Inequitable Housing Practices and Youth Internalizing Symptoms: Mediation Via Perceptions of Neighborhood Cohesion

Disordered urban environments negatively impact mental health symptoms and disorders. While many aspects of the built environment have been studied, one influence may come from inequitable, discriminatory housing practices such as redlining, blockbusting, and gentrification. The patterns of disinvestment and reinvestment that follow may be an underlying mechanism predicting poor mental health. In this study, we examine pathways between such practices and internalizing symptoms (i.e., anxiety and depression) among a sample of African American youth in Baltimore, Maryland, considering moderation and mediation pathways including neighborhood social cohesion and sex. In our direct models, the inequitable housing practices were not significant predictors of social cohesion. In our sex moderation model, however, we find negative influences on social cohesion: for girls from gentrification, and for boys from blockbusting. Our moderated mediation model shows that girls in gentrifying neighborhoods who experience lower social cohesion have higher levels of internalizing symptoms. Likewise for boys, living in a formerly blockbusted neighborhood generates poorer social cohesion, which in turn drives higher rates of internalizing symptoms. A key implication of this work is that, in addition to standard measures of the contemporary built environment, considering other invisible patterns related to discriminatory and inequitable housing practices is important in understanding the types of neighborhoods where anxiety and depression are more prevalent. And while some recent work has discussed the importance of considering phenomena like redlining in considering long‐term trajectories of neighborhoods, other patterns such as blockbusting and gentrification may be equally important

Inequitable Housing Practices and Youth Internalizing Symptoms: Mediation Via Perceptions of Neighborhood Cohesion

Disordered urban environments negatively impact mental health symptoms and disorders. While many aspects of the built environment have been studied, one influence may come from inequitable, discriminatory housing practices such as redlining, blockbusting, and gentrification. The patterns of disinvestment and reinvestment that follow may be an underlying mechanism predicting poor mental health. In this study, we examine pathways between such practices and internalizing symptoms (i.e., anxiety and depression) among a sample of African American youth in Baltimore, Maryland, considering moderation and mediation pathways including neighborhood social cohesion and sex. In our direct models, the inequitable housing practices were not significant predictors of social cohesion. In our sex moderation model, however, we find negative influences on social cohesion: for girls from gentrification, and for boys from blockbusting. Our moderated mediation model shows that girls in gentrifying neighborhoods who experience lower social cohesion have higher levels of internalizing symptoms. Likewise for boys, living in a formerly blockbusted neighborhood generates poorer social cohesion, which in turn drives higher rates of internalizing symptoms. A key implication of this work is that, in addition to standard measures of the contemporary built environment, considering other invisible patterns related to discriminatory and inequitable housing practices is important in understanding the types of neighborhoods where anxiety and depression are more prevalent. And while some recent work has discussed the importance of considering phenomena like redlining in considering long-term trajectories of neighborhoods, other patterns such as blockbusting and gentrification may be equally important

Prenatal Protein Malnutrition Produces Resistance to Distraction Similar to Noradrenergic Deafferentation of the Prelimbic Cortex in a Sustained Attention Task

Exposure to malnutrition early in development increases likelihood of neuropsychiatric disorders, affective processing disorders, and attentional problems later in life. Many of these impairments are hypothesized to arise from impaired development of the prefrontal cortex. The current experiments examine the impact of prenatal malnutrition on the noradrenergic and cholinergic axons in the prefrontal cortex to determine if these changes contribute to the attentional deficits seen in prenatal protein malnourished rats (6% casein vs. 25% casein). Because prenatally malnourished animals had significant decreases in noradrenergic fibers in the prelimbic cortex with spared innervation in the anterior cingulate cortex and showed no changes in acetylcholine innervation of the prefrontal cortex, we compared deficits produced by malnutrition to those produced in adult rats by noradrenergic lesions of the prelimbic cortex. All animals were able to perform the baseline sustained attention task accurately. However, with the addition of visual distractors to the sustained attention task, animals that were prenatally malnourished and those that were noradrenergically lesioned showed cognitive rigidity, i.e., were less distractible than control animals. All groups showed similar changes in behavior when exposed to withholding reinforcement, suggesting specific attentional impairments rather than global difficulties in understanding response rules, bottom-up perceptual problems, or cognitive impairments secondary to dysfunction in sensitivity to reinforcement contingencies. These data suggest that prenatal protein malnutrition leads to deficits in noradrenergic innervation of the prelimbic cortex associated with cognitive rigidity

Multi-ancestry genome-wide association study of major depression aids locus discovery, fine mapping, gene prioritization and causal inference

Most genome-wide association studies (GWAS) of major depression (MD) have been conducted in samples of European ancestry. Here we report a multi-ancestry GWAS of MD, adding data from 21 cohorts with 88,316 MD cases and 902,757 controls to previously reported data. This analysis used a range of measures to define MD and included samples of African (36% of effective sample size), East Asian (26%) and South Asian (6%) ancestry and Hispanic/Latin American participants (32%). The multi-ancestry GWAS identified 53 significantly associated novel loci. For loci from GWAS in European ancestry samples, fewer than expected were transferable to other ancestry groups. Fine mapping benefited from additional sample diversity. A transcriptome-wide association study identified 205 significantly associated novel genes. These findings suggest that, for MD, increasing ancestral and global diversity in genetic studies may be particularly important to ensure discovery of core genes and inform about transferability of findings.</p

Social vulnerability, COVID-19 impact, and decision making among adults in a low-resource community

Socially vulnerable individuals, including those with greater exposure to adversity and social instability, are at greater risk for a variety of negative outcomes following exposure to public health crises. One hypothesized mechanism linking social vulnerability to poor health outcomes is delay discounting, the behavioral tendency to select smaller immediately available rewards relative to larger delayed rewards. However, little research has examined the impact of real-world disease outbreaks, such as the COVID-19 pandemic, on the relation between social vulnerability and delay discounting. This study examined whether the severity of COVID-19 impact moderated the association between social vulnerability and delay discounting in a diverse sample of 72 human adults (M(age) = 42.4; 69% Black; 87% female) drawn from two low-resource urban areas. Contrary to hypotheses, results indicated that exposure to more severe COVID-19 impacts did not affect decision making among individuals with higher levels of social vulnerability. Conversely, findings suggest that individuals with lower levels of social vulnerability who reported more significant impacts of COVID-19 evidenced a greater tendency to select larger, delayed rewards relative to individuals with greater social vulnerability. Findings suggest the recent pandemic may influence the relation between social vulnerability and behavioral processes underlying health decision-making

Designing and Validating a Novel Method for Assessing Delay Discounting Associated With Health Behaviors: Ecological Momentary Assessment Study

BackgroundDelay discounting quantifies an individual’s preference for smaller, short-term rewards over larger, long-term rewards and represents a transdiagnostic factor associated with numerous adverse health outcomes. Rather than a fixed trait, delay discounting may vary over time and place, influenced by individual and contextual factors. Continuous, real-time measurement could inform adaptive interventions for various health conditions. ObjectiveThe goals of this paper are 2-fold. First, we present and validate a novel, short, ecological momentary assessment (EMA)–based delay discounting scale we developed. Second, we assess this tool’s ability to reproduce known associations between delay discounting and health behaviors (ie, substance use and craving) using a convenience-based sample. MethodsParticipants (N=97) were adults (age range 18-71 years), recruited on social media. In phase 1, data were collected on participant sociodemographic characteristics, and delay discounting was evaluated via the traditional Monetary Choice Questionnaire (MCQ) and our novel method (ie, 7-item time-selection and 7-item monetary-selection scales). During phase 2 (approximately 6 months later), participants completed the MCQ, our novel delay discounting measures, and health outcomes questions. The correlations between our method and the traditional MCQ within and across phases were examined. For scale reduction, a random number of items were iteratively selected, and the correlation between the full and random scales was assessed. We then examined the association between our time- and monetary-selection scales assessed during phase 2 and the percentage of assessments that participants endorsed using or craving alcohol, tobacco, or cannabis. ResultsIn total, 6 of the 7 individual time-selection items were highly correlated with the full scale (r>0.89). Both time-selection (r=0.71; P0.94). Greater delay discounting measured via the time-selection measure (adjusted mean difference=5.89, 95% CI 1.99-9.79), but not the monetary-selection scale (adjusted mean difference=–0.62, 95% CI –3.57 to 2.32), was associated with more past-hour tobacco use endorsement in follow-up surveys. ConclusionsThis study evaluated a novel EMA-based scale’s ability to validly and reliably assess delay discounting. By measuring delay discounting with fewer items and in situ via EMA in natural environments, researchers may be better able to identify individuals at risk for poor health outcomes

Testing gene by community disadvantage moderation of sexual health outcomes among urban women.

We examined whether the interplay between community disadvantage and a conduct disorder polygenic risk score (CD PRS) was associated with sexual health outcomes among urban women. Participants (N = 511; 75.5% African American) were originally recruited to participate in a school-based intervention and were followed into adulthood. Community disadvantage was calculated using census data when participants were in first grade. At age 20, blood or saliva samples were collected and participants reported on their condom use, sexual partners, and sexually transmitted infections. A CD PRS was created based on a genome-wide association study conducted by Dick et al. [2010]. Higher levels of community disadvantage was associated with greater sexually transmitted infections among women with a higher CD PRS. Implications of the study findings are discussed

Shared Genetic Etiology between Cortical Brain Morphology and Tobacco, Alcohol, and Cannabis Use

Genome-wide association studies (GWAS) have identified genetic variants associated with brain morphology and substance use behaviors (SUB). However, the genetic overlap between brain structure and SUB has not been well characterized. We leveraged GWAS summary data of 71 brain imaging measures and alcohol, tobacco, and cannabis use to investigate their genetic overlap using linkage disequilibrium score regression. We used genomic structural equation modeling to model a "common SUB genetic factor"and investigated its genetic overlap with brain structure. Furthermore, we estimated SUB polygenic risk scores (PRS) and examined whether they predicted brain imaging traits using the Adolescent Behavior and Cognitive Development (ABCD) study. We identified 8 significant negative genetic correlations, including between (1) alcoholic drinks per week and average cortical thickness, and (2) intracranial volume with age of smoking initiation. We observed 5 positive genetic correlations, including those between (1) insula surface area and lifetime cannabis use, and (2) the common SUB genetic factor and pericalcarine surface area. SUB PRS were associated with brain structure variation in ABCD. Our findings highlight a shared genetic etiology between cortical brain morphology and SUB and suggest that genetic variants associated with SUB may be causally related to brain structure differences.</p