modern phenomenon, obesity was recorded during the Palaeolithic through small statuettes of the female form (Venus figurines). Even if the phenotype was rare, these statuettes indicate that some women achieved large body sizes during the last glacial maximum, a period of nutritional stress. To explore this paradox, we develop an eco-life-course conceptual framework that integrates the effects of dietary transitions with intergenerational biological mechanisms. We assume that Palaeolithic populations exposed to glaciations had high lean mass and high dietary protein requirements. We draw on the protein leverage hypothesis, which posits that low-protein diets drive overconsumption of energy to satisfy protein needs. We review evidence for an increasing contribution of plant foods to diets as the last glacial maximum occurred, assumed to reduce dietary protein content. We consider physiological mechanisms through which maternal overweight impacts the obesity susceptibility of the offspring during pregnancy. Integrating this evidence, we suggest that the last glacial maximum decreased dietary protein content and drove protein leverage, increasing body weight in a process that amplified across generations. Through the interaction of these mechanisms with environmental change, obesity could have developed among women with susceptible genotypes, reflecting broader trade-offs between linear growth and adiposity and shifts in the population distribution of weight. Our approach may stimulate bioarchaeologists and paleoanthropologists to examine paleo-obesity in greater detail and to draw upon the tenets of human biology to interpret evidence.

Background and objectives: For thousands of years, betel nut has been used as a psychoactive agent in Asian and Oceanian populations. Betel nut chewing was associated with the alteration of human oral microbiome and with diseases such as oral cancer and periodontitis, but only in populations of Asian cultural background. We studied the influence of betel nut chewing on the oral microbiome in Papua New Guinea, where half of the population uses betel nut and the prevalence of these diseases is one of the highest in the world.

Methodology: We characterized the oral microbiomes of 100 Papua New Guineans. We defined two cohorts of betel chewers (n = 50) and non-chewers (n = 50) based on a genetic approach to identify the presence of betel nut in saliva. We statistically compared the alpha and beta microbial diversities between the two cohorts. We performed linear discriminant analyses to identify bacterial species more prevalent in each cohort.

Results: We found that oral microbial diversity is significantly different between betel chewers and non-chewers. The dysbiosis observed in betel chewers, led to an increase of pathogenic bacterial species including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, known to be in the aetiology of periodontal diseases.

Conclusions and implications: Our study strongly supports the alteration of human oral microbiome by betel nut use, potentially leading to periodontal diseases. It also shows the need to consider local specificities (e.g. different habits, betel nut types, and oral microbial diversities) to better characterize the impact of betel nut chewing on health.

Many postpartum women experience sexual dysfunction, characterised by reduced sexual motivation and libido, and pain during intercourse. Menstruation is also suppressed in breastfeeding women (lactational amenorrhoea). Lactational amenorrhoea has been discussed in an evolutionary context due to its positive impacts on birth spacing. In contrast, postpartum sexual dysfunction has not been viewed through an evolutionary lens. Might postpartum sexual dysfunction also be under selection? We discuss possible evolutionary explanations for postpartum sexual dysfunction. In particular, we suggest that sexual conflict, a widespread phenomenon that occurs when the evolutionary interests of males and females diverge, may be a cause of disrupted postpartum sex. This sexual conflict-based explanation generates predictions relevant to the health and well-being of new mothers that warrant testing.

Perinatal mood and anxiety disorders (PMADs) are estimated to affect as many as 17.7% of mothers in agricultural and postindustrial societies. Various lines of research converge to suggest that PMADs may be 'diseases of modernity', arising from a mismatch between the environments in which humans evolved over hundreds of thousands of years and contemporary postindustrial lifestyles. Here we highlight the social context of childrearing by focusing on three sources of mismatch associated with PMADs: closer interbirth spacing, lack of allomaternal support and lack of prior childcare experience. The transitions to agriculture and industrialization disrupted traditional maternal support networks, allowing closer birth spacing without compromising infant survival but increasing maternal isolation. Caring for closely spaced offspring is associated with high levels of parenting stress, and poses a particular challenge in the context of social isolation. The mother's kin and community play a critical role in allomothering (childcare participation) in all contemporary hunter-gatherer societies, facilitating a system of simultaneous care for children of a range of ages with unique age-specific needs. The absence of social support and assistance from allomothers in postindustrial societies leaves mothers at increased risk for PMADs due to elevated caregiving burdens. Furthermore, the traditional system of allomothering that typified human evolutionary history afforded girls and women experience and training before motherhood, which likely increased their self-efficacy. We argue that the typical postindustrial motherhood social experience is an evolutionary anomaly, leading to higher rates of PMADs.

Market integration (MI), or the shift from subsistence to market-based livelihoods, profoundly influences health, yet its impacts on infectious diseases remain underexplored. Here, we synthesize the current understanding of MI and infectious disease to stimulate more research, specifically aiming to leverage concepts and tools from disease ecology and related fields to generate testable hypotheses. Embracing a One Health perspective, we examine both human-to-human and zoonotic transmission pathways in their environmental contexts to assess how MI alters infectious disease exposure and susceptibility in beneficial, detrimental and mixed ways. For human-to-human transmission, we consider how markets expand contact networks in ways that facilitate infectious disease transmission while also increasing access to hygiene products and housing materials that likely reduce infections. For zoonotic transmission, MI influences exposures to pathogens through agricultural intensification and other market-driven processes that may increase or decrease human encounters with disease reservoirs or vectors in their shared environments. We also consider how MI-driven changes in noncommunicable diseases affect immunocompetence and susceptibility to infectious disease. Throughout, we identify statistical, survey and laboratory methods from ecology and the social sciences that will advance interdisciplinary research on MI and infectious disease.