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BackgroundSouth Africa's rates of psychiatric morbidity are among the highest in sub-Saharan Africa and are foregrounded by the country's long history of political violence during apartheid. Growing evidence suggests that in utero stress exposure is a potent developmental risk factor for future mental illness risk, yet the extent to which the psychiatric effects of prenatal stress impact the next generation are unknown. We evaluate the intergenerational effects of prenatal stress experienced during apartheid on psychiatric morbidity among children at ages 17-18 and also assess the moderating effects of maternal age, social support, and past household adversity.MethodsParticipants come from Birth-to-Twenty, a longitudinal birth cohort study in Soweto-Johannesburg, South Africa's largest peri-urban township which was the epicentre of violent repression and resistance during the final years of the apartheid regime. Pregnant women were prospectively enrolled in 1990 and completed questionnaires assessing social experiences, and their children's psychiatric morbidity were assessed at ages 17-18.ResultsFull data were available from 304 mother-child pairs in 2007-8. Maternal prenatal stress in 1990 was not directly associated greater psychiatric morbidity during at ages 17-18. Maternal age and past household adversity moderated the intergenerational mental health effects of prenatal stress such that children born to younger mothers and late adolescent/young adult children experiencing greater household adversity exhibited worse psychiatric morbidity at ages 17-18. Social support did not buffer against the long-term psychiatric impacts of prenatal stress.ConclusionsGreater prenatal stress from apartheid predicted adverse psychiatric outcomes among children born to younger mothers and adolescents/young adults who experienced greater concurrent stress. Our findings suggest that prenatal stress may affect adolescent mental health, have stress-sensitising effects, and represent possible intergenerational effects of trauma experienced under apartheid in this sample.

ObjectivesAlterations in adult hypothalamic-pituitary-adrenal (HPA) axis activity have increasingly been linked with early life stress and adult depression, but a limited number of studies have used longitudinal data to explore HPA axis dysregulation as an underlying mechanism driving the long-term depressive impacts of early stressors. Here we address potential long-term impacts of early life, family-based stress on depressive symptoms among young adults in a longitudinal birth cohort study begun in 1983 in the Philippines.Materials and methodsWe relate a composite measure of family-based stressors experienced between birth and adolescence to circadian dynamics in adult salivary cortisol and depressive risk measured at 21-22 years of age. Multiple regression analyses were conducted to examine the relationship between early life stress levels and risk of adult depressive symptoms, as well as the role of adult diurnal cortisol activity in this relationship.ResultsGreater levels of early life familial stress predicted more severe depressive symptomatology at age 21-22 in a dose-response fashion (p

Developmental plasticity is a widespread property of living organisms, but different individuals in the same species can vary greatly in how susceptible they are to environmental influences. In humans, research has sought to link variation in plasticity to physiological traits such as stress reactivity, exposure to prenatal stress-related hormones such as cortisol, and specific genes involved in major neurobiological pathways. However, the determinants of individual differences in plasticity are still poorly understood. Here we present the novel hypothesis that, in both sexes, higher exposure to androgens during prenatal and early postnatal life should lead to increased plasticity in traits that display greater male variability (i.e., a majority of physical and behavioral traits). First, we review evidence of greater phenotypic variation and higher susceptibility to environmental factors in males; we then consider evolutionary models that explain greater male variability and plasticity as a result of sexual selection. These empirical and theoretical strands converge on the hypothesis that androgens may promote developmental plasticity, at least for traits that show greater male variability. We discuss a number of potential mechanisms that may mediate this effect (including upregulation of neural plasticity), and address the question of whether androgen-induced plasticity is likely to be adaptive or maladaptive. We conclude by offering suggestions for future studies in this area, and considering some research designs that could be used to empirically test our hypothesis.

A 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.

Objectives: External environmental heat exposure during gestation impacts the physiology of human development in utero, but evidence for these impacts has not yet been explored in dentition. We examined deciduous teeth for fluctuating asymmetry (FA), a measure of developmental instability, together with gestational environmental temperature data drawn from historical weather statistics. Materials and Methods: We measured dental casts from the longitudinal Burlington Growth Study, representing 172 participants (ages 3–6 years) with health records. FA was calculated from crown dimensions and intercuspal distances that develop during gestation. Multiple regression separated by sex (nfemale = 81) examined the effects of mean temperatures in each trimester, controlling for birth year. Results: In females, increased temperatures during the first trimester are significantly associated with an increase in FA (p = 0.03), specifically during the second and third prenatal months (p = 0.03). There is no relationship between temperature and FA for either sex in the second or third trimesters, when enamel is formed. Discussion: Dental instability may be sensitive to temperature in the first trimester in females during the scaffolding of crown shape and size in the earliest stages of tooth formation. Sexual dimorphism in growth investment strategies may explain the differences in results between males and females. Using enduring dental characteristics, these results advance our understanding of the effects of temperature on fetal physiology within a discrete period. [ABSTRACT FROM AUTHOR]

Objectives: Recent discussions in human biology have highlighted how local ecological contexts shape the relationship between social stressors and health across populations. Chronic low‐grade inflammation has been proposed as a pathway linking social stressors to health, with evidence concentrated in high‐income Western contexts. However, it remains unclear whether this is an important pathway in populations where prevalence is lower due to lower adiposity and greater infectious exposures. To investigate this further, we tested associations between multiple types of intimate partner violence (IPV), a highly prevalent stressor and health crisis globally, and C‐reactive protein (CRP), a commonly used measure of chronic low‐grade inflammation, in Cebu, Philippines. For reference, we compared results for CRP to depression, a well‐established and consistently observed health outcome of IPV. Methods: Data came from 1601 currently partnered women (ages 35–69 years) as part of the Cebu Longitudinal Health and Nutrition Survey. IPV exposures included physical, emotional, and controlling behavior. Depression scores were measured using a modified version of the Center for Epidemiologic Studies‐Depression Scale for this population, whereas plasma CRP was measured from overnight‐fasted morning blood samples. Results: All three types of IPV were associated with a higher depression score. However, none of the IPV measures were associated with CRP. In a post hoc interaction test, emotional IPV became positively associated with CRP as waist circumference increased above the mean. Conclusions: Our results suggest a complex relationship between social stressors and chronic low‐grade inflammation, which is likely dependent on the population‐specific context of lifestyle and environmental factors. [ABSTRACT FROM AUTHOR]

A central prediction of evolutionary theory is that energy invested into reproduction comes at the expense of somatic maintenance and repair, accelerating biological aging. Supporting this prediction are findings that high fertility among women predicts shorter lifespan and poorer health later in life. However, biological aging is thought to begin before age-related health declines, limiting the applicability of morbidity and mortality for studying the aging process earlier in life. Here, we examine the relationship between reproductive history and biological aging in a sample of young (20 to 22yo) men and women from the Cebu Longitudinal Health and Nutrition Survey, located in the Philippines (n = 1,735). We quantify biological aging using six measures, collectively known as epigenetic clocks, reflecting various facets of cellular aging, health, and mortality risk. In a subset of women, we test whether longitudinal changes in gravidity between young and early-middle adulthood (25 to 31yo) are associated with changes in epigenetic aging during that time. Cross-sectionally, gravidity was associated with all six measures of accelerated epigenetic aging in women (n = 825). Furthermore, longitudinal increases in gravidity were linked to accelerated epigenetic aging in two epigenetic clocks (n = 331). In contrast, the number of pregnancies a man reported fathering was not associated with epigenetic aging among same-aged cohort men (n = 910). These effects were robust to socioecological, environmental, and immunological factors, consistent with the hypothesis that pregnancy accelerates biological aging and that these effects can be detected in young women in a high-fertility context. [ABSTRACT FROM AUTHOR]

Objectives: Maternal experiences before pregnancy predict birth outcomes, a key indicator of health trajectories, but the timing and pathways for these effects are poorly understood. Here we test the hypothesis that maternal pre‐adult growth patterns predict pregnancy glucose and offspring fetal growth in Cebu, Philippines. Methods: Using multiple regression and path analysis, gestational age‐adjusted birthweight and variables reflecting infancy, childhood, and post‐childhood/adolescent weight gain (conditional weights) were used to predict pregnancy HbA1c and offspring birth outcomes among participants in the Cebu Longitudinal Health and Nutrition Survey. Results: Maternal early/mid‐childhood weight gain predicted birth weight, length, and head circumference in female offspring. Late‐childhood/adolescent weight gain predicted birth length, birth weight, skinfold thickness, and head circumference in female offspring, and head circumference in male offspring. Pregnancy HbA1c did not mediate relationships between maternal growth and birth size parameters. Discussion: In Cebu, maternal growth patterns throughout infancy, childhood, and adolescence predict fetal growth via a pathway independent of circulating glucose, with stronger impacts on female than male offspring, consistent with a role of developmental nutrition on offspring fetal growth. Notably, the strength of relationships followed a pattern opposite to what occurs in response to acute pregnancy stress, with strongest effects on head circumference and birth length and weakest on skinfolds. We speculate that developmental sensitivities are reversed for stable, long‐term nutritional cues that reflect average local environments. These findings are relevant to public health and life‐history theory as further evidence of developmental influences on health and resource allocation across the life course. [ABSTRACT FROM AUTHOR]

Objectives: The COVID‐19 pandemic in South Africa introduced new societal adversities and mental health threats in a country where one in three individuals are expected to develop a psychiatric condition sometime in their life. Scientists have suggested that psychosocial stress and trauma during childhood may increase one's vulnerability to the mental health consequences of future stressors—a process known as stress sensitization. This prospective analysis assessed whether childhood adversity experienced among South African children across the first 18 years of life, coinciding with the post‐apartheid transition, exacerbates the mental health impacts of psychosocial stress experienced during the 2019 coronavirus (COVID‐19) pandemic (ca. 2020–2021). Materials and Methods: Data came from 88 adults who participated in a follow‐up study of a longitudinal birth cohort study in Soweto, South Africa. Childhood adversity and COVID‐19 psychosocial stress were assessed as primary predictors of adult PTSD risk, and an interaction term between childhood adversity and COVID‐19 stress was calculated to evaluate the potential effect of stress sensitization. Results: Fifty‐six percent of adults exhibited moderate‐to‐severe PTSD symptoms. Greater childhood adversity and higher COVID‐19 psychosocial stress independently predicted worse post‐traumatic stress disorder symptoms in adults. Adults who reported greater childhood adversity exhibited non‐significantly worse PTSD symptoms from COVID‐19 psychosocial stress. Discussion: These results highlight the deleterious mental health effects of both childhood trauma and COVID‐19 psychosocial stress in our sample and emphasize the need for greater and more accessible mental health support as the pandemic progresses in South Africa. [ABSTRACT FROM AUTHOR]

Objectives: The drivers of human life expectancy gains over the past 200 years are not well‐established, with a potential role for historical reductions in infectious disease. We investigate whether infectious exposures in infancy predict biological aging using DNA methylation‐based markers that forecast patterns of morbidity and mortality later in life. Methods: N = 1450 participants from the Cebu Longitudinal Health and Nutrition Survey—a prospective birth cohort initiated in 1983—provided complete data for the analyses. Mean chronological age was 20.9 years when venous whole blood samples were drawn for DNA extraction and methylation analysis, with subsequent calculation of three epigenetic age markers: Horvath, GrimAge, and DunedinPACE. Unadjusted and adjusted least squares regression models were evaluated to test the hypothesis that infectious exposures in infancy are associated with epigenetic age. Results: Birth in the dry season, a proxy measure for increased infectious exposure in the first year of life, as well as the number of symptomatic infections in the first year of infancy, predicted lower epigenetic age. Infectious exposures were associated with the distribution of white blood cells in adulthood, which were also associated with measures of epigenetic age. Conclusions: We document negative associations between measures of infectious exposure in infancy and DNA methylation‐based measures of aging. Additional research, across a wider range of epidemiological settings, is needed to clarify the role of infectious disease in shaping immunophenotypes and trajectories of biological aging and human life expectancy. [ABSTRACT FROM AUTHOR]

Objectives: The gut microbiome (GM) connects physical and social environments to infant health. Since the infant GM affects immune system development, there is interest in understanding how infants acquire microbes from mothers and other household members. Materials and Methods: As a part of the Cebu Longitudinal Health and Nutrition Survey (CLHNS), we paired fecal samples (proxy for the GM) collected from infants living in Metro Cebu, Philippines at 2 weeks (N = 39) and 6 months (N = 36) with maternal interviews about prenatal household composition. We hypothesized that relationships between prenatal household size and composition and infant GM bacterial diversity (as measured in fecal samples) would vary by infant age, as well as by household member age and sex. We also hypothesized that infant GM bacterial abundances would differ by prenatal household size and composition. Results: Data from 16 S rRNA bacterial gene sequencing show that prenatal household size was the most precise estimator of infant GM bacterial diversity, and that the direction of the association between this variable and infant GM bacterial diversity changed between the two time points. The abundances of bacterial families in the infant GM varied by prenatal household variables. Conclusions: Results highlight the contributions of various household sources to the bacterial diversity of the infant GM, and suggest that prenatal household size is a useful measure for estimating infant GM bacterial diversity in this cohort. Future research should measure the effect of specific sources of household bacterial exposures, including social interactions with caregivers, on the infant GM. [ABSTRACT FROM AUTHOR]