Children's empathy moderates the association between perceived interparental conflict and child health.

Interparental conflict is known to negatively impact child well-being, including behavioral and physiological well-being. Children's empathy - that is, vicariously experiencing others' emotions - may increase children's sensitivity to and the biological repercussions of interparental conflict. Although empathy represents a valued trait and is an important part of socioemotional development, its influence on children's physical health is unknown. This study examined whether empathy moderates the association between perceived interparental conflict and both child systemic inflammation and parent-rated overall child health in a sample of children between the ages of seven to nine. Children and their parents participating in the long-term evaluation of the Family Foundations program, a randomized trial of a perinatal preventative intervention, provided data approximately eight years following enrollment into the program. We collected peripheral blood samples via dried blood spots, anthropometric measurements, and child and parent psychosocial questionnaires. Results indicated significant positive main effects of child empathy on both C-reactive protein (CRP; B = 0.26, SE = 0.11, p =.026) and Interleukin-6 (IL-6; B = 0.20, SE = 0.10, p =.045) levels. Further, child affective empathy moderated the associations between perceived interparental conflict and both CRP (B = 0.39, SE = 0.19, p =.050) and parent-reported child health (B = 0.30, SE = 0.13, p =.021), such that greater empathy strengthened the negative associations between interparental conflict and child health. Overall, findings suggests that there may be a biological cost of being more empathic in high-conflict environments and highlight the need for tools to help more empathic children appropriately manage vicarious emotions.

Mean affect and affect variability may interact to predict inflammation.

INTRODUCTION: Individuals with greater affect variability (i.e., moment-to-moment fluctuations possibly reflecting emotional dysregulation) are at risk for greater systemic inflammation, which is associated with cardiovascular disease. Some evidence suggests that affect variability is linked with poorer health indicators only among those with higher average levels of affect, particularly for positive affect (PA), and that associations may be non-linear. The present study sought to examine whether links between both PA and negative affect (NA) variability and inflammation are moderated by average level of affect. METHODS: Participants (N = 300, 50 % female, ages 21-70, 60 % non-Hispanic White, 19 % Hispanic, 15 % non-Hispanic Black) completed a lab assessment and provided a blood sample to measure systemic inflammation (i.e., TNF-α, IL-6, CRP). Affect was collected via a two-day ecological momentary assessment protocol where reports were collected about every 45-min during waking hours. Momentary affect ratings were averaged across both days (i.e., iM), separately for PA and NA, for each participant. Affect variability was calculated as the person-specific SD (i.e., iSD) of affect reports, separately for PA and NA. Linear and quadratic interactions were tested. Models included covariates for sex, race, and body mass index. RESULTS: There were significant interactions between NA iM and NA iSD predicting TNF-α (b = 6.54; p < 0.05) and between PA iM and PA iSD predicting IL-6 (b = 0.45; p < 0.05). Specifically, the association between these affect variability indicators and inflammatory markers were suggestive of a positive association among those with higher average affect but a negative association among those with lower average affect. There was no evidence of non-linear associations between affect and inflammation. DISCUSSION: Incorporating interactive effects between affect variability and average affect may be an important consideration in understanding affective-inflammatory associations.

First-generation College Students Have Greater Systemic Inflammation than Continuing-Generation College Students Following the Initial College Transition: A Brief Report.

BACKGROUND: First-generation college students ("first-gens") are often at a disadvantage socially and academically; whether they are at risk physiologically is unknown despite the well-established link between greater education and better long-term health. PURPOSE: To examine whether first-gens have higher levels of cardiovascular disease (CVD) risk markers relative to continuing-generation college students ("continuing-gens"). METHODS: A panel of CVD risk markers was assessed among 87 emerging adults (41 first-gens) twice over their first year of college. RESULTS: Compared to continuing-gens, first-gens had greater systemic inflammation (composite of averaged z-scores for C-reactive protein and interleukin-6; B = 0.515, SE = 0.171, p = .003) during the fall but not spring semester (p > .05). Associations were independent of family home ownership and childhood adversity, even though first-gens were more likely to live in rental homes and reported riskier home environments. Lower childhood subjective social status (SSS) accounted for greater systemic inflammation among first-gens as evidenced by an indirect effect of college generation status on systemic inflammation through childhood SSS (a1b1 = 0.261, bootstrapped SE = 0.103, 95% boot CI [0.078, 0.482]). There were no differences in metabolic risk and latent virus regulation by college generation status in either semester (p > .10). CONCLUSIONS: This is the first study to find that first-gens have higher levels of systemic inflammation than continuing-gens following the college transition and that childhood SSS may be one explanatory pathway. First-gens may benefit from university resources that address social class differences, which should be provided early on so that first-gens can reap the health-relevant benefits of higher education, at least in the short term.

Assembling a cohort for in-depth, longitudinal assessments of the biological embedding of child maltreatment: Methods, complexities, and lessons learned.

As championed by the work of Ed Zigler, investing in nurturing environments for all children is a chief tenet of primary prevention that will have far-reaching benefits to the health and welfare of all members of society. Children who endure child maltreatment (CM) are among society's most vulnerable. Prospective longitudinal research aimed at a comprehensive understanding of the mechanisms linking CM to subsequent adverse health consequences is needed to improve outcomes and to strengthen causal inference. This paper outlines the methods of the Child Health Study (CHS), a large, state-wide longitudinal cohort of recently maltreated and nonmaltreated youth aged 8-13 who will be assessed every 2 years. The CHS is designed to include in-depth assessments of multiple environmental, behavioral, neural, physiological, and molecular mechanisms through which CM may impact a broad spectrum of youth development, including behavioral and physical health outcomes. In addition to describing the conceptual framework and methods underlying the CHS, we provide information on valuable "lessons learned" in the hopes of supporting future research efforts facing similar challenges. The ultimate goal of this research is demonstrating how policies regarding CM impact the well-being, resilience and recovery of survivors and that they are worthy of large public investment.

Neuroendocrine coordination and youth behavior problems: A review of studies assessing sympathetic nervous system and hypothalamic-pituitary adrenal axis activity using salivary alpha amylase and salivary cortisol.

Externalizing and internalizing behavior problems can have deleterious psychosocial consequences for youth. Both sympathetic nervous system (SNS) and hypothalamic-pituitary adrenal (HPA) axis activity and reactivity may contribute to behavior problems but have largely been studied separately, with inconsistent findings. Because the SNS and HPA axis interact to carry out physiological processes (e.g., responding to stressors), considering SNS and HPA axis activity jointly may elucidate disparate findings. This review discusses studies that simultaneously assessed SNS and HPA axis (re)activity and youth behavior problems using measures of salivary alpha amylase (sAA) and salivary cortisol. Multiple patterns of SNS and HPA axis coordination were associated with problem behaviors, especially when considering individual differences and youth's psychosocial context. Importantly, many study findings may be artifacts of widespread methodological differences. The reviewed studies lay the foundation for future research on neuroendocrine coordination as a contributing factor to youth problem behaviors and some recommendations for future research are discussed.

Prospective Relations Between Prenatal Maternal Cortisol and Child Health Outcomes.

OBJECTIVE: The aim of the study was to investigate prospective, longitudinal associations between maternal prenatal cortisol response to an interpersonal stressor and child health for the subsequent 3 years. METHODS: One hundred twenty-three women expecting their first child provided salivary cortisol samples between 12 and 32 weeks of gestation (M (SD) = 22.4 (4.9) weeks) before and after a videotaped couple conflict discussion with their partner. Mothers reported on overall child health and several indicators of child illness (sick doctor visits, fevers, ear, and respiratory infections) when children were 6 months (n = 114), 1 (n = 116), and 3 (n = 105) years old. Associations between maternal prenatal cortisol reactivity and recovery and later child health at each of the three time points were analyzed using longitudinal regression models. RESULTS: Greater cortisol reactivity in response to the couple conflict discussion was associated with maternal self-report of better overall child health (p = .016, 95% CI = 0.06-1.30, Cohen's f = 0.045) across the study period. Greater cortisol reactivity was also associated with lower incidence rate ratios for maternal reports of sick doctor visits (incidence rate ratio 95% CI = 0.25-0.83, p = .006), fevers (95% CI = 0.25-0.73, p = .002), ear infections (95% CI = 0.25-0.58, p < .001), and respiratory infections (95% CI = 0.08-1.11, p = .073). Cortisol recovery was unrelated to study outcomes (all p's > 0.05). Maternal prenatal depressive symptoms moderated the association between cortisol reactivity and overall child health (p = .034, 95% CI = 0.07-1.87 for interaction term) but no other health outcomes (p's > 0.05). Among women with lower depressive symptoms, cortisol reactivity was not associated with overall child health; among women with higher levels of depressive symptoms, greater cortisol reactivity was associated with better overall child health. CONCLUSIONS: This study provides longitudinal evidence that greater maternal cortisol reactivity to a salient interpersonal stressor during pregnancy is associated with fewer child health problems and better maternal report of overall child health during infancy and into early childhood. TRIAL REGISTRATION: Clinicaltrials.gov ID NCT01901536.

Aspects of the parent-child relationship and parent metabolic outcomes.

Much is known about the effect of parent-child relationships on child health; less is known about how parent-child relationships influence parent health. To assess the association between aspects of the parent-child relationship and parent metabolic outcomes, and whether these associations are moderated by parent gender. Five metabolic outcomes (systolic and diastolic blood pressure, heart rate, total cholesterol and glycated hemoglobin) were assessed among 261 parents (45.83 ± 5.50 years) of an adolescent child (14.57 ± 1.072 years). Parents completed questionnaires assessing their child's hassles and the quality of their days with their child. Parents' perceptions of their child's hassles were associated with parent heart rate (B = 2.954, SE = 1.267, p = 0.021) and cholesterol (B = 0.028, SE = 0.011, p = 0.010), such that greater perceived child hassles were associated with higher heart rate and cholesterol levels, on average. These associations were not moderated by parent gender (all ps > 0.30). Parent report of their day with their child was not associated with parent metabolic outcomes (all ps > 0.20). Parent gender moderated the association between parent report of their day with their child and parent systolic blood pressure (B = 13.861, SE = 6.200, p = 0.026), such that less positive reports were associated with higher blood pressure readings among fathers, but not mothers. This study suggests that parent metabolic health may in part be influenced by aspects of the parent-child relationship.

Is Sexual Abuse a Unique Predictor of Sexual Risk Behaviors, Pregnancy, and Motherhood in Adolescence?

This study tested sexual abuse as a unique predictor of subsequent adolescent sexual behaviors, pregnancy, and motherhood when in company with other types of maltreatment (physical abuse, neglect) and alternative behavioral, family, and contextual risk factors in a prospective, longitudinal study of maltreated (n = 275) and comparison (n = 239) nulliparous females aged 14-19 years old assessed annually through 19 years old. Hierarchical regression was used to disentangle risk factors that account for the associations of maltreatment type on risky sexual behaviors at 19 years old, adolescent pregnancy, and adolescent motherhood. Findings indicate that sexual and physical abuse remain significant predictors of risky sexual behaviors, and that sexual abuse remains a significant predictor of adolescent motherhood when alternative explanatory variables are controlled.

Chronic Family Stress and Adolescent Health: The Moderating Role of Emotion Regulation.

OBJECTIVE: The aim of the study was to assess whether the association between chronic family stress and physiological measures is moderated by emotion regulation strategies in an adolescent sample. METHODS: Chronic family stress was assessed via a semistructured interview and emotion regulation strategies (cognitive reappraisal and suppression) via questionnaire among 261 adolescents (14.57 (1.07) years). Several metabolic (waist-hip ratio, systolic and diastolic blood pressure) and inflammatory markers (basal and stimulated proinflammatory cytokine production in response to bacterial challenge) as well as glucocorticoid sensitivity were assessed. RESULTS: There were no main effects of chronic family stress, cognitive reappraisal, or suppression on physiological measures (all p's > .10). Emotion regulation moderated the association between chronic family stress and physiological measures. As chronic family stress increased, adolescents higher in cognitive reappraisal had smaller waist-hip ratios (B = -.003, SE = .001, p = .015) and lower systolic blood pressure (B = -.303, SE = .143, p = .035), although no moderation was found with respect to inflammatory markers and glucocorticoid sensitivity (all p's > .30). In addition, as chronic family stress increased, adolescents higher in suppression showed evidence of higher stimulated proinflammatory cytokine production (B = .046, SE = .020, p = .021) and lower glucocorticoid sensitivity (B = .051, SE = .021, p = .015), although basal inflammation and metabolic measures were not moderated by suppression (all p's > .50). CONCLUSIONS: This study suggests that the types of emotion regulation strategies used by adolescents may affect the extent to which chronic family stress affects important metabolic and immune processes.

Low-Grade Inflammation and Ambulatory Cortisol in Adolescents: Interaction Between Interviewer-Rated Versus Self-Rated Acute Stress and Chronic Stress.

OBJECTIVE: To determine whether the association between self-rated or interviewer-rated recent acute stress exposures and low-grade inflammation and daily cortisol production in adolescents is moderated by chronic stress ratings. METHODS: Acute and chronic stress exposures were assessed in 261 adolescents aged 13 to 16 years using a semistructured life stress interview. The negative impact of acute stressors was independently rated by both adolescents (self-rated) and interviewers (interviewer-rated). Markers of inflammation (interleukin (IL)-6, IL-1ra, C-reactive protein) were measured from peripheral blood samples obtained via antecubital venipuncture. Participants collected 4 saliva samples at home on each of 6 consecutive days for the analysis of diurnal salivary cortisol profiles. RESULTS: There were no main effects of acute stressors (self- and interviewer-rated) and chronic family or peer stress on adolescent inflammation markers and cortisol (p values > .10). However, the interaction between interviewer-rated acute stress and chronic family stress was significantly associated with adolescent inflammation markers (IL-6, IL-1ra). Specifically, as chronic family stress increased, the association between acute stressor impact (interviewer-rated) and inflammation markers became more positive (IL-6 (B = .054, SE = .023, p = .022); IL-1ra (B = .030, SE = .014, p = .034)). Interactions between self-rated acute stress and chronic family stress were not associated with any biological measures (p values > .10). Interactions between acute stressor impact (both self- and interviewer-rated) and chronic peer stress were also not significantly associated with any biological measures (p values > .05). CONCLUSIONS: Among adolescents, interviewer-based ratings of acute stressor impact may allow for better prediction of health-relevant inflammation markers than adolescents' own ratings.

Social role conflict predicts stimulated cytokine production among men, not women.

OBJECTIVE: To assess whether perceived role conflict is associated with stimulated pro-inflammatory cytokine production and glucocorticoid sensitivity, and whether these associations are moderated by sex. METHODS: 153 healthy adults (aged 45.8±5.5years, 78% female) listed their 3 main social roles and indicated the amount of role conflict they perceived between each pair of social roles. Subsequently, participants underwent blood draws and leukocyte response to microbial challenge and glucocorticoid sensitivity were assessed by incubating whole blood with lipopolysaccharide (LPS) in the presence or absence of hydrocortisone. Stimulated levels of Interleukin (IL)-1ß, IL-6, IL-8, and tumor necrosis factor alpha (TNFα) were measured. RESULTS: Multiple regression analyses controlling for sociodemographics revealed significant sex×role conflict interactions for LPS-stimulated production of IL-1ß, IL-6, and TNFα (all interaction ps<0.05), and a marginal interaction on LPS-stimulated IL-8 production (interaction p<0.10). Greater perceived role conflict was associated with greater pro-inflammatory cytokine production in response to microbial stimulation only among men, not women. There also were significant sex×role conflict interactions with respect to glucocorticoid sensitivity for IL-1ß, IL-6, and TNFα production (all interaction ps<0.05) and a marginal interaction for IL-8 (interaction p<0.10). Greater perceived role conflict was unrelated to glucocorticoid sensitivity among women, but associated with less sensitivity to glucocorticoid signaling among men. CONCLUSIONS: Perceived social role conflict, indicating greater perceived demand across multiple social roles, may take a greater toll on the regulation of inflammatory processes among men compared to women.

Lifetime exposure to traumatic and other stressful life events and hair cortisol in a multi-racial/ethnic sample of pregnant women.

We examined whether lifetime exposure to stressful and traumatic events alters hypothalamic-pituitary-adrenal (HPA) axis functioning, as indexed by hair cortisol, regardless of associated psychopathology, among pregnant women of different racial/ethnic backgrounds. 180 women provided hair samples for measurement of integrated cortisol levels throughout pregnancy and information regarding their lifetime exposure to stressful and traumatic life events. Results indicate that increased lifetime exposure to traumatic events was associated with significantly greater hair cortisol over the course of pregnancy. Similarly, greater lifetime exposure to stressful and traumatic events weighted by reported negative impact (over the previous 12 months) was associated with significantly greater hair cortisol during pregnancy. All analyses controlled for maternal age, education, body mass index (BMI), use of inhaled corticosteroids, race/ethnicity, and post-traumatic stress disorder (PTSD) and depressive symptoms. Following stratification by race/ethnicity, associations between stressful and traumatic life events and hair cortisol were found among Black women only. This is the first study to consider associations between lifetime stress exposures and hair cortisol in a sociodemographically diverse sample of pregnant women. Increased exposure to stressful and traumatic events, independent of PTSD and depressive symptoms, was associated with higher cortisol production, particularly in Black women. Future research should investigate the influence of such increased cortisol exposure on developmental outcomes among offspring.

Mercury and psychosocial stress exposure interact to predict maternal diurnal cortisol during pregnancy.

BACKGROUND: Disrupted maternal prenatal cortisol production influences offspring development. Factors influencing the hypothalamic-pituitary-adrenal axis include social (e.g., stressful life events) and physical/chemical (e.g., toxic metals) pollutants. Mercury (Hg) is a common contaminant of fish and exposure is widespread in the US. No prior study has examined the joint associations of stress and mercury with maternal cortisol profiles in pregnancy. OBJECTIVES: To investigate potential synergistic influences of prenatal stress and Hg exposures on diurnal cortisol in pregnant women. METHODS: Analyses included 732 women (aged 27.4 ± 5.6 years) from a Mexico City pregnancy cohort. Participants collected saliva samples on two consecutive days (mean 19.52 ± 3.00 weeks gestation) and reported life stressors over the past 6 months. Hg was assessed in toe nail clippings collected during pregnancy. RESULTS: There were no main effects of Hg or psychosocial stress exposure on diurnal cortisol (ps > .20) but strong evidence of interaction effects on cortisol slope (interaction B = .006, SE = .003, p = .034) and cortisol at times 1 and 2 (interaction B = -.071, SE = .028, p = .013; B = -.078, SE = .032, p = .014). Women above the median for Hg and psychosocial stress exposure experienced a blunted morning cortisol response compared to women exposed to higher stress but lower Hg levels. CONCLUSIONS: Social and physical environmental factors interact to alter aspects of maternal diurnal cortisol during pregnancy. Research focusing solely on either domain may miss synergistic influences with potentially important consequences to the offspring.

Family chaos and adolescent inflammatory profiles: the moderating role of socioeconomic status.

OBJECTIVE: To test whether family chaos influences adolescents' inflammatory profiles and whether adolescents from low socioeconomic status (SES) environments are at higher risk for experiencing adverse inflammatory profiles from living in chaotic family environments. METHODS: A total of 244 families with an adolescent aged 13 to 16 years participated. Parents completed measures of family SES and family chaos. Both systemic inflammation and stimulated proinflammatory cytokine production in response to bacterial challenge were assessed in adolescents. RESULTS: Our results suggest that SES moderates the detrimental effect of family chaos on systemic inflammation and interleukin-6 (B = -0.010, standard error [SE] = 0.004, p = .026), but not C-reactive protein (B = 0.009, SE = 0.006, p = .11), and on stimulated proinflammatory cytokine production (B = -0.098, SE = 0.044, p = .026) in adolescents, such that a chaotic family environment is positively associated with greater systemic inflammation and greater stimulated proinflammatory cytokine production in adolescents as family SES declines. CONCLUSIONS: These findings indicate that living in chaotic family environments places youth who may be vulnerable based on socioeconomic factors at a potentially higher risk for inflammation-related diseases.

Stress and food allergy: mechanistic considerations.

Recent years have seen a marked increase in food allergy prevalence among children, particularly in Western countries, that cannot be explained by genetic factors alone. This has resulted in an increased effort to identify environmental risk factors underlying food allergies and to understand how these factors may be modified through interventions. Food allergy is an immune-mediated adverse reaction to food. Consequently, considerations of candidate risk factors have begun to focus on environmental influences that perturb the healthy development of the emerging immune system during critical periods of development (eg, prenatally and during early childhood), particularly in the gut. Given that psychosocial stress is known to play an important role in other allergic and inflammatory diseases, such as asthma, its potential role in food allergy is a growing area of research. However, research to date has largely focused on animal studies. This review synthesizes relevant animal research and epidemiological data, providing proof of concept for moderating influences of psychological stress on food allergy outcomes in humans. Pathways that may underlie associations between psychosocial stress and the expression of food allergy are discussed.

Cross-Tissue Comparison of Epigenetic Aging Clocks in Humans.

Epigenetic clocks are a common group of tools used to measure biological aging - the progressive deterioration of cells, tissues and organs. Epigenetic clocks have been trained almost exclusively using blood-based tissues but there is growing interest in estimating epigenetic age using less-invasive oral-based tissues (i.e., buccal or saliva) in both research and commercial settings. However, differentiated cell types across body tissues exhibit unique DNA methylation landscapes and age-related alterations to the DNA methylome. Applying epigenetic clocks derived from blood-based tissues to estimate epigenetic age of oral-based tissues may introduce biases. We tested the within-person comparability of common epigenetic clocks across five tissue types: buccal epithelial, saliva, dry blood spots, buffy coat (i.e., leukocytes), and peripheral blood mononuclear cells. We tested 284 distinct tissue samples from 83 individuals aged 9-70 years. Overall, there were significant within-person differences in epigenetic clock estimates from oral-based versus blood-based tissues, with average differences of almost 30 years observed in some age clocks. In addition, most epigenetic clock estimates of blood-based tissues exhibited low correlation with estimates from oral-based tissues despite controlling for cellular proportions and other technical factors. Our findings indicate that application of blood-derived epigenetic clocks in oral-based tissues may not yield comparable estimates of epigenetic age, highlighting the need for careful consideration of tissue type when estimating epigenetic age.

Cross-tissue comparison of telomere length and quality metrics of DNA among individuals aged 8 to 70 years.

Telomere length (TL) is an important biomarker of cellular aging, yet its links with health outcomes may be complicated by use of different tissues. We evaluated within- and between-individual variability in TL and quality metrics of DNA across five tissues using a cross-sectional dataset ranging from 8 to 70 years (N = 197). DNA was extracted from all tissue cells using the Gentra Puregene DNA Extraction Kit. Absolute TL (aTL) in kilobase pairs was measured in buccal epithelial cells, saliva, dried blood spots (DBS), buffy coat, and peripheral blood mononuclear cells (PBMCs) using qPCR. aTL significantly shortened with age for all tissues except saliva and buffy coat, although buffy coat was available for a restricted age range (8 to 15 years). aTL did not significantly differ across blood-based tissues (DBS, buffy coat, PBMC), which had significantly longer aTL than buccal cells and saliva. Additionally, aTL was significantly correlated for the majority of tissue pairs, with partial Spearman's correlations controlling for age and sex ranging from ⍴ = 0.18 to 0.51. We also measured quality metrics of DNA including integrity, purity, and quantity of extracted DNA from all tissues and explored whether controlling for DNA metrics improved predictions of aTL. We found significant tissue variation: DNA from blood-based tissues had high DNA integrity, more acceptable A260/280 and A260/230 values, and greater extracted DNA concentrations compared to buccal cells and saliva. Longer aTL was associated with lower DNA integrity, higher extracted DNA concentrations, and higher A260/230, particularly for saliva. Model comparisons suggested that incorporation of quality DNA metrics improves models of TL, although relevant metrics vary by tissue. These findings highlight the merits of using blood-based tissues and suggest that incorporation of quality DNA metrics as control variables in population-based studies can improve TL predictions, especially for more variable tissues like buccal and saliva.

Self-rated mental and physical health are prospectively associated with psychosocial and academic adjustment to college.

Objective: To examine prospective associations between physical and mental self-rated health (SRH), college generation status and college adjustment among first-year college students. Participants and methods: Eighty-seven first-year college students (41 first-generation college students) reported their SRH when starting college, and then, reported on psychosocial and academic adjustment and health behaviors midway through each semester. Results: Better physical and mental SRH were associated with better psychosocial adjustment in both semesters and academic adjustment in the fall but were generally not predictive of health behaviors. Specifically, better physical SRH was associated with less loneliness (fall: B = -.192, p = .048; spring: B = -.233, p = .008) and fewer anxiety symptoms in both semesters (fall: B = -.236, p = .011; spring: B = -.210, p = .014) and fewer depressive symptoms (fall: B = -.134, p = .016) and more fall semester credits (B = .965, p = .002). Better mental SRH was associated with greater sense of belonging (fall: B = .317, p < .001; spring: B = .242, p = .009), less loneliness (fall: -.210, p = .008; spring: B = -.181, p = .012), and fewer anxiety symptoms (fall: -.193, p = .011; spring: -.195, p = .006) in both semesters and higher fall semester grade point average (B = .129, p = .032). Independent effects of physical and mental SRH are also discussed. Largely, college generation status did not matter for college adjustment within this sample. Conclusions: Physical and mental SRH when starting college may be important indicators of psychosocial adjustment over the first year and academic adjustment in the fall.

First-Generation College Students, Emotional Support, and Systemic Inflammation Following the College Transition.

PURPOSE: To examine whether emotional support moderates the association between college generation status and concurrent and prospective levels of systemic inflammation during the college transition among a sample of older U.S. adolescents. METHODS: At an undergraduate tertiary institution, 41 first-generation college students (first-gens) and 46 continuing-generation college students (continuing-gens) in their first semester of college reported on basic demographic information and perceived emotional support. They also had their blood drawn midway through both the first and second semester to measure C-reactive protein and interleukin-6. An inflammatory composite for each semester was created by averaging the standardized scores for log-transformed C-reactive protein and interleukin-6. RESULTS: Compared to continuing-gens, first-gens had greater systemic inflammation in the first semester regardless of their level of emotional support (B = 0.515, p = .003). However, emotional support moderated the association between college generation status and prospective systemic inflammation in the second semester (B = -0.525, p = .007) such that first-gens had greater systemic inflammation compared to continuing-gens, but only if they reported lower levels of emotional support (B = 0.826, p = .002). This moderation effect held after further adjusting for systemic inflammation in the first semester (B = -0.374, p = .022). Also discussed are results of secondary analyses examining sources of support. DISCUSSION: Compared to continuing-gens, first-gens had greater systemic inflammation in the first semester irrespective of emotional support, suggesting all first-gens may stand to benefit from college resources provided early in the college transition. Furthermore, first-gens who reported lower levels of emotional support may benefit from additional college resources provided beyond the first semester.

A perinatal coparenting intervention: Effects of a randomized trial on parent cardiometabolic risk and self-reported health.

BACKGROUND: The transition to parenthood is a common yet stressful experience faced by many young and midlife adults, and the risk of cardiometabolic conditions also begins to rise at this time. Consequently, parenthood represents an opportune time to intervene with adults to support their psychological and physical health. PURPOSE: We examined whether the benefits of the Family Foundations program, a perinatal preventative intervention promoting positive coparenting, extend beyond documented mental health and family relationship outcomes to better cardiometabolic risk factors among parents. METHODS: We analyzed data from 183 couples (n = 366 participants) who, eight years prior, were randomly assigned to the 9-session perinatal preventative intervention program or a control condition. We collected dried blood spots to measure C-reactive protein (CRP), interleukin-6 (IL-6), and cholesterol; parents also reported on their self-rated health. RESULTS: Randomization to the intervention condition was associated with lower cholesterol (B=-.081, p = .049). Among parents who demonstrated more negative communication styles at pretest (during pregnancy), the intervention was further associated with better self-rated health (B=.181, p = .018). Participation in the intervention program was also marginally associated with lower CRP (B=-.261, p = .077), particularly among mothers (B=-.428, p = .076). CONCLUSIONS: These findings indicate that coparenting-focused interventions, such as Family Foundations, can lead to benefits beyond psychosocial and behavioral outcomes, and suggest that Family Foundations may improve parents' longer-term physical health, with potentially more benefits among couples who demonstrated more negative communication styles during pregnancy.