Recent work demonstrated that allostatic load (AL), a metric of multisystem physiological dysregulation, incurred during sensitive periods of development, imparts lasting consequences on adult health outcomes. We expand on this work to examine how childhood AL mediates the relationship between childhood adversity and adult cardiometabolic outcomes. Using data from the Great Smoky Mountains Study, a longitudinal study tracking psychiatric and physical functioning outcomes in children ages 9-13 assessed annually into adulthood, we evaluated survey, blood sample, and demographic data to determine childhood adversity, childhood AL, and adult cardiometabolic health (n=650). Childhood adversity was determined through interviews evaluating various stress dimensions, including threat, loss, unpredictability, maltreatment, poverty, and other adverse events reported by child or parent within 3 months preceding interviews. AL scores were calculated from biomarkers representing immune, metabolic, and neuroendocrine function. Adult cardiometabolic health was determined from blood pressure, BMI, and waist-hip-ratio at age 30. We used confirmatory factor analysis to examine the relationship between stress dimensions and a latent adversity variable. The latent adversity construct was primarily driven by maltreatment and poverty, although all dimensions of stress contributed significantly (p<0.001). Using structural equation modeling (SEM), we examined direct and indirect paths between this latent variable and measured indicators of AL and adult outcomes, controlling for sex, race, age and pubertal stage. SEM results showed that childhood AL mediates the relationship between childhood adversity and adult cardiometabolic outcomes (p<0.005), while the direct path was non-significant. These results highlight AL as a key mechanism linking early adversity to long-term risk.

Lower birth weight (BW) has been widely shown to predict elevated risk for cardiovascular diseases (CVD) like hypertension, diabetes and atherosclerosis. Building on this finding, it has been hypothesized that the higher rates of CVD among Black Americans may trace, in part, to socially-driven inequities in BW. A critical review of empirical tests of this idea yielded a paradox: although Black Americans have lower BWs and higher CVD, and even though lower BW has been widely shown to predict future CVD risk, studies generally report stronger inverse BW–CVD relationships in white compared to Black samples. Drawing on recent clarifications in intergenerational pathways, we propose an updated model that could help explain the weaker BW–CVD relationship in Black Americans: Structural racism not only elevates offspring CVD risk through intergenerational pathways that reduce BW (e.g. maternal stress or hypertension), but also increases the likelihood of maternal weight gain and elevated gestational glucose, which elevate future offspring CVD risk but increase BW. We review evidence that these offsetting, “push–pull” effects on BW operate across the full spectrum of maternal gestational glucose and offspring BW. As a result, when BW is used as a marker, a dimension of CVD risk is rendered invisible, proportionate to the strength of these opposing pathways. BW will thus be particularly uncoupled from CVD risk in minoritized US populations, who face psychosocial stress but are also more likely to be exposed to environments that lead to weight gain and metabolic dysregulation.

Famines, defined as severe hunger crises, have often been studied within the developmental origins of health and disease (DOHaD) framework, which hypothesizes that harmful environmental exposures during critical periods of development induce epigenetic and/or physiological changes which alter metabolism and increase risk of disease. With increasing rates of cardiometabolic disease, it is imperative to understand how exposures during development contribute to worsening health in later-life. We explored the effects of famine on subsequent hypertension and type 2 diabetes risk observed in countries at varying income levels and nutrition transitions. Following MOOSE and PRISMA protocols, we identified papers that examined famine exposure across peri-natal, childhood and adolescence. Overall, exposure to famine at the perinatal stage was positively associated with both hypertension and diabetes (pooled OR 1.17, 95% CI 1.08-1.25, p =< 0.0001; pooled OR 1.31, 95% CI 1.20-1.42, p =< 0.0001). Strong positive associations were apparent for combined early, middle and late childhood exposure with hypertension and diabetes in adulthood (pooled OR 1.30, 95% CI 1.19-1.42, p=< 0.0001; pooled OR 1.30, 95% CI 1.18-1.42, p=< 0.0001). Sex based analysis revealed that females were more affected across all developmental stages for both hypertension and diabetes (pooled OR 1.41, 95% CI 1.16-1.70, p=0.0004; pooled OR 1.27, 95% CI 1.11-1.43, p=0.0002). Overall, the study establishes that the effects of famine can be seen beyond the peri-natal stage, suggesting that developmental plasticity extends well into childhood. These results can help us anticipate disease risk as well as answer bigger questions on human evolution and development.

Attention-Deficit/Hyperactivity Disorder (ADHD) is a prevalent neurodevelopmental disorder characterised by persistent inattention, hyperactivity, and impulsivity, often extending into adulthood. Adult ADHD frequently co-occurs with depression and anxiety, reflecting overlapping neurobiological mechanisms, including dysregulation of catecholaminergic signalling and the hypothalamic–pituitary–adrenal (HPA) axis. However, limited research in India has examined these interactions among young adults.

This cross-sectional study assessed 1,634 young adults (18–25 years) in Delhi-NCR, India, using the ASRS-V1.1, Beck Depression Inventory (BDI), Perceived Stress Scale (PSS), and Beck Anxiety Inventory (BAI).

ADHD was strongly associated with depression, anxiety, and elevated stress, suggesting a biological vulnerability. Individuals with ADHD showed 4.7-fold higher odds of moderate/severe depression, 5.1-fold higher odds of moderate/severe anxiety, and 18.6-fold higher odds of high stress. Mediation analysis indicated that stress and anxiety partially mediated the ADHD–depression relationship. The indirect effects via stress (β = 3.82, 95% CI [3.06–4.58], p < .001) and anxiety (β = 4.23, 95% CI [3.40–5.06], p < .001) were significant, while the direct effect remained, highlighting both direct and indirect pathways linking ADHD to depressive symptoms.

Among ADHD subtypes, the combined subtype (ADHD-C) exhibited the highest burden of depression, anxiety, and stress, while inattentive (ADHD-I) and hyperactive/impulsive (ADHD-H) subtypes also showed elevated mental health risks. These findings suggest that understanding the neurobiological and stress-related pathways connecting ADHD to depression may enhance early identification, inform targeted interventions, and guide biologically informed strategies for prevention and treatment of comorbid mental health conditions in young adults with ADHD.

The Texas Rural Health and Heritage Project studies the social and historical contexts of health disparities for middle aged and older adults in the rural Blackland Prairie regions of Texas. In addition to exploring the relationship between the histories of plantation ecologies, farming, and embodiment in the rural South over the lifespan, we are investigating the ways that individuals create communities of support to buffer the specific challenges of rural life. This paper explores the relationship between social support and healthy aging using survey and biometric data from over 6000 Texans in the more urban Dallas-Fort Worth Metroplex. Our findings suggest that for this comparative population, older women report higher levels of worry, anxiety and depression than their male counterparts, while also describing higher levels of social support. Notably, this pattern persists for married men and women. Narratives about rural life and farming often center male perspectives on work and weathering, while women’s perspectives remain secondary. These findings suggest that across rural and urban spaces greater attention should be paid to the costs of connectedness, variability in experiences of social support, the gendered dynamics of sociality for older individuals, and their potential implications differential markers of aging in these communities.

The COVID-19 pandemic worsened health disparities by disrupting access to care, especially for marginalized populations. Latinas, who faced barriers to prenatal care, may have experienced emotional distress in response to pandemic-related disruptions in access to prenatal care. This study investigates how healthcare access disruptions during COVID-19 are associated with maternal mental health among Latinas receiving publicly funded prenatal health care in El Paso, Texas. We hypothesized that disruptions to prenatal care, such as delayed appointments, telehealth transitions, or difficulty scheduling appointments, would be associated with levels of psychological distress. Using cross-sectional survey data from pregnant Latinas interviewed between 2020-2022, we assessed self-reported healthcare disruptions and emotional distress levels using the Kessler Psychological Distress Scale (K10). We also examined associations with a history of healthcare avoidance to financial costs. Statistical analysis was conducted in R, using multivariable linear regression models to test for associations between healthcare disruptions and distress, adjusting for covariates, including country of birth, maternal age, parity, and gestational age at interview. Analyses suggest that healthcare disruptions predicted elevated psychological distress in the domains of difficulty accessing general healthcare (b=5.42, p-value≤0.001) or prenatal care services (b=5.90, p-value≤0.001), delayed initiation of prenatal care (b=4.03, p-value=0.01), and having fewer prenatal appointments scheduled (b=5.10, p-value=0.01). Previous experiences of avoiding healthcare visits due to cost for participants (b=6.09, p-value≤0.001), their children (b=2.56, p-value=0.04), or household members (b=4.58, p-value≤0.001) were also associated with psychological distress scores. Findings highlight the need for policies that ensure equitable access to prenatal care during crises for marginalized populations.

Food and water insecurity often co-occur, jointly contributing to malnutrition, psychosocial stress, and risk of infectious and non-communicable diseases, including diabetes. This pattern is especially pronounced in the Galapagos Islands, where rapid socioeconomic and epidemiological changes and geographic isolation pose significant challenges to human health. In July 2025, a mixed-methods pilot study was conducted on San Cristóbal Island in households (n=25) with at least one adult diagnosed with diabetes or prediabetes to explore associations between food and water security status and measured metabolic health outcomes. Surveys included sociodemographic, water and food security, and diabetes-related variables. Metabolic biomarkers, blood pressure, and anthropometric measurements were collected for all adults in the households (n=40). 48% of households experienced either water or food insecurity, while 44% faced both water and food insecurity. The severity of insecurity was similar between single and doubly insecure households. Among those with diabetes or prediabetes, HbA1c, systolic blood pressure, HDL, and waist-to-height ratio (WHtR) were higher in households with one insecurity compared to households with both, though triglycerides were lower. Notably, doubly insecure households had higher diabetes medication use. Among other household members, HbA1c and WHtR were higher in single insecure households, while higher triglycerides, systolic blood pressure, and lower HDL were more common in doubly insecure ones. No statistically significant differences were observed, possibly due to the limited sample size. Poorer metabolic outcomes associated with only food or water insecurity are surprising but may reflect differing physiological stress and instability across the groups.

Access to adequate food is a significant challenge of homelessness in the United States. Even with support from the Supplemental Nutrition Assistance Program (SNAP) and community programs, many people experiencing homelessness (PEH) cope with high levels of food insecurity (FI). This study explores the factors associated with FI among PEH in a mid-sized city in Oregon. FI was assessed using a modified USDA Food Insecurity Module, and associated factors were assessed using validated and internally developed measures likely related to food insecurity based on literature and our pilot work. 298 participants completed the FI portion of the questionnaire, and a subset of 45 participated in qualitative interviews where food access was discussed. Of the 298 questionnaire participants, 80.2% were food insecure. In bivariate analysis, FI was significantly associated (p < 0.05) with common mental disorders (higher anxiety and depression scale scores; reported diagnosis of PTSD, anxiety, and depression), stressful experiences (higher ACE and perceived stress scale scores, more police encounters), having an injury resulting in chronic pain or disability, and living in temporary shelter. Further multivariate analyses will examine individual, social, and structural factors associated with FI. Qualitative findings demonstrate that even when strategically utilizing SNAP, PEH are often hungry. Community and nonprofit efforts to address this need periodically meet caloric needs but not nutritional or cultural ones. Given the high levels of food insecurity in this population, this work points to the need for more stable and comprehensive nutrition support programs for PEH and sustained investment in SNAP.

During reproduction, many altered or new physiological processes place significant demands on the maternal body. Water and energy demands increase dramatically during both pregnancy and lactation. In limited-resource environments, it is unclear how these reproductive states contribute to physiological stress. Using longitudinal data collected by the Daasanach Human Biology Project between 2022-2024, we assessed the association between reproductive status (pregnant, lactating, non-pregnant/non-lactating) and fingernail cortisol concentration (FCC) among semi-nomadic pastoralist Daasanach women (n=217 reproductive-age individuals, defined as aged 16-51, with 293 observations; n=247 total individuals with 378 observations) in northern Kenya. We estimated random-effects panel linear regression models to test these relationships, adjusting for water and food insecurity among other covariates. Lactating status, but not pregnancy or non-pregnant/non-lactating status, was significantly associated with log-transformed FCC for reproductive-age women (β=0.10, SE=0.04, p=0.01) and overall (β=0.09, SE=0.04, p<0.05). Cortisol levels were lower in women above the reproductive age cutoff than in reproductive-age women (t=2.27, df=77.7, p=0.03), but water insecurity (p=0.70) and food insecurity (p=0.96) levels did not differ between these groups. Since age did not predict FCC, this suggests that when women are lactating they have significantly higher chronic stress regardless of water stress, and that the reproductive years confer social or familial responsibilities which also increase stress. Further work is needed to understand how the maternal body adapts to the stress of increased resource demands during reproductive events, particularly in resource-limited environments.

Early life environments shape future health outcomes. However, gaps exist in our understanding of the mechanisms responsible for these patterns. Gut microbes represent one potential pathway through which early life environments can influence physiology and health in infancy and beyond. Infants are born mostly sterile and acquire microbes from contact with caregivers and the environment during the first three years of life. Many of the microbiome traits obtained during this period may be retained into adulthood, and gut microbes have been shown to affect host metabolism, immune function, and even behavior across the lifecourse. Here, we use a long-term birth cohort, the Cebu Longitudinal Health and Nutrition Survey (CLHNS) in the Philippines, to examine the association between early life environments and the subsequent composition of the gut microbiome. We characterized gut microbiome composition and functional potential in 105 women in 2017 and related it to survey data collected for them at birth in 1983-1984. We found significant associations between early life microbial exposures and overall gut microbiome composition (PERMANOVA F1,84= 4.3, p = 0.009). We also found that early life microbial exposure accounted for 77% of the microbial functional pathways that differed in relative abundance across individuals, many of which were associated with amino acid metabolism. These findings suggest that early life environments can be embodied via impacts on the gut microbiome and that these impacts can persist until adulthood. Implications for physiology and health must be further explored.

Many cross-sectional studies have examined determinants of gut microbiota diversity and composition, but the long-term effects of early-life exposures remain poorly understood. This study aimed to explore associations between prenatal heavy metal exposure and gut microbiota diversity and composition at age 15, and to examine how early-life growth and neurodevelopment relate to later microbial profiles. The study was based on a hospital-based birth cohort established in 2008 in the Terai region of Nepal, an area where heavy metal exposure and child growth retardation have been recognized as public health concerns. Among 100 infants originally recruited, 74 adolescents participated in the 2022–2023 follow-up. Cord blood samples were analyzed for heavy metal concentrations (As, Cu), and fecal samples at age 15 were sequenced using MiSeq. Data were processed using QIIME2 pipelines, and associations were analyzed with R software. α-diversity metrics (Shannon index, observed ASVs) were positively correlated with cord blood As and Cu, while weight, height, and BMI at 14 years were negatively correlated with diversity. β-diversity (unweighted UniFrac) was significantly associated with anthropometric indices, and height at 6 months and psychomotor development index at 24 months were linked to weighted UniFrac distances. Taxonomic analyses revealed significant associations at both phylum (Firmicutes, Actinobacteriota) and genus (Dorea_A lineage) levels. These findings suggest that prenatal heavy metal exposure and early-life developmental conditions may shape adolescent gut microbiota, highlighting the importance of developmental and environmental factors in long-term microbial ecology.

Low-resource communities face disproportionately greater exposure to environmental contaminants, many of which are both directly obesogenic and influence the gut microbiome in ways that further increase obesity risk. In this study, we used a multi-omics approach to investigate how gut microbiome composition mediates the relationship between environmental contaminants and body mass index (BMI) in two low-resource communities in the United States. Our sample included anthropometrics and fecal samples collected from 185 individuals living in southwest Illinois (n=97) and the Mississippi Delta (n=88) in 2022 and 2023 as part of the REACH Study. Fecal samples were analyzed using 16S rRNA sequencing and untargeted metabolomics – a technique that measures as many metabolites, as possible in a biological sample, unlike the limited data provided by targeted approaches. High-dimensional mediation analysis revealed nineteen metabolites that were significantly associated with gut microbiome composition and BMI, including six known chemical contaminants. All known contaminants had a significant negative relationship with adiposity, including 4-Methylquinoline, a probable human carcinogen (B = -1.50, p = 0.05). 4-Methylquinoline was also associated with the abundance of an anti-inflammatory, short-chain fatty acid-producing Clostridium species (B = -0.17, p = 0.04). Several bacterial metabolites were associated with BMI, including trans-3-Indoleacrylic acid (B = 2.24, p = 0.03), a tryptophan metabolite. Our results suggest a bidirectional relationship where environmental contaminants affect microbiome composition and specific microbes modify contaminant toxicity. By clarifying the biological pathways that mediate environmental disparities and human health, this research provides data that could inform future public health interventions.

Human biologists are increasingly attentive to how pollutant exposures disrupt endocrine systems, with consequences for health and human variation. The calcium–parathyroid hormone (PTH)–vitamin D axis is a central regulatory pathway for mineral metabolism, skeletal biology, and adaptation to ecological stressors. Its disruption is both clinically significant and anthropologically meaningful: parathyroid disorders are shaped by sex, age, and gendered life course processes, with incidence rising sharply in midlife and disproportionately affecting women. Metals such as lead (Pb), cadmium (Cd), and mercury (Hg) plausibly disrupt calcium–PTH regulation, yet their influence in population-based settings remains underexplored.

This study examines how heavy metal exposure alters continuous variation in calcium, PTH, and derived indices (calcium/phosphorus ratio, parathyroid function index), conceptualizing these measures as biomarkers of endocrine disruption rather than diagnostic thresholds. Data are drawn from NHANES 2003–2006, the only U.S. cycles with concurrent intact PTH, serum calcium, 25(OH)D, phosphorus, and biomonitoring for Pb, Cd, and Hg. Multivariable models estimate associations between metals and both biomarkers and composite indices, adjusting for demographic and nutritional covariates. When analyzed as an exposure mixture, metals showed a positive, monotonic association with both PTH and the parathyroid function index. Weighted quantile sum regression indicated Cd contributed the largest weight to the mixture effect, followed by Pb and Hg. These associations reflect chronic, low-level endocrine disruption of a homeostatic regulatory system. By treating the calcium–PTH axis as a sensitive target of endocrine disruption, this research highlights how low-level metal exposures shape human biology and health across the life course.

Transgender and nonbinary (TNB) people experience significant exposure to anti-TNB enacted stigma at all stages of life, yet few studies examine health effects from a life course perspective. To understand how early life adversity becomes embodied, we analyzed baseline survey and biomarker data from the longitudinal Transgender Resilience and Health Study among TNB people in the United States (N = 147). T-tests compared those reporting experiences of anti-trans enacted stigma before age 18 (ESU18; n = 90) to those who did not (n = 57), and linear regressions tested the associations between exposure to ESU18 and adult health. Biomarker analyses controlled for age, BMI, medication use, and chronic disease. Mental health analyses were age-adjusted. Mental health and cardiovascular function did not significantly differ between those who experienced ESU18 and those who did not (p > .50). Among participants reporting ESU18, the amount of enacted stigma was positively associated with adulthood anxiety (B = .335, 95% CI: [.008, .663], p = .045), but not depression (B = .147, 95% CI: [-.212, .506], p = .418). Contrary to our hypotheses, greater ESU18 exposure was significantly associated with lower diastolic blood pressure (B = -.659, 95% CI: [-1.307, -.011], p = .046), suggesting increased autonomic nervous system regulation. Systolic blood pressure (B = -.195, 95% CI: [-1.056, .667], p = .654) was not. Though early life experiences of enacted stigma may impact TNB adult health, decreasing chronic exposure over the life course is key for TNB health.

Resilience is generally understood to positively affect health, yet there is less discussion about the role of adversity in developing resilience. To understand how resilience from past adversity (i.e., hard-earned resilience) influences health, we analyzed baseline data from the Transgender Resilience and Health Study, a longitudinal study among transgender and nonbinary people in the United States (N = 153). Data collected at baseline included semi-structured interviews, surveys, and several types of biomarker samples. During the interview, participants were asked what contributed to their resilience. Then we conducted two rounds of systematic, multi-coder theme identification, coding, and analysis to explore the theme of hard-earned resilience. One subtheme we identified was post-traumatic growth (i.e., growth from previous experiences of adversity). We then used t-tests and ANCOVA to compare how cardiovascular function differed between participants reporting post-traumatic growth (n = 57, 37.3%) from those who did not (n = 96, 62.7%). Age, smoking, medication use, and BMI were covariates. Diastolic blood pressure (DBP) was significantly higher among participants reporting post-traumatic growth compared to those who did not (MPTG = 84.2, MnoPTG = 79.4, p = .01). Systolic blood pressure (MPTG = 121.1, MnoPTG = 118.9, p = .36) and heart rate did not significantly differ (MPTG = 73.9, MnoPTG = 71.4, p = .11). Results suggest chronic stress related to prior adversity precipitating post-traumatic growth may contribute to higher DBP suggesting decreased vascular relaxation. These results highlight the physiological scars that past adversity can leave alongside perceived positive mental growth.