African Americans disproportionately suffer more severe and debilitating morbidity from chronic pain than do non-Hispanic Whites. These differences may arise from differential exposure to psychosocial and environmental factors such as adverse childhood experiences, racial discrimination, low socioeconomic status, and depression, all of which have been associated with chronic stress and chronic pain. Race, as a social construct, makes it such that African Americans are more likely to experience different early life conditions, which may induce epigenetic changes that sustain racial differences in chronic pain. Epigenetics is one mechanism by which environmental factors such as childhood stress, racial discrimination, economic hardship, and depression can affect gene expression without altering the underlying genetic sequence. This article provides a narrative review of the literature on epigenetics as a mechanism by which differential environmental exposure could explain racial differences in chronic pain. Most studies of epigenetic changes in chronic pain examine DNA methylation. DNA methylation is altered in the glucocorticoid (stress response) receptor gene, NR3C1 , which has been associated with depression, childhood stress, low socioeconomic status, and chronic pain. Similarly, DNA methylation patterns of immune cytokine genes have been associated with chronic stress states. Thus, DNA methylation changes may play an essential role in the epigenetic modulation of chronic pain in different races with a higher incidence of epigenetic alterations contributing to more severe and disabling chronic pain in African Americans.

Background:Eating disorders are a significant cause of morbidity and mortality. The etiology and maintenance of eating-disorder symptoms are not well understood. Evidence suggests that there may be gustatory alterations in patients with eating disorders.Objective:This article systematically reviews research assessing gustatory differences in patients with anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED).Method:A systematic review was performed, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, examining taste and eating disorders. We reviewed electronic databases and identified 1,490 peer-reviewed English-language studies. Of these, 49 met inclusion criteria.Results:Studies employed psychophysical measures (n = 27), self-reported questionnaires (n = 5), and neuroimaging techniques (i.e., electroencephalography, functional magnetic resonance imaging; n = 17). Psychophysical studies showed that individuals with BN, in general, had greater preference for sweetness than healthy controls, and those with AN had a greater aversion for fat than controls. In neuroimaging studies, findings suggested that predictable administration of sweet-taste stimuli was associated with reduced activation in taste-reward regions of the brain among individuals with AN (e.g., insula, ventral, and dorsal striatum) but increased activation in BN and BED.Discussion:To our knowledge, this systematic review is the first to synthesize literature on taste differences in AN, BN, and BED. The inconsistency and variability in methods used across studies increased difficulties in comparing studies and disease processes. Further studies with well-defined population parameters are warranted to better understand how taste varies in patients with eating disorders.

Ultra-processed food consumption has increased world-wide, yet little is known about the potential links with taste preference and sensitivity. This exploratory study aimed to (i) compare sweet and salty taste detection thresholds and preferences following consumption of ultra-processed and unprocessed diets, (ii) investigate whether sweet and salty taste sensitivity and preference were associated with taste-substrates (i.e. sodium and sugar) and ad libitum nutrient intake, and (iii) examine associations of taste detection thresholds and preferences with blood pressure (BP) and anthropometric measures following consumption of ultra-processed and unprocessed diets. In a randomized crossover study, participants (N=20) received ultra-processed or unprocessed foods for 2 weeks, followed by the alternate diet. Baseline food intake data were collected prior to admission. Taste detection thresholds and preferences were measured at the end of each diet arm. Taste-substrate/nutrient intake, body mass index (BMI), and body weight (BW) were measured daily. No significant differences were observed in participant salt and sweet detection thresholds or preferences after two weeks on ultra-processed or unprocessed diets. There was no significant association between salt and sweet taste detection thresholds, preferences, and nutrient intakes on either diet arm. A positive correlation was observed between salt taste preference and systolic BP (r=0.59; p=0.01), BW (r=0.47, p= 0.04), and BMI (r=0.50; p=0.03) following consumption of the ultra-processed diet. Thus, a two-week consumption of an ultra-processed diet does not appear to acutely impact sweet or salty taste sensitivity or preference..

Background: Obesity is common among kidney transplant recipients; However biological mediators of obesity are not well understood in this population. Because subcutaneous adipose tissue can be easily obtained during kidney transplant surgery, it provides a unique avenue for studying the mechanisms of obesity for this group. Although differential gene expression patterns were previously profiled for kidney transplant patients, gene co-expression patterns can shed light on gene modules not yet explored on the coordinative behaviors of gene transcription in biological and disease processes from a systems perspective. Methods: In this study, we collected 29 demographic and clinical variables and matching microarray expression data for 26 kidney transplant patients. We conducted Weighted Gene Correlation Network Analysis (WGCNA) for 5758 genes with the highest average expression levels and related gene co-expression to clinical traits. Results: A total of 35 co-expression modules were detected, two of which showed associations with obesityrelated traits, mainly at baseline. Gene Ontology (GO) enrichment was found for these two clinical traitassociated modules. One module consisting of 129 genes was enriched for a variety of processes, including cellular homeostasis and immune responses. The other module consisting of 36 genes was enriched for tissue development processes. Conclusions: Our study generated gene co-expression modules associated with obesity-related traits in kidney transplant patients and provided new insights regarding the cellular biological processes underlying obesity in this population.