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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]

• Socioeconomic status (SES) predicts numerous health outcomes. • Chronic inflammation and immunosenescence are implicated pathways. • Studies on SES and immune function outside high income countries are limited. • In Cebu, Philippines, SES was negatively associated with measures of immunosenescence. • SES was positively associated with inflammation and mediated by adiposity. Socioeconomic status (SES) gradients in health are well-documented, and while biological pathways are incompletely understood, chronic inflammation and accelerated immune aging (immunosenescence) among lower SES individuals have been implicated. However, previous findings have come from samples in higher income countries, and it is unclear how generalizable they are to lower- and middle-income countries (LMIC) with different infectious exposures and where adiposity—an important contributor to chronic inflammation—might show different SES patterning. To address this gap, we explored associations between SES and inflammation and immunosenescence in a sample of women in Cebu, Philippines. Data came from the mothers of the Cebu Longitudinal Health and Nutrition Survey birth cohort (mean age: 47.7, range: 35–69 years). SES was measured as a combination of annual household income, education level, and assets. Chronic inflammation was measured using C-reactive protein (CRP) in plasma samples from 1,834 women. Immunosenescence was measured by the abundance of exhausted CD8T (CD8 + CD28-CD45RA-) and naïve CD8T and CD4T cells, estimated from DNA methylation in whole blood in a random subsample of 1,028. Possible mediators included waist circumference and a collection of proxy measures of pathogen exposure. SES was negatively associated with the measures of immunosenescence, with slight evidence for mediation by a proxy measure for pathogen exposure from the household's drinking water source. In contrast, SES was positively associated with CRP, which was explained by the positive association with waist circumference. Similar to higher income populations, in Cebu there is an SES-gradient in pathogen exposures and immunosenescence. However, lifestyle changes occurring more rapidly among higher SES individuals is contributing to a positive association between SES and adiposity and inflammation. Our results suggest more studies are needed to clarify the relationship between SES and inflammation and immunosenescence across LMIC. [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]

Epigenetic clocks quantify regular changes in DNA methylation that occur with age, or in relation to biomarkers of ageing, and are strong predictors of morbidity and mortality. Here, we assess whether measures of fetal nutrition and growth that predict adult chronic disease also predict accelerated biological ageing in young adulthood using a suite of commonly used epigenetic clocks. Data come from the Cebu Longitudinal Health and Nutrition Survey (CLHNS), a long-running cohort followed since birth in metropolitan Cebu, Philippines. Past work has shown that birth weight (BW) and the mother's arm fat during pregnancy (a measure of pregnancy energy status) relate inversely to health outcomes in the CLHNS but primarily in males. Genome-wide DNA methylation was assessed in whole blood using the Infinium EPIC array. Participants included males (n=895) and females (n=803) measured in 2005 (20.8–22.5 years). Clocks included the Hannum and Horvath clocks trained on chronological age, the DNAmPhenoAge and DNAmGrimAge clocks trained on clinical biomarkers, the Dunedin pace of ageing (DunedinPACE) clock trained on longitudinal changes in ageing biomarkers, and the DNAmTL clock trained on leukocyte telomere length. In males, lower BW predicted advanced biological ageing using the Hannum, DNAmPhenoAge, DunedinPoAm, and DNAmTL clocks. In contrast, BW did not predict any clock in female participants. Participants' mothers' pregnancy arm fat only predicted DNAmTL in males. These findings suggest that epigenetic clocks are a useful tool for gauging long-term outcomes predicted by fetal growth, and add to existing evidence in the CLHNS for sex differences in these relationships. [ABSTRACT FROM AUTHOR]

Alloparental caregiving is key to humans' highly flexible reproductive strategies. Across species and across societies, alloparental care is more common in harsh and/or unpredictable environments (HUEs). Currently, however, it is unclear whether HUEs predict intra-population variation in alloparental care, or whether early life HUEs might predict later alloparental care use in adulthood, consistent with adaptive developmental plasticity. We test whether harshness measures (socioeconomic status (SES), environmental hygiene, crowding) and unpredictability measures (parental unemployment, paternal absence, household moves) predicted how much alloparental assistance families in Cebu, Philippines received, in a multigenerational study with data collected across four decades. Though worse environmental hygiene predicted more concurrent alloparental care in 1994, we found little evidence that HUEs predict within-population variation in alloparental care in this large-scale, industrialized society. Indeed, less-crowded conditions and higher SES predicted more alloparental care, not less, in the 1980s and in 2014 respectively, while paternal absence in middle childhood predicted less reliance on alloparental care in adulthood. In this cultural context, our results generally do not provide support for the translation of interspecific or intersocietal patterns linking HUEs and alloparental care to intra-population variation in alloparental care, nor for the idea that a reproductive strategy emphasizing alloparental care use may be preceded by early life HUEs. [ABSTRACT FROM AUTHOR]

Current evolutionary theory conceptualizes fathers' childcare as highly facultative and likely contingent on a variety of local socioecological predictors. Much of the evolutionarily-motivated work on the predictors of paternal care has focused on smaller-scale societies, while similar, potentially complementary research in larger-scale societies has focused on theoretical frameworks from (e.g.) economics and developmental psychology. Due to the different emphases, relatively few studies have incorporated information on variables known to predict paternal care in one context with those known to predict it in the other. Here, we assess whether paternal care conforms to predictions derived from the facultative fathering hypothesis and life history theory in Cebu, the Philippines. We evaluated which of 6 variables—hours worked outside the home, age and number of children, number of other caregivers, family residence pattern, and fathers' educational attainment—predicted the number of hours fathers reported spending on 12 common caregiving tasks. Consistent with the basic premise of facultative fathering, men who worked more spent less time on childcare. Additionally, the time fathers spent on different types of caregiving reflected changes in demand as children age. However, alloparental care appears to be a complement to, rather than a substitute for, paternal care in this context, in contrast to the predictions of the facultative fathering hypothesis. We also found that men with more education reported spending more time on childcare, consistent with a caregiving strategy that emphasizes heavy investment in embodied capital across generations. Our data illustrate the context-specific nature of 'facultative' caregiving in humans, and highlight the importance of considering locally-relevant predictors when testing predictions derived from evolutionary theory. [ABSTRACT FROM AUTHOR]

Objective: Cross‐culturally, men's T declines in response to pairbonding and fatherhood, but less is known about what happens to T during and after life history transitions that theoretically lead to renewed mating effort. We tested whether men's T rises (or declines less with age) as their children age, or when pairbonds end, independent of changes in fatherhood‐related variables such as co‐residence with children. Methods: We used demographic, behavioral, and salivary hormone data (waking and pre‐bed T) collected in 2009 and 2014 for the Cebu Longitudinal Health and Nutrition Survey (n = 571 men). Results: Fathers with older children tended to have attenuated decline in pre‐bedtime T between 2009 and 2014 compared to men with younger children, after controlling for pairbonding (ß = 1.58, SE = 0.88, P = 0.074). Separated men had higher pre‐bedtime T than pairbonded men, controlling for fatherhood‐related variables (ß = 11.74, SE = 4.33, P = 0.007). Change in T did not significantly differ for men who separated between the two surveys, relative to men who remained pairbonded throughout. Conclusion: We found modest support for the prediction that men experience less of an age‐related drop in T as their youngest child ages, a trend that might strengthen as children age further. We also replicate the finding that separated men have higher T, although longitudinal changes in the hormone were not significantly different in these men. Our data suggest that, of two life history transitions that may predict renewed mating effort, pair bond loss is more strongly endocrine mediated than potential mating effort shifts related to the aging of children. [ABSTRACT FROM AUTHOR]

Because cross-species evidence suggests that high testosterone (T) may interfere with paternal investment, the relationships between men's transition to parenting and changes in their T are of growing interest. Studies of human males suggest that fathers who provide childcare often have lower T than uninvolved fathers, but no studies to date have evaluated how nighttime sleep proximity between fathers and their offspring may affect T. Using data collected in 2005 and 2009 from a sample of men (n = 362; age 26.0 ± 0.3 years in 2009) residing in metropolitan Cebu, Philippines, we evaluated fathers' T based on whether they slept on the same surface as their children (same surface cosleepers), slept on a different surface but in the same room (roomsharers), or slept separately from their children (solitary sleepers). A large majority (92%) of fathers in this sample reported practicing same surface cosleeping. Compared to fathers who slept solitarily, same surface cosleeping fathers had significantly lower evening (PM) T and also showed a greater diurnal decline in T from waking to evening (both p<0.05). Among men who were not fathers at baseline (2005), fathers who were cosleepers at follow-up (2009) experienced a significantly greater longitudinal decline in PM T over the 4.5-year study period (p<0.01) compared to solitary sleeping fathers. Among these same men, baseline T did not predict fathers' sleeping arrangements at follow-up (p>0.2). These results are consistent with previous findings indicating that daytime father-child interaction contributes to lower T among fathers. Our findings specifically suggest that close sleep proximity between fathers and their offspring results in greater longitudinal decreases in T as men transition to fatherhood and lower PM T overall compared to solitary sleeping fathers. [ABSTRACT FROM AUTHOR]

Background: Although maternal infection and inflammation during pregnancy can adversely affect offspring birth weight (BW), whether low grade inflammation in the non-pregnant state predicts BW is unknown. Aim: To evaluate relationships between offspring BW and pro- and anti-inflammatory factors measured in parous but non-pregnant women. Subjects and methods: Data come from 234 parous Filipino females (21.5 ± 0.3 years) in the Cebu Longitudinal Health and Nutrition Survey, a population-based birth cohort in Metropolitan Cebu, Philippines. Pro-inflammatory [Interleukin-6 (IL-6), Interleukin-1 beta (IL-1β), tumour necrosis factor alpha (TNFα), C-reactive protein (CRP)] and anti-inflammatory [Interleukin-10 (IL-10)] factors were measured in fasting plasma when the women were not pregnant, and related to recalled offspring BW. Results: BW in female offspring was lower only among women with high IL-1β. Although pro-inflammatory cytokines did not predict BW in male offspring, women with higher anti-inflammatory IL-10 gave birth to larger males. Women with a combination of low inflammatory (IL-6) and high anti-inflammatory (IL-10) factors (interaction p < 0.104) gave birth to the largest males. Conclusion: Immune factors measured outside of pregnancy predict offspring BW in these young women. Stable variation in inflammatory phenotype could impact the gestational environment of offspring, thus pointing to potential inter-generational effects of chronic low-grade inflammation. [ABSTRACT FROM AUTHOR]