Contributions of Structural Racism to the Food Environment: A Photovoice Study of Black Residents With Hypertension in Baltimore, MD.

BACKGROUND: Disproportionate exposure to poor food environments and food insecurity among Black Americans may partially explain critical chronic disease disparities by race and ethnicity. A complex set of structural factors and interactions between Black residents and their food environments, including store types, quantity, proximity, and quality of goods and consumer interactions within stores, may affect nutritional behaviors and contribute to higher cardiovascular and kidney disease risk. METHODS: We used the Photovoice methodology to explore the food environment in Baltimore, MD, through the perspectives of Black residents with hypertension between August and November 2019. Twenty-four participants were enrolled in the study (mean age: 65.1 years; 67% female). After a brief photography training, participants captured photos of their food environment, which they discussed in small focus groups over the course of 5 weeks. Discussions were audiotaped and analyzed for emergent themes using a line-by-line inductive approach. Themes were, then, organized into a collective narrative. RESULTS: Findings describe physical and social features of the food environment as well as participants' perceptions of its origins and holistic and generational health effects. The study illustrates the interrelationships among the broader socio-political environment, the quality and quantity of stores in the food landscape, and the ways in which they engage with the food environment as residents and consumers who have been marginalized due to their race and/or social class. The following meta-themes emerged from the data: (1) social injustice; (2) structural racism and classism; (3) interpersonal racism; (4) generational effects; (5) mistrust; (6) social programs; and (7) community asset-based approaches, including advocacy and civic engagement. CONCLUSIONS: Understanding residents' perceptions of the foundations and effects of the food environment on their health may help stakeholders to cocreate multilevel interventions alongside residents to improve access to healthy food and health outcomes among disparities affected populations.

Housing Insecurity and Risk of Adverse Kidney Outcomes.

Background: Housing insecurity is characterized by high housing costs or unsafe living conditions that prevent self-care and threaten independence. We examined the relationship of housing insecurity and risk of kidney disease. Methods: We used longitudinal data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study (Baltimore, MD). We used multivariable regression to quantify associations between housing insecurity and rapid kidney function decline (loss of >5 ml/min per 1.73 m2 of eGFR per year) and, among those without kidney disease at baseline, incident reduced kidney function (eGFR <60 ml/min per 1.73 m2) and incident albuminuria (urine albumin-creatinine ratio [ACR] ≥30 mg/g). Results: Among 1262 participants, mean age was 52 years, 40% were male and 57% were black. A total of 405 (32%) reported housing insecurity. After a median of 3.5 years of follow-up, rapid kidney function decline, incident reduced kidney function, and incident albuminuria occurred in 199 (16%), 64 (5%), and 74 (7%) participants, respectively. Housing insecurity was associated with increased odds of incident albuminuria (unadjusted OR, 2.04; 95% CI, 1.29 to 3.29; adjusted OR, 3.23; 95% CI, 1.90 to 5.50) but not rapid kidney function decline or incident reduced kidney function. Conclusions: In this urban population, housing insecurity was associated with increased risk of subsequent albuminuria. Increased recognition of housing insecurity as a social determinant of kidney disease is needed, and risk-reduction efforts that specifically target populations experiencing housing insecurity should be considered.

The kappa opioid receptor modulates GABA neuron excitability and synaptic transmission in midbrainprojections from the insular cortex.

As an integrative hub, the insular cortex (IC) translates external cues into interoceptive states that generate complex physiological, affective, and behavioral responses. However, the precise circuit and signaling mechanisms in the IC that modulate these processes are unknown. Here, we describe a midbrain-projecting microcircuit in the medial aspect of the agranular IC that signals through the Gαi/o-coupled kappa opioid receptor (KOR) and its endogenous ligand dynorphin (Dyn). Within this microcircuit, Dyn is robustly expressed in layer 2/3, while KOR is localized to deep layer 5, which sends a long-range projection to the substantia nigra (SN). Using ex vivo electrophysiology, we evaluated the functional impact of KOR signaling in layer 5 of the IC. We found that bath application of dynorphin decreased GABA release and increased glutamate release on IC-SN neurons, but did not alter their excitability. Conversely, dynorphin decreased the excitability of GABA neurons without altering synaptic transmission. Pretreatment with the KOR antagonist nor-BNI blocked the effects of dynorphin in IC-SN neurons and GABA neurons, indicating that the changes in synaptic transmission and excitability were selectively mediated through KOR. Selective inhibition of IC GABA neurons using a KOR-derived DREADD recapitulated these effects. This work provides insight into IC microcircuitry and indicates that Dyn/KOR signaling may act to directly reduce activity of layer 5 GABA neurons. In turn, KOR-driven inhibition of GABA promotes disinhibition of IC-SN neurons, which can modulate downstream circuits. Our findings present a potential mechanism whereby chronic upregulation of IC Dyn/KOR signaling can lead to altered subcortical function and downstream activity.