Parental incarceration and child physical health outcomes from infancy to adulthood: A critical review and multilevel model of potential pathways.

BACKGROUND: There are currently 2.2 million people incarcerated in U.S. prisons and jails, representing a 500% increase over the past 40 years. An emerging literature suggests the impact of mass incarceration extends beyond the prison, jail, or detention center to the families of incarcerated individuals. Less scholarship has considered consequences of parental incarceration for their children's physical health. METHODS: We conduct a critical review of the literature investigating an association between parental incarceration and children's physical health outcomes from infancy to adulthood. RESULTS: Studies varied substantially in study design, sample composition, and methodological approach. Most studies suggest an association between parental incarceration and adverse physical health outcomes. Evidence is more consistent for outcomes such as infant and child mortality, lower healthcare access, and negative health behaviors and more mixed for measures such as self-reported/general health. CONCLUSION: We propose a multilevel model of mechanistic pathways to stimulate future research on the potential pathways through which parental incarceration could influence children's physical health.

Students of color show health advantages when they attend schools that emphasize the value of diversity.

As the United States becomes more diverse, the ways in which mainstream institutions recognize and address race and ethnicity will be increasingly important. Here, we show that one novel and salient characteristic of an institutional environment, that is, whether a school emphasizes the value of racial and ethnic diversity, predicts better cardiometabolic health among adolescents of color. Using a diverse sample of adolescents who attend more than 100 different schools in predominantly urban locations, we find that when schools emphasize the value of diversity (operationalized as mentioning diversity in their mission statements), students of color, but not white students, have lower values on a composite of five biomarkers of inflammation, have less insulin resistance and compensatory ß-cell activity, and have fewer metabolic syndrome signs and score lower on a continuous metabolic syndrome composite. These results suggest that institutions that emphasize diversity may play an unacknowledged role in protecting the health of people of color and, thus, may be a site for future interventions to reduce health disparities.

The Relationship Between Disproportionate Social Support and Metabolic and Inflammatory Markers: Moderating Role of Socioeconomic Context.

OBJECTIVE: The present study examines the association of disproportionate social support (the relative balance of support given versus received) on metabolic and inflammatory outcomes and whether effects vary by socioeconomic context. METHODS: We enrolled a sample of 307 parental caregivers living with a child with a chronic illness. Parents were assessed on four dimensions of social support: emotional support received, instrumental support received, emotional support given, and instrumental support given. Disproportionate social support was calculated as the difference between support received and support given. Participants provided sociodemographic information, were interviewed about financial stress, and were assessed on metabolic (systolic blood pressure, diastolic blood pressure, total cholesterol, body fat percent, and body mass index) and inflammatory (interleukin 6 and C-reactive protein) outcomes. RESULTS: More disproportionate instrumental and emotional support was associated with higher inflammation (b = 0.10, SE = 0.04, p = .014; b = 0.0.09, SE = 0.05, p = .042, respectively). We observed significant interactions between disproportionate social support and income (b = -0.04, SE = 0.02, p = .021). Parents from lower-income households who gave more emotional support than they received had higher inflammation compared with those from higher-income households. We also observed a significant interaction between disproportionate instrumental support and income (b = 0.04, SE = 0.02, p = .006). Parents from lower-income households who received more instrumental support than they gave had worse metabolic outcomes compared with parents from higher-income households. Parallel interaction patterns were observed using an interview-based measure of financial stress. CONCLUSIONS: These findings show that disproportionate social support has implications for physical health, particularly for caregivers from socioeconomically disadvantaged households.

The costs of high self-control in Black and Latino youth with asthma: Divergence of mental health and inflammatory profiles.

Emerging evidence in psychology suggests a paradox whereby high levels of self-control when striving for academic success among minority youth can have physical health costs. This study tested the skin-deep resilience hypothesis in asthma- whether minority youth who are striving hard to succeed academically experience good psychological outcomes but poor asthma outcomes. Youth physician-diagnosed with asthma (N = 276, M age = 12.99; 155 = White, 121 = Black/Latino) completed interviews about school stress and a self-control questionnaire. Outcomes included mental health (anxiety/depression) and ex-vivo immunologic processes relevant to asthma (lymphocyte Th-1 and Th-2 cytokine production, and sensitivity to glucocorticoid inhibition). Physician contacts were tracked over a one-year follow-up. For minority youth experiencing high levels of school stress, greater self-control was associated with fewer mental health symptoms (beta = -0.20, p < .05), but worse asthma inflammatory profiles (larger Th-1 and Th-2 cytokine responses, lower sensitivity to glucocorticoid inhibition), and more frequent physician contacts during the one-year follow-up (beta's ranging from 0.22 to 0.43, p's < .05). These patterns were not evident in White youth. In minority youth struggling with school, high levels of self-control are detrimental to asthma inflammatory profiles and clinical outcomes. This suggests the need for health monitoring to be incorporated into academic programs to ensure that 'overcoming the odds' does not lead to heightened health risks in minority youth.

SWI/SNF chromatin remodeling regulates alcohol response behaviors in Caenorhabditis elegans and is associated with alcohol dependence in humans.

Alcohol abuse is a widespread and serious problem. Understanding the factors that influence the likelihood of abuse is important for the development of effective therapies. There are both genetic and environmental influences on the development of abuse, but it has been difficult to identify specific liability factors, in part because of both the complex genetic architecture of liability and the influences of environmental stimuli on the expression of that genetic liability. Epigenetic modification of gene expression can underlie both genetic and environmentally sensitive variation in expression, and epigenetic regulation has been implicated in the progression to addiction. Here, we identify a role for the switching defective/sucrose nonfermenting (SWI/SNF) chromatin-remodeling complex in regulating the behavioral response to alcohol in the nematode Caenorhabditis elegans. We found that SWI/SNF components are required in adults for the normal behavioral response to ethanol and that different SWI/SNF complexes regulate different aspects of the acute response to ethanol. We showed that the SWI/SNF subunits SWSN-9 and SWSN-7 are required in neurons and muscle for the development of acute functional tolerance to ethanol. Examination of the members of the SWI/SNF complex for association with a diagnosis of alcohol dependence in a human population identified allelic variation in a member of the SWI/SNF complex, suggesting that variation in the regulation of SWI/SNF targets may influence the propensity to develop abuse disorders. Together, these data strongly implicate the chromatin remodeling associated with SWI/SNF complex members in the behavioral responses to alcohol across phyla.

Neighborhood Social Conditions, Family Relationships, and Childhood Asthma.

BACKGROUND AND OBJECTIVES: Poor neighborhood conditions have established associations with poorer child health, but little is known about protective factors that mitigate the effects of difficult neighborhood conditions. In this study, we tested if positive family relationships can buffer youth who live in dangerous and/or disorderly neighborhoods from poor asthma outcomes. METHODS: A total of 308 youths (aged 9-17) who were physician-diagnosed with asthma and referred from community pediatricians and/or family practitioners participated in this cross-sectional study. Neighborhood conditions around families' home addresses were coded by using Google Street View images. Family relationship quality was determined via youth interviews. Clinical asthma outcomes (asthma symptoms, activity limitations, and forced expiratory volume in 1 second percentile), asthma management behaviors (family response to asthma symptoms and integration of asthma into daily life), and asthma-relevant immunologic processes (lymphocyte T helper 1 and T helper 2 cytokine production and sensitivity to glucocorticoid inhibition) were assessed via questionnaires, interviews, spirometry, and blood draws. RESULTS: Significant interactions were found between neighborhood conditions and family relationship quality (ß = |.11-.15|; P < .05). When neighborhood danger and/or disorder was low, family relationships were not associated with asthma. When neighborhood danger and/or disorder was high, better family relationship quality was associated with fewer asthma symptoms, fewer activity limitations, and higher forced expiratory volume in 1 second percentile. Similar patterns emerged for asthma management behaviors. With immunologic measures, greater neighborhood danger and/or disorder was associated with greater T helper 1 and T helper 2 cytokine production and reduced glucocorticoid sensitivity. CONCLUSIONS: When youth live in dangerous and/or disorderly neighborhoods, high family relationship quality can buffer youth from poor asthma outcomes. Although families may not be able to change their neighborhoods, they may nonetheless be able to facilitate better asthma outcomes in their children through strong family relationships.

Early-life socioeconomic disadvantage, not current, predicts accelerated epigenetic aging of monocytes.

Low socioeconomic status (SES) in early-life and adulthood independently contribute to increased risk for aging-related chronic diseases. One mechanistic hypothesis for these associations involves faster cellular aging of immune cells, which could plausibly contribute to chronic disease pathogenesis by compromising host resistance and/or up-regulating inflammation. However, little is known about the association between life-course SES and cellular aging. The present study examines the association of early-life and current SES with a novel biomarker of cellular aging termed the "epigenetic clock," in monocytes. Additionally, we examine health behaviors and depressive symptoms as potential explanatory pathways. The study involved 335 participants between the ages of 15 and 55 from Vancouver, Canada and surrounding areas. Enrolled participants had to fit into four life-course SES trajectories, corresponding to low-low, low-high, high-low and high-high combinations of early-life (ages 0 to 5) and current SES respectively. Cellular aging of monocytes was measured using Horvath's DNA methylation derived measure of epigenetic age acceleration. Results indicated that socioeconomic disadvantage during early-life, but not later in life, was associated with accelerated epigenetic aging of monocytes. No early-life SES by current SES interaction was detected, suggesting that socioeconomic mobility is unrelated to epigenetic age acceleration. In path analyses, neither current health behaviors nor current depressive symptoms emerged as mediators of the early-life SES effect. These findings suggest socioeconomic disadvantage in early-life is independently predictive of cellular aging of immune cells, with potential implications for aging-related diseases later in life.