Suchergebnisse

Many biological systems have critical periods that overlap with the age of maternal provisioning via placenta or lactation. As such, they serve as conduits for phenotypic information transfer between generations and link maternal experience with offspring biology and disease outcomes. This review critically evaluates proposals for an adaptive function of these responses in humans. Although most models assume an adult function for the metabolic responses to nutritional stress, these specific traits have more likely been tailored for effects during fetal life and infancy. Other biological functions are under stronger evolutionary selection later in life and thus are better candidates for predictive plasticity. Given the long human life cycle and environmental changes that are unpredictable on decadal timescales, plastic responses that evolved to confer benefits in adolescence or adulthood likely rely on cues that integrate matrilineal experiences prior to gestation. We conclude with strategies for testing the timescale and adaptive significance of developmental responses to early environments.

AbstractA well‐established literature demonstrates executive function (EF) deficits in obese children and adults relative to healthy weight comparisons. EF deficits in obesity are associated with overeating and impulsive consumption of high calorie foods leading to excess weight gain and to problems with metabolic regulation and low‐grade inflammation that detrimentally affect the structure and function of prefrontal cortex. Here, we test a complementary explanation for the relation between EF and body mass index (BMI) grounded in the energy demand of the developing brain. Recent work shows that the brain accounts for a lifetime peak of 66% of resting metabolic rate in childhood and that developmental changes in brain energetics and normative changes in body weight gain are closely inversely related. This finding suggests a trade‐off in early childhood between energy used to support brain development versus energy used to support physical growth and fat deposition. To test this theorized energetic trade‐off, we analyzed data from a large longitudinal sample (N = 1,292) and found that change in EF from age 3 to 5 years, as a proxy for brain development in energetically costly prefrontal cortex, is inversely related to change in BMI from age 2 to 5 years. Greater linear decline in BMI predicted greater linear increase in EF. We interpret this finding as tentative support for a brain–body energetic trade‐off in early childhood with implications for lifetime obesity risk.

▪ Abstract  We use an expanded framework of multiple epidemiologic transitions to review the issues of re/emerging infection. The first epidemiologic transition was associated with a rise in infectious diseases that accompanied the Neolithic Revolution. The second epidemiologic transition involved the shift from infectious to chronic disease mortality associated with industrialization. The recent resurgence of infectious disease mortality marks a third epidemiologic transition characterized by newly emerging, re- emerging, and antibiotic resistant pathogens in the context of an accelerated globalization of human disease ecologies. These transitions illustrate recurring sociohistorical and ecological themes in human–disease relationships from the Paleolithic Age to the present day.

Individuals who are minoritized as a result of race, sexual identity, gender, or socioeconomic status experience a higher prevalence of many diseases. Understanding the biological processes that cause and maintain these socially driven health inequities is essential for addressing them. The gut microbiome is strongly shaped by host environments and affects host metabolic, immune, and neuroendocrine functions, making it an important pathway by which differences in experiences caused by social, political, and economic forces could contribute to health inequities. Nevertheless, few studies have directly integrated the gut microbiome into investigations of health inequities. Here, we argue that accounting for host-gut microbe interactions will improve understanding and management of health inequities, and that health policy must begin to consider the microbiome as an important pathway linking environments to population health.

Individuals who are minoritized as a result of race, sexual identity, gender, or socioeconomic status experience a higher prevalence of many diseases. Understanding the biological processes that cause and maintain these socially driven health inequities is essential for addressing them. The gut microbiome is strongly shaped by host environments and affects host metabolic, immune, and neuroendocrine functions, making it an important pathway by which differences in experiences caused by social, political, and economic forces could contribute to health inequities. Nevertheless, few studies have directly integrated the gut microbiome into investigations of health inequities. Here, we argue that accounting for host–gut microbe interactions will improve understanding and management of health inequities, and that health policy must begin to consider the microbiome as an important pathway linking environments to population health.