Race and ethnic variation in college students’ allostatic regulation of racism-related stress

Racism-related stress is thought to contribute to widespread race/ethnic health inequities via negative emotion and allostatic stress process up-regulation. Although prior studies document race-related stress and health correlations, due to methodological and technical limitations, they have been unable to directly test the stress-reactivity hypothesis in situ. Guided by theories of constructed emotion and allostasis, we developed a protocol using wearable sensors and daily surveys that allowed us to operationalize and time-couple self-reported racism-related experiences, negative emotions, and an independent biosignal of emotional arousal. We used data from 100 diverse young adults at a predominantly White college campus to assess racism-related stress reactivity using electrodermal activity (EDA), a biosignal of sympathetic nervous system activity. We find that racism-related experiences predict both increased negative emotion risk and heightened EDA, consistent with the proposed allostatic model of health and disease. Specific patterns varied across race/ethnic groups. For example, discrimination and rumination were associated with negative emotion for African American students, but only interpersonal discrimination predicted increased arousal via EDA. The pattern of results was more general for Latinx students, for whom interpersonal discrimination, vicarious racism exposure, and rumination significantly modulated arousal. As with Latinx students, African students were particularly responsive to vicarious racism while 1.5 generation Black students were generally not responsive to racism-related experiences. Overall, these findings provide support for allostasis-based theories of mental and physical health via a naturalistic assessment of the emotional and sympathetic nervous system responding to real-life social experiences.

Racism in the United States shapes interracial social interactions (1) and, mirroring society-wide trends in the racialization of American politics (2, 3), the situation may be worsening with rising racial animosity (4, 5). Consequently, racism-related stress is hypothesized to contribute to widespread minority health disparities (6) and Black/White mortality differentials on a scale sufficient to influence election outcomes (7). One possible explanation for these disparities is that race-related stress increases negative emotions and physiological wear and tear via modulation of the sympathetic-adrenal-medullary (SAM) axis, hypothalamic-pituitary-adrenal (HPA) axis, and immune system (8). Up-regulation of these systems, often referred to generically as “the stress process,” is the outcome of the brain’s predictive modeling and regulation of the body’s energetic needs, or allostasis (9). Here, race-related stress is thought to increase energy demands as the brain prepares the body to deal with threats by marshaling oxygen, glucose, and other energetic mediators (10). Consequently, researchers have argued that ongoing allostatic up-regulation of the autonomic and endocrine systems, combined with immune activity modulation, in response to racism-related threats is physiologically taxing and over time increases vulnerability to chronic disease (11, 12). For example, downstream physiological adaptions to a body energized on high alert are thought to increase risks for excess adiposity, hypertension, diabetes, and cardiovascular disease (13–15), traditionally the leading cause of death in the United States.Despite the theoretical importance of regulatory allostatic processes for understanding racial health inequities, racism-related physiological responding has not been directly measured in real time in the real world. Conducting these assessments is challenging because the timing of many socially mediated experiences, such as racism-related incidents, occur in “social time”; that is, they are dependent upon actions beyond the control of the individual, are largely unobserved, and are highly variable and stochastic. Acute physiological changes are thus responses to temporally variable stimuli and are modulated on precise time scales in the order of seconds (i.e., SAM) and minutes (i.e., HPA). Although systematic and metaanalytic reviews find evidence that discriminatory experiences are correlated with mental and physical health both early (6) and later in life (16), most studies are cross-sectional, retrospective, and rely on behavioral and psychological self-reports, even when employing temporally sensitive methodologies (17). Although a few recent studies in natural settings incorporating biomarkers consistent with models of allostasis have begun filtering into the literature (18), their measurement strategies are not time-synchronized with race-related experiences. These studies provide post hoc evidence of allostatic process modulation, but do not measure allostatic regulation concurrently as it transpires in situ.Our study was designed to address these limitations and to directly test allostatic modulation of the sympathetic component of the SAM response to racism-related stress. To these ends, we developed a prospective protocol capturing events throughout the day, including the timing of racism-related experiences of perceived interpersonal discrimination, rumination on racism, and vicarious racism exposure, as well as negative emotions. Our design also included a wearable device that continuously tracked SAM activity using an electrodermal activity (EDA) sensor, a direct measure of the sympathetic nervous system (SNS) division of the autonomic nervous system that indexes affective arousal. This approach facilitated approximate time-synchronization of racism-related experiences with the SNS-mediated first-stage allostatic stress-response pathway. We were therefore able to operationalize two key aspects of stress-response dynamics temporally coupled with racism-related stressors: Negative emotion and SNS arousal. To our knowledge, this study provides a temporally coregistered and ecologically embedded assessment of the dynamic links between race-related stressors, negative emotions, and the SAM-mediated SNS component of a stress response among individuals of diverse ethnic backgrounds.     

Low Dopamine D2/D3 Receptor Availability is Associated with Steep Discounting of Delayed Rewards in Methamphetamine Dependence

Background:

Individuals with substance use disorders typically exhibit a predilection toward instant gratification with apparent disregard for the future consequences of their actions. Indirect evidence suggests that low dopamine D₂-type receptor availability in the striatum contributes to the propensity of these individuals to sacrifice long-term goals for short-term gain; however, this possibility has not been tested directly. We investigated whether striatal D₂/D₃ receptor availability is negatively correlated with the preference for smaller, more immediate rewards over larger, delayed alternatives among research participants who met DSM-IV criteria for methamphetamine (MA) dependence.

Methods:

Fifty-four adults (n = 27 each: MA-dependent, non-user controls) completed the Kirby Monetary Choice Questionnaire, and underwent positron emission tomography scanning with [¹⁸F]fallypride.

Results:

MA users displayed steeper temporal discounting (p = 0.030) and lower striatal D₂/D₃ receptor availability (p < 0.0005) than controls. Discount rate was negatively correlated with striatal D₂/D₃ receptor availability, with the relationship reaching statistical significance in the combined sample (r = -0.291, p = 0.016) and among MA users alone (r = -0.342, p = 0.041), but not among controls alone (r = -0.179, p = 0.185); the slopes did not differ significantly between MA users and controls (p = 0.5).

Conclusions:

These results provide the first direct evidence of a link between deficient D₂/D₃ receptor availability and steep temporal discounting. This finding fits with reports that low striatal D₂/D₃ receptor availability is associated with a higher risk of relapse among stimulant users, and may help to explain why some individuals choose to continue using drugs despite knowledge of their eventual negative consequences. Future research directions and therapeutic implications are discussed.     

COVID-19 risk index (CRI): a simple and validated emergency department risk score that predicts mortality and the need for mechanical ventilation

Journal of Thrombosis and Thrombolysis - Although certain risk factors have been associated with morbidity and mortality, validated emergency department (ED) derived risk prediction models specific...     

Leveraging the Medical Context to Increase Upper Extremity Reconstruction Among Patients With Tetraplegia: A Qualitative Analysis

Objectives

To (1) characterize patients' medical experiences from initial injury until they become candidates for upper extremity reconstruction (UER); and (2) identify points in this medical context that may be most amenable to interventions designed to increase UER utilization.

Modifiable Failures in the Colorectal Cancer Screening Process and Their Association With Risk of Death

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Infection with Hemotropic Mycoplasma Species in Patients with or without Extensive Arthropod or Animal Contact

PCR amplification targeting the 16S rRNA gene was used to test individuals with and without extensive arthropod and animal contact for the possibility of hemotropic mycoplasma infection. The prevalence of hemotropic mycoplasma infection (4.7%) was significantly greater in previously reported cohorts of veterinarians, veterinary technicians, spouses of veterinary professionals, and others with extensive arthropod exposure and/or frequent animal contact than in a previously reported cohort of patients examined by a rheumatologist because of chronic joint pain or evidence of small-vessel disease (0.7%). Based upon DNA sequence analysis, a Mycoplasma ovis-like species was the most prevalent organism detected; however, infection with “Candidatus Mycoplasma haematoparvum” and a potentially novel, but incompletely characterized, hemotropic Mycoplasma species was also documented. Historical exposure to animals and arthropod vectors that can harbor hemotropic Mycoplasma spp. should be considered during epidemiological investigations and in the evaluation of individual patients.     

FBXO28 causes developmental and epileptic encephalopathy with profound intellectual disability

Chromosome 1q41‐q42 deletion syndrome is a rare cause of intellectual disability, seizures, dysmorphology, and multiple anomalies. Two genes in the 1q41‐q42 microdeletion, WDR26 and FBXO28, have been implicated in monogenic disease. Patients with WDR26 encephalopathy overlap clinically with those with 1q41‐q42 deletion syndrome, whereas only one patient with FBXO28 encephalopathy has been described. Seizures are a prominent feature of 1q41‐q42 deletion syndrome; therefore, we hypothesized that pathogenic FBXO28 variants cause developmental and epileptic encephalopathies (DEEs). We describe nine new patients with FBXO28 pathogenic variants (four missense, including one recurrent, three nonsense, and one frameshift) and analyze all 10 known cases to delineate the phenotypic spectrum. All patients had epilepsy and 9 of 10 had DEE, including infantile spasms (3) and a progressive myoclonic epilepsy (1). Median age at seizure onset was 22.5 months (range 8 months to 5 years). Nine of 10 patients had intellectual disability, which was profound in six of nine and severe in three of nine. Movement disorders occurred in eight of 10 patients, six of 10 had hypotonia, four of 10 had acquired microcephaly, and five of 10 had dysmorphic features, albeit different to those typically seen in 1q41‐q42 deletion syndrome and WDR26 encephalopathy. We distinguish FBXO28 encephalopathy from both of these disorders with more severe intellectual impairment, drug‐resistant epilepsy, and hyperkinetic movement disorders.