The balance of giving versus receiving social support and all-cause mortality in a US national sample.

While numerous studies exist on the benefits of social support (both receiving and giving), little research exists on how the balance between the support that individuals regularly give versus that which they receive from others relates to physical health. In a US national sample of 6,325 adults from the National Survey of Midlife Development in the United States, participants were assessed at baseline on hours of social support given and received on a monthly basis, with all-cause mortality data collected from the National Death Index over a 23-y follow-up period. Participants who were relatively balanced in the support they gave compared to what they received had a lower risk of all-cause mortality than those who either disproportionately received support from others (e.g., received more hours of support than they gave each month) or disproportionately gave support to others (e.g., gave many more hours of support a month than they received). These findings applied to instrumental social support (e.g., help with transportation, childcare). Additionally, participants who gave a moderate amount of instrumental social support had a lower risk of all-cause mortality than those who either gave very little support or those who gave a lot of support to others. Associations were evident over and above demographic, medical, mental health, and health behavior covariates. Although results are correlational, one interpretation is that promoting a balance, in terms of the support that individuals regularly give relative to what they receive in their social relationships, may not only help to strengthen the social fabric of society but may also have potential physical health benefits.

Prospective associations between neighborhood violence and monocyte pro-inflammatory transcriptional activity in children.

Individuals exposed to persistent neighborhood violence are at increased risk for developing mental and physical health problems across the lifespan. The biological mechanisms underlying this phenomenon are not well understood. Thus, we examined the relationship between children's exposure to neighborhood violence and inflammatory activity, a process involved in the pathogenesis of multiple health problems. 236 children from the Chicago area participated in a two-year longitudinal study (mean age at baseline, 13.9 years; 67% female; 39% White, 34% Black, 33% Hispanic). Neighborhood violence was measured as the homicide frequency in a child's Census block group in the five years before study entry. Fasting blood was drawn at study entry and two years later (in eighth and tenth grade). The blood was used to quantify protein biomarkers of systemic inflammatory activity and perform genome-wide expression profiling of isolated monocytes. Neighborhood violence was associated with higher systemic inflammatory activity at both assessments. It also was associated with a monocyte transcriptional profile indicative of increased signaling along the nuclear factor-kappa B (NF-κB) and activator protein 1 (AP-1) control pathways, which are key orchestrators of pro-inflammatory effector functions. Neighborhood violence also was associated with transcriptional indications of higher beta-adrenergic and lower glucocorticoid signaling, which could function as neuroendocrine conduits linking threatening experiences with inflammatory activity. Neighborhood violence was not associated with two-year changes in protein biomarkers, although it did presage a transcriptional profile indicative of increasing AP-1 and declining glucocorticoid signaling over follow-up. Collectively, these observations highlight cellular and molecular pathways that could underlie health risks associated with neighborhood violence.

Out of the Laboratory and Into the Field: Validation of Portable Cell Culture Protocols.

OBJECTIVE: Field-based research on inflammation and health is typically limited to baseline measures of circulating cytokines or acute-phase proteins, whereas laboratory-based studies can pursue a more dynamic approach with ex vivo cell culture methods. The laboratory infrastructure required for culturing leukocytes limits application in community-based settings, which in turn limits scientific understandings of how psychosocial, behavioral, and contextual factors influence the regulation of inflammation. We aim to address this gap by validating two "field-friendly" cell culture protocols, one using a small volume of venous whole blood and another using finger-stick capillary whole blood. METHODS: We evaluated the performance of both protocols against a standard laboratory-based protocol using matched venous and capillary blood samples collected from young adults (n = 24). Samples were incubated with lipopolysaccharide and hydrocortisone, and the production of proinflammatory cytokines interleukin 1ß, interleukin 6, and tumor necrosis factor α was measured in response. RESULTS: Comparisons indicate a high level of agreement in responses across the protocols and culture conditions. The overall correlation in results was 0.88 between the standard and small-volume protocols and 0.86 between the standard and capillary blood protocols. Repeatability for the small-volume and capillary blood protocols was high, with mean coefficients of variation across five replicates of 6.2% and 5.4%, respectively. CONCLUSIONS: These results demonstrate the feasibility of culturing cells and quantifying the inflammatory response to challenge outside the laboratory, with a wide range of potential applications in biobehavioral research in community-based and remote field settings.

Developing a neurobehavioral animal model of poverty: Drawing cross-species connections between environments of scarcity-adversity, parenting quality, and infant outcome.

Children reared in impoverished environments are at risk for enduring psychological and physical health problems. Mechanisms by which poverty affects development, however, remain unclear. To explore one potential mechanism of poverty's impact on social-emotional and cognitive development, an experimental examination of a rodent model of scarcity-adversity was conducted and compared to results from a longitudinal study of human infants and families followed from birth (N = 1,292) who faced high levels of poverty-related scarcity-adversity. Cross-species results supported the hypothesis that altered caregiving is one pathway by which poverty adversely impacts development. Rodent mothers assigned to the scarcity-adversity condition exhibited decreased sensitive parenting and increased negative parenting relative to mothers assigned to the control condition. Furthermore, scarcity-adversity reared pups exhibited decreased developmental competence as indicated by disrupted nipple attachment, distress vocalization when in physical contact with an anesthetized mother, and reduced preference for maternal odor with corresponding changes in brain activation. Human results indicated that scarcity-adversity was inversely correlated with sensitive parenting and positively correlated with negative parenting, and that parenting fully mediated the association of poverty-related risk with infant indicators of developmental competence. Findings are discussed from the perspective of the usefulness of bidirectional-translational research to inform interventions for at-risk families.

Salivary cortisol and cognitive development in infants from low-income communities.

Early stress exposure is proposed to have significant lasting effects on cognitive development. The glucocorticoid hormone cortisol, a product of the hypothalamic-pituitary-adrenal (HPA) axis, is a particular focus of research, however, the majority of past research has been based on studies of older children and adults. Evidence linking cortisol levels in infancy with cognitive development is lacking. In a large cohort sample of infants (N = 1091) oversampled for psychosocial risk, we tested whether basal cortisol levels and cortisol reactivity to emotional stressors administered at 7 and 15 months of age were associated with cognitive development measured at 15 months. Cognitive development was measured using the Mental Development Index of the Bayley Scales of Infant Development. Multiple regression analyses indicated that basal cortisol levels at 15 months, and to a lesser extent at seven months, were inversely associated with infant cognitive development after adjusting for psychosocial and obstetric risk. The findings provide some of the first evidence that HPA axis activity in infancy is associated with early cognitive development.

Exploring longitudinal associations between neighborhood disadvantage and cortisol levels in early childhood.

Children who grow up in poverty are more likely to experience chronic stressors that generate "wear" on stress regulatory systems including the hypothalamus-pituitary-adrenal (HPA) axis. This can have long-term consequences for health and well-being. Prior research has examined the role of proximal family and home contributions to HPA axis functioning. However, there is evidence to suggest that more distal levels of context, including neighborhoods, also matter. Prior evidence has primarily focused on adolescents and adults, with little evidence linking the neighborhood context with HPA activity in infancy and toddlerhood. We tested whether neighborhood disadvantage (indexed by US Census data) was associated with basal salivary cortisol levels at 7, 15, and 24 months of child age in a large sample of families (N = 1,292) residing in predominately low-income and rural communities in the United States. Multilevel models indicated that neighborhood disadvantage was positively associated with salivary cortisol levels and that this effect emerged across time. This effect was moderated by the race/ethnicity of children such that the association was only observed in White children in our sample. Findings provide preliminary evidence that the neighborhood context is associated with stress regulation during toddlerhood, elucidating a need for future work to address possible mechanisms.

Maternal-child adrenocortical attunement in early childhood: continuity and change.

This study evaluated continuity and change in maternal-child hypothalamic-pituitary-adrenal axis attunement in early childhood. Participants were drawn from a prospective study of 1,292 mother-child dyads, which were racially diverse, predominantly low-income, and non-urban. Child focused stress tasks designed to elicit anger, fear, and frustration were administered during early infancy, later infancy, and toddlerhood. Mothers' and children's saliva samples (later assayed for cortisol) were collected before and after the tasks. The strength of mother-child adrenocortical attunement was conserved across infancy and toddlerhood. The magnitude of maternal-child adrenocortical attunement decreased in response to the child-focused stress tasks. Maternal sensitivity and the child's task-related emotional reactivity moderated adrenocortical attunement across the task, with greater maternal sensitivity during a free-play, and lower levels of child emotional reactivity during the stress tasks, stabilizing attunement from pre- to post-task levels. The findings advance our understanding of individual differences in the social regulation of adrenocortical activity in early childhood.

Interpersonal violence exposure and inflammation during adolescence and young adulthood.

Exposure to violence increases young peoples' risk of developing mental and physical health problems. Chronic stress-related upregulation of innate immune system activity and the development of low-grade inflammation may partially underlie this health risk. However, much of the previous research has been limited to cross-sectional studies utilizing between-person analytic designs, susceptible to confounding by unmeasured factors. In this six-wave panel study of N=157 female adolescents and young adults, we tested within-person associations between interpersonal violence exposure and multiple measures of inflammatory activity. Ex vivo culture studies suggested that participants' immune cells were more reactive to microbial stimulation and less sensitive to inhibition by glucocorticoids after violence. Numbers of circulating monocyte cells increased after violence, but serum levels of interleukin-6 and c-reactive protein did not. Findings from this within-person analysis suggest that violence exposure up-regulates innate immune system activity during adolescence and young adulthood in ways that may increase mental and physical health risk.

Toward a neuroscience of interactive parent-infant dyad empathy.

In accord with social neuroscience's progression to include interactive experimental paradigms, parents' brains have been activated by emotionally charged infant stimuli - especially of their own infant - including baby cry and picture. More recent research includes the use of brief video clips and opportunities for maternal response. Among brain systems important to parenting are those involved in empathy. This research may inform recent studies of decreased societal empathy, offer mechanisms and solutions.

Parental brain and socioeconomic epigenetic effects in human development.

Critically significant parental effects in behavioral genetics may be partly understood as a consequence of maternal brain structure and function of caregiving systems recently studied in humans as well as rodents. Key parental brain areas regulate emotions, motivation/reward, and decision making, as well as more complex social-cognitive circuits. Additional key environmental factors must include socioeconomic status and paternal brain physiology. These have implications for developmental and evolutionary biology as well as public policy.

Childhood Violence Exposure, Inflammation, and Cardiometabolic Health.

Exposure to interpersonal violence during childhood, a severe and often traumatic form of social stress, is an enduring problem that an emerging body of work suggests may be relevant to cardiometabolic health and the progression of cardiovascular disease (CVD) across the life course. Less is known about this association causally, and consequently, the biological mechanisms that may confer risk for, and resilience to, poor health outcomes in the aftermath of violence are not well understood. Drawing on recent theoretical insights and empirical research in both humans and non-human animal models, the current paper articulates a hypothesis for one way that childhood violence could get "under the skin" to influence CVD. Based on this emerging literature, one plausible way that childhood violence exposure could increase susceptibility to CVD in later life is by sensitizing stress-response neurobiology and immune processes that regulate and promote inflammation, which is a key pathogenic mechanism in CVD. This is inherently a developmental process that begins in early life and that unfolds across the life course, although less is known about the specific mechanisms through which this occurs. The goal of this paper is to articulate some of these plausible mechanisms and to suggest areas for future research that aims to reduce the burden of disease among individuals who are exposed to violence.

Association of Wealth With Longevity in US Adults at Midlife.

Importance: Wealthy adults tend to live longer than those with less wealth. However, a challenge in this area of research has been the reduction of potential confounding by factors associated with the early environment and heritable traits, which could simultaneously affect socioeconomic circumstances in adulthood and health across the life course. Objective: To identify the association between net worth at midlife and subsequent all-cause mortality in individuals as well as within siblings and twin pairs. Design Setting and Participants: This cohort study conducted a series of analyses using data from the Midlife in the United States (MIDUS) study, an ongoing national study of health and aging. The sample included adults (unrelated individuals, full siblings, and dizygotic and monozygotic twins) aged 20 to 75 years, who participated in wave 1 of the MIDUS study, which occurred from 1994 to 1996. The analyses were conducted between November 16, 2019, and May 18, 2021. Exposures: Self-reported net worth (total financial assets minus liabilities) at midlife (the middle years of life). Main Outcomes and Measures: All-cause mortality was tracked over nearly 24 years of follow-up, with a censor date of October 31, 2018. Survival models tested the association between net worth and all-cause mortality. Discordant sibling and twin analyses compared longevity within siblings and twin pairs who, given their shared early experiences and genetic backgrounds, were matched on these factors. Results: The full sample comprised 5414 participants, who had a mean (SD) age of 46.7 (12.7) years and included 2766 women (51.1%). Higher net worth was associated with lower mortality risk (hazard ratio [HR], 0.95; 95% CI, 0.94-0.97; P < .001). Among siblings and twin pairs specifically (n = 2490), a similar within-family association was observed between higher net worth and lower mortality (HR, 0.94; 95% CI, 0.91-0.97; P = .001), suggesting that the sibling or twin with more wealth tended to live longer than their co-sibling or co-twin with less wealth. When separate estimates were performed for the subsamples of siblings (HR, 0.94; 95% CI, 0.90-0.97; P = .002), dizygotic twins (HR, 0.94; 95% CI, 0.86-1.02; P = .19), and monozygotic twins (HR, 0.95; 95% CI, 0.87-1.04; P = .34), the within-family estimates of the net worth-mortality association were similar, although the precision of estimates was reduced among twins. Conclusions and Relevance: This cohort study found that wealth accumulation at midlife was associated with longevity in US adults. Discordant sibling analyses suggested that this association is unlikely to be simply an artifact of early experiences or heritable characteristics shared by families.

Resting-State Functional Connectivity of the Central Executive Network Moderates the Relationship Between Neighborhood Violence and Proinflammatory Phenotype in Children.

BACKGROUND: Neighborhood violence increases children's risk for a variety of health problems. Yet, little is known about biological pathways involved or neural mechanisms that might render children more or less vulnerable. Here, we address these questions by considering whether neighborhood violence is associated with the expression of a proinflammatory phenotype and whether this relationship is moderated by resting-state functional connectivity (rsFC) of the central executive network (CEN). METHODS: The study involved 217 children (13.9 years old; 66.4% female; 36.9% Black; 30.9% Latinx), enrolled in eighth grade and reassessed 2 years later. At time 1, geocoding was used to estimate murder frequency in children's neighborhoods, and functional magnetic resonance imaging was used to characterize CEN rsFC. At both visits, children gave antecubital blood for ex vivo studies, where leukocytes were incubated with stimulators and inhibitors of inflammation, and cytokine production was measured. RESULTS: Consistent with our hypotheses, the relationship between neighborhood murder and inflammatory activity was moderated by CEN rsFC. Among children with lower rsFC, neighborhood violence covaried with a proinflammatory phenotype, reflected in larger cytokine responses to triggering stimuli and lower sensitivity to inhibitory agents. These associations were generally not apparent for children with higher rsFC, although occasionally they ran in the opposite direction. The same patterns were apparent 2 years later. CONCLUSIONS: These results advance the understanding of neighborhood violence and its relationship with processes involved in the initiation and resolution of inflammation. They also deepen understanding of variability in children's immunologic responses to stress and suggest that the CEN may be a neurobiological contributor to resilience.

Community violence and cellular and cytokine indicators of inflammation in adolescents.

Neighborhood violence is associated with a range of health consequences but little is known about the biological processes involved. Research in disease pathogenesis has identified low-grade inflammation as a process that, beginning in the first decades of life, is both induced by chronic stress and a contributor to multiple cardiometabolic diseases that present throughout the lifecourse. Previous research has examined whether neighborhood violence is associated with inflammatory biomarkers, but has been limited to cytokine indicators of inflammation. In a sample of adolescents (n = 203) residing in Chicago, we tested cross-sectional associations between neighborhood violence and cellular and cytokine indicators of inflammation. Neighborhood-level violence was measured in multiple ways (as murder rates of Census block groups and as the sum of homicides within 1 and ½ mile zones) in the areas surrounding where youth lived and attended school. At the individual level, violence exposure was measured by self-report (direct victimization, witnessing violence, and/or victimization of family or friends in the past year). Adolescents residing in high-violence neighborhoods evidenced higher numbers of pro-inflammatory classical (CD14++CD16-) monocytes relative to those in less violent neighborhoods. In contrast, neighborhood-level violence was not consistently associated with cytokine levels across different model specifications. Self-reported violence exposure was also not consistently associated with inflammatory biomarkers. Neighborhood-level violence and self-reported violence exposure interacted, such that the positive association between neighborhood-level violence and classical monocytes was observed only among adolescents who reported being exposed to violence. Associations were largely specific to the neighborhoods in which youth lived as opposed to those in which they attended school. Findings provide the first evidence that youth residing in high-violence neighborhoods show mobilization of classical monocytes, suggesting a pro-inflammatory mechanism through which contextual stressors such as neighborhood violence may compromise health.

Parenting in poverty: Attention bias and anxiety interact to predict parents' perceptions of daily parenting hassles.

Research has long acknowledged the centrality of parents' subjective experiences in the caregiving role for the organization of parenting behaviors and family functioning. Recent scientific advances in cognitive process models and in the neurobiology of parenting indicate that parenting is shaped in part by conscious and nonconscious cognitive processes. This study extends a growing literature on neurocognitive models of parenting by exploring the extent to which attention processes in parents operate independently and interactively with intrapsychic processes, proximal interpersonal stressors, and the larger socioeconomic context to predict perceptions of parenting hassles in primarily low-income Latino/a parents of young children living in urban areas of concentrated disadvantage (N = 185). Analyses indicated that parent reports of anxiety, intimate partner violence, and perceptions of financial hardship each uniquely predicted parents' perceptions of daily parenting hassles. Parents' attentional bias toward threat interacted with anxiety symptoms such that parents experiencing high levels of attention bias toward threat in combination with high levels of anxiety reported significantly more daily parenting hassles. Findings from the current study provide insight into the ways in which neurocognitive processes affect one aspect of parenting, with implications for programs and policies designed to support parenting for families in poverty. (PsycINFO Database Record

Psychobiological influences on maternal sensitivity in the context of adversity.

This study evaluated prospective longitudinal relations among an index of poverty-related cumulative risk, maternal salivary cortisol, child negative affect, and maternal sensitivity across the first 2 postpartum years. Participants included 1,180 biological mothers residing in rural and predominantly low-income communities in the United States. Multilevel growth curve analyses indicated that an index of cumulative risk was positively associated with maternal cortisol across the postpartum (study visits occurring at approximately 7, 15, and 24 months postpartum) over and above effects for African American ethnicity, time of day of saliva collection, age, parity status, having given birth to another child, contraceptive use, tobacco smoking, body mass index, and breastfeeding. Consistent with a psychobiological theory of mothering, maternal salivary cortisol was negatively associated with maternal sensitivity observed during parent-child interactions across the first 2 postpartum years over and above effects for poverty-related cumulative risk, child negative affect, as well as a large number of covariates associated with cortisol and maternal sensitivity. Child negative affect expressed during parent-child interactions was negatively associated with observed maternal sensitivity at late (24 months) but not early time points of observation (7 months) and cumulative risk was negatively associated with maternal sensitivity across the postpartum and this effect strengthened over time. Results advance our understanding of the dynamic, transactional, and psychobiological influences on parental caregiving behaviors across the first 2 postpartum years. (PsycINFO Database Record

Poverty and language development: roles of parenting and stress.

Socioeconomic status affects a variety of mental and physical health outcomes, such as language development. Indeed, with poverty, disparities in the development of language processing are arguably among the most consistently found- with decreases in vocabulary, phonological awareness, and syntax at many different developmental stages. In this review, after considering basic brain systems affected by low socioeconomic status that are important for language development and related peripartum issues, we focus on two theoretical models that link poverty with the brain systems affected in language problems. The family stress model connects poverty with parental emotional distress that affects parenting, whereas the parental investment model involves a focus on basic needs that affects children's language. Understanding the mechanisms through which poverty affects the brain, parenting behaviors and language development may have implications for identification and treatment of individuals as well as social policy.

Parenting and Beyond: Common Neurocircuits Underlying Parental and Altruistic Caregiving.

Interpersonal relationships constitute the foundation on which human society is based. The infant-caregiver bond is the earliest and most influential of these relationships. Driven by evolutionary pressure for survival, parents feel compelled to provide care to their biological offspring. However, compassion for non-kin is also ubiquitous in human societies, motivating individuals to suppress their own self-interests to promote the well-being of non-kin members of the society. We argue that the process of early kinship-selective parental care provides the foundation for non-exclusive altruism via the activation of a general Caregiving System that regulates compassion in any of its forms. We propose a tripartite structure of this system that includes (1) the perception of need in another, (2) a caring motivational or feeling state, and (3) the delivery of a helping response to the individual in need. Findings from human and animal research point to specific neurobiological mechanisms including activation of the insula and the secretion of oxytocin that support the adaptive functioning of this Caregiving System.