Fatherhood and Psychobiology in the Philippines: Perspectives on Joint Profiles and Longitudinal Changes of Fathers’ Estradiol and Testosterone

Objectives: Research on the psychobiology of partnering and fathering has focused on testosterone (T), oxytocin, and prolactin (PRL) as mechanisms that potentially mediate life history trade-offs related to those roles. Less is known about other hormones that might be responsive to life history transitions and implicated in fathering, such as estradiol (E2). We examined how E2 changed during the transition to marriage and fatherhood, its correlation with fathers’ caregiving, and its joint within-individual production with other hormones (T, PRL). Methods: Data were collected from a total of 913 Filipino men (aged 25.9 years ± 0.3 SD at follow-up) enrolled in a longitudinal cohort study. Morning saliva samples collected at baseline (2005) and follow-up (2009) were assayed for T and E2 (n = 329), dried blood spots from baseline were assayed for PRL. Fathers reported on caregiving in 2009. Results: When compared with men who remained single non-fathers over the study period, men who became married residential fathers experienced larger declines in E2. This effect was non-significant when we controlled for longitudinal changes in T. E2 was not significantly related to fathers’ caregiving, controlling for T. In cross-sectional analyses for PRL, T, and E2, married residential fathers exhibited within-individual profiles of reduced T and elevated PRL, whereas single non-fathers exhibited the opposite profile of elevated T and reduced PRL. Conclusions: Our findings point to the need for future research to consider the mutually regulatory dynamics and/or combinatorial implications of multiple physiological axes acting within individuals to underpin life history trade-offs and behavioral strategies

The Roles of Parents in Shaping Fathering Across Generations in Cebu, Philippines

Objective: This study examined how parental caregiving and parent–child closeness are associated with future fathering among 335 Filipino men who are participants in a long-running birth cohort study. Background Few studies have multidecade longitudinal data to test the pathways through which parenting is transmitted across generations, with most relevant research conducted in the United States, Europe, and other similar settings. The roles of mothers and fathers in shaping their sons’ future parenting is particularly understudied despite fathers having the potential to positively influence child health and development. Method: Participants’ mothers (Generation 1 [G1]) reported on caregiving during Generation 2 (G2) participants’ early life, and the G2 males reported parent–child closeness during adolescence. G2 fathers reported on their own child-care involvement and the salience of care- giving to their parenting identity. We tested whether parent–child closeness moderated the effect of early-life care to predict later-life fathering. Results: G1-G2 closeness moderated the association between G1 parents’ caregiving and G2 fathers’ parenting identity (for both G1 parents) and caregiving time (for G1 fathers only). When the G1-G2 mother–son relationship was not close, there was a negative correlation between G1 maternal care and G2 fathers’ caregiving identity. For G2 men who were close to their fathers, there were positive associations between G1 paternal care and G2 fathers’ caregiving identity and time, respectively. Among G2 men who were not close to their fathers, the slopes relating G1 paternal care to G2 fathers’ care- giving identity and time, respectively, were negative. Conclusion: These findings reflect that developmental experiences with both mothers and fathers are predictive of men’s identity as parents in adulthood and that closeness between fathers and sons moderates whether sons’ paternal care tends to emulate or diverge from their fathers’ caregiving patterns

Exploring the Links between Early Life and Young Adulthood Social Experiences and Men’s Later Life Psychobiology as Fathers

Early life cues of environmental harshness and unpredictability have been hypothesized to influence within-species variation in the timing of life history transitions and the dynamics of reproductive strategies, such as investments in mating and parenting. It is also believed that adolescence is an influential developmental period for male reproductive strategies, with those who achieve greater social and sexual success during that period maintaining faster life history strategies into adulthood. If correct, such early life and post-pubertal experiences could also help shape the psychobiological pathways that mediate reproductive strategies, including the well-documented physiological shifts that occur when some men become parents. Drawing on a large sample of Filipino men (n = 417), we evaluate whether men who experienced cues of harshness or unpredictability in childhood or have earlier ages at sexual debut have elevated testosterone (T) as fathers. We also test whether males who experienced a combination of early life experiences of harshness or unpredictability and had earlier ages of sexual debut during adolescence had the most elevated T as fathers. We found that fathers who experienced early life harshness and who engaged in sex at an earlier age had elevated waking T. Among men transitioning to fatherhood across the 4.5-year follow-up period of this study, those who experienced unpredictability and who engaged in sex at an earlier age showed attenuated declines in waking T between baseline and follow-up. Complementing these findings, we found that fathers who first engaged in sex at later ages had greater acute declines in T when they played with their toddlers. We suggest that these patterns could reflect programming effects of sociosexual experiences during the years following the marked biological transitions that accompany puberty, which occur along with the better-studied effects of earlier life exposures to stressors. Overall, our results support the hypothesis that early life circumstances and social and sexual experiences, from early life to young adulthood, help calibrate physiological axes as key mechanisms coordinating dynamic life history strategies

Sociosexuality, testosterone, and life history status: Prospective associations and longitudinal changes among men in Cebu, Philippines

Sociosexuality is defined as an individual\u27s interest in uncommitted sexual activity and can be measured in terms of both psychological orientations and behavioral expression. In socio-ecological contexts in which adults monogamously partner and cooperate to raise children, individuals with unrestricted sociosexuality are likely to prioritize mating/competition over committed partnering and parenting. Given the importance of mother-father cooperation in the evolutionary past, humans may have the capacity to facultatively and opportunistically downregulate sociosexuality to focus on priorities related to invested partnering and parenting. To date, no prior studies have used longitudinal data to track within-individuals changes in sociosexuality as it relates to such life history transitions. Given the lack of prior longitudinal research in this area, it is likewise unknown what physiological mechanisms might mediate within-individual changes in sociosexuality through time but testosterone is a plausible candidate. To explore these questions, we drew on a large, long-running study of Filipino men (n=288), who were single non-fathers at 25.9 years of age and were followed up 4–5 years later. We found that men with more unrestricted sociosexuality at baseline were more likely to experience relationship dissolution by follow-up, consistent with past work. Compared to men who remained single non-fathers at follow-up, men who became married residential fathers showed shifts towards more restricted global sociosexuality as well as sociosexual behavior. Relative to their own baseline values, married residential fathers also had more restricted sociosexuality in all domains at follow-up. They were the only group for whom this was found. We found theoretically-consistent but modest support for positive correlations between men\u27s testosterone and their sociosexuality, but no evidence that the two change in tandem together through time. Our results suggest that some amount of between-individual differences in sociosexuality are not stable and can facultatively shift alongside other aspects of male reproductive effort

Evolutionary life history theory as an organising framework for cohort studies : insights from the Cebu Longitudinal Health and Nutrition Survey

By tracking a group of individuals through time, cohort studies provide fundamental insights into the developmental time course and causes of health and disease. Evolutionary life history theory seeks to explain patterns of growth, development, reproduction and senescence, and inspires a range of hypotheses that are testable using the longitudinal data from cohort studies. Here we review two decades of life history theory-motivated work conducted in collaboration with the Cebu Longitudinal Health and Nutrition Survey (CLHNS), a birth cohort study that enrolled more than 3000 pregnant women in the Philippines in 1983 and has since followed these women, their offspring and grandoffspring. This work has provided evidence that reproduction carries “costs” to cellular maintenance functions, potentially speeding senescence, and revealed an unusual form of genetic plasticity in which the length of telomeres inherited across generations is influenced by reproductive timing in paternal ancestors. Men in Cebu experience hormonal and behavioural changes in conjunction with changes in relationship and fatherhood status that are consistent with predictions based upon other species that practice bi-parental care. The theoretical expectation that early life cues of mortality or environmental unpredictability will motivate a “fast” life history strategy are confirmed for behavioural components of reproductive decision making, but not for maturational tempo, while our work points to a broader capacity for early life developmental calibration of systems like immunity, reproductive biology and metabolism. Our CLHNS findings illustrate the power of life history theory as an integrative, lifecourse framework to guide longitudinal studies of human populations

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types