Health Disparities in Colorectal Cancer Screening in United States: Race/ethnicity or Shifting Paradigms?

Background: Colorectal cancer (CRC) remains the third leading cause of cancer death in the United States. The incidence, mortality, and screening vary by race/ethnicity, with African Americans and Hispanics being disproportionately represented. Early detection through screening prolongs survival and decreases mortality. CRC screening (CRCS) varies by race/ethnicity, with lower prevalence rates observed among minorities, but the factors associated with such disparities remain to be fully understood. The current study aimed to examine the ethnic/racial disparities in the prevalence of CRCS, and the explanatory factors therein in a large sample of U.S. residents, using the National Health Interview Survey, 2003. Materials and Methods: A cross-sectional, epidemiologic design was used with a chi squareto assess the prevalence of CRCS, while a survey logistic regression model was used to assess the odds of being screened. Results: There was a significant variability in CRCS, with minorities demonstrating lower prevalence relative to Caucasians χ2 (3) = 264.4, p\u3c 0.0001. After controlling for the covariates, racial/ethnic disparities in CRCS persisted. Compared to Caucasians, African Americans/Blacks were 28% (adjusted prevalence odds ratio [APOR] = 0.72, 99% CI, 0.60-0.80), while Hispanics 33% (APOR, 0.67, 99% CI, 0.53-0.84) and Asians 37% (APOR, 0.63, 99% CI, 0.43-0.95) were less likely to be screened for CRC. Conclusion: Among older Americans, racial/ethnic disparities in CRCS exist, which was unexplained by racial/ethnic variance in the covariates associated with CRCS. These findings recommend further studies in enhancing the understanding of confounders and mediators of disparities in CRCS and the application of these factors including the health belief model in improving CRCS among ethnic/racial minorities

Aberrant Epigenomic Modulation of Glucocorticoid Receptor Gene (NR3C1) in Early Life Stress and Major Depressive Disorder Correlation: Systematic Review and Quantitative Evidence Synthesis

Early life stress (ELS) induced by psychological trauma, child maltreatment, maternal separation, and domestic violence predisposes to psycho-behavioral pathologies during adulthood, namely major depressive disorder (MDD), anxiety, and bipolar affective disorder. While environmental data are available in illustrating this association, data remain to be established on the epigenomic underpinning of the nexus between ELS and MDD predisposition. Specifically, despite the observed aberrant epigenomic modulation of the NR3C1, a glucocorticoid receptor gene, in early social adversity and social threats in animal and human models, reliable scientific data for intervention mapping in reducing social adversity and improving human health is required. We sought to synthesize the findings of studies evaluating (a) epigenomic modulations, mainly DNA methylation resulting in MDDfollowing ELS, (b) epigenomic modifications associated with ELS, and (c) epigenomic alterations associated with MDD. A systematic review and quantitative evidence synthesis (QES) were utilized with the random effect meta-analytic procedure. The search strategy involved both the PubMed and hand search of relevant references. Of the 1534 studies identified through electronic search, 592 studies were screened, 11 met the eligibility criteria for inclusion in the QES, and 5 examined ELS and MDD; 4 studies assessed epigenomic modulation and ELS, while 2 studies examined epigenomic modulations and MDD. The dense DNA methylation of the 1F exon of the NR3C1, implying the hypermethylated region of the glucocorticoid receptor gene, was observed in the nexus between ELS andMDD,common effect size (CES) = 14.96, 95%CI, 10.06–19.85. With respect to epigenomic modulation associated with child ELS, hypermethylation was observed, CES = 23.2%, 95%CI, 8.00–38.48. In addition, marginal epigenomic alteration was indicated in MDD, where hypermethylation was associated with increased risk of MDD, CES = 2.12%, 95%CI, −0.63–4.86. Substantial evidence supports the implication of NR3C1 and environmental interaction, mainly DNA methylation, in the predisposition to MDD following ELS. This QES further supports aberrant epigenomic modulation identified in ELS as well as major depressive episodes involving dysfunctional glucocorticoid-mediated negative feedback as a result of allostatic overload. These findings recommend prospective investigation of social adversity and its predisposition to the MDD epidemic via aberrant epigenomic modulation. Such data will facilitate early intervention mapping in reducing MDD in the United States population

Implication of Spiritual Network Support System in Epigenomic Modulation and Health Trajectory

With challenges in understanding the multifactorial etiologies of disease and individual treatment effect heterogeneities over the past four decades, much has been acquired on how physical, chemical and social environments a ffect human health, predisposing certain subpopulations to adverse health outcomes, especially the socio-environmentally disadvantaged (SED). Current translational data on gene and adverse environment interaction have revealed how adverse gene-environment interaction, termed aberrant epigenomic modulation, translates into impaired gene expression via messenger ribonucleic acid (mRNA) dysregulation, reflecting abnormal protein synthesis and hence dysfunctional cellular differentiation and maturation. The environmental influence on gene expression observed in most literature includes physical, chemical, physicochemical and recently social environment. However, data are limited on spiritual or religious environment network support systems, which reflect human psychosocial conditions and gene interaction. With this limited information, we aimed to examine the available data on spiritual activities characterized by prayers and meditation for a possible explanation of the nexus between the spiritual network support system (SNSS) as a component of psychosocial conditions, implicated in social signal transduction, and the gene expression correlate. With the intent to incorporate SNSS in human psychosocial conditions, we assessed the available data on bereavement, loss of spouse, loneliness, social isolation, low socio-economic status (SES), chronic stress, low social status, social adversity (SA) and early life stress (ELS), as surrogates for spiritual support network connectome. Adverse human psychosocial conditions have the tendency for impaired gene expression through an up-regulated conserved transcriptional response to adversity (CTRA) gene expression via social signal transduction, involving the sympathetic nervous system (SNS), beta-adrenergic receptors, the hypothalamus-pituitary-adrenal (HPA) axis and the glucocorticoid response. This review specifically explored CTRA gene expression and the nuclear receptor subfamily 3 group C member 1 (NR3C1) gene, a glucocorticoid receptor gene, in response to stress and the impaired negative feedback, given allostatic overload as a result of prolonged and sustained stress and social isolation as well as the implied social interaction associated with religiosity. While more remains to be investigated on psychosocial and immune cell response and gene expression, current data on human models do implicate appropriate gene expression via the CTRA and NR3C1 gene in the SNSS as observed in meditation, yoga and thai-chi, implicated in malignant neoplasm remission. However, prospective epigenomic studies in this context are required in the disease causal pathway, prognosis and survival, as well as cautious optimism in the application of these findings in clinical and public health settings, due to unmeasured and potential confoundings implicated in these correlations

Black-White Risk Differentials in COVID-19 (SARS-COV2) Transmission, Mortality and Case Fatality in the United States: Translational Epidemiologic Perspective and Challenges

Background: Social and health inequities predispose vulnerable populations to adverse morbidity and mortality outcomes of epidemics and pandemics. While racial disparities in cumulative incidence (CmI) and mortality from the influenza pandemics of 1918 and 2009 implicated Blacks with survival disadvantage relative to Whites in the United States, COVID-19 currently indicates comparable disparities. We aimed to: (a) assess COVID-19 CmI by race, (b) determine the Black-White case fatality (CF) and risk differentials, and (c) apply explanatory model for mortality risk differentials. Methods: COVID-19 data on confirmed cases and deaths by selective states health departments were assessed using a cross-sectional ecologic design. Chi-square was used for CF independence, while binomial regression model for the Black-White risk differentials. Results: The COVID-19 mortality CmI indicated Blacks/AA with 34% of the total mortality in the United States, albeit their 13% population size. The COVID-19 CF was higher among Blacks/AA relative to Whites; Maryland, (2.7% vs. 2.5%), Wisconsin (7.4% vs. 4.8%), Illinois (4.8% vs. 4.2%), Chicago (5.9% vs. 3.2%), Detroit (Michigan), 7.2% and St. John the Baptist Parish (Louisiana), 7.9%. Blacks/AA compared to Whites in Michigan were 15% more likely to die, CmI risk ratio (CmIRR) = 1.15, 95% CI, 1.01-1.32. Blacks/AA relative to Whites in Illinois were 13% more likely to die, CmIRR = 1.13, 95% CI, 0.93-1.39, while Blacks/AA compared to Whites in Wisconsin were 51% more likely to die, CmIRR = 1.51, 95% CI, 1.10-2.10. In Chicago, Blacks/AA were more than twice as likely to die, CmIRR = 2.24, 95% CI, 1.36-3.88. Conclusion: Substantial racial/ethnic disparities are observed in COVID-19 CF and mortality with Blacks/AA disproportionately affected across the United States

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Désavantage de la survie spécifique du cancer du sein à cinq ans chez les femmes afro-américaines.

Racial/ethnic disparities in female breast cancer survival continue to persist in United States. However, disparities comparing African Americans (AA), Asians and Caucasians remain to be assessed. We aimed to assess multi-racial/ethnic disparities in breast cancer survival, and to examine the factors that may explain the variability. A total of 6,951 women diagnosed with breast cancer between 1992 and 1998 were identified from Surveillance, Epidemiology, and End Results tumor registries. The effect of race/ethnicity and the prognostic factors on survival was assessed using Cox proportional hazard model. AA demonstrated a survival disadvantage. Compared to Asians, Caucasians had 74% increased risk of dying (HR= 1.74, 95% CI = 1.31 – 2.33), while AA were almost three times as likely as Asians to die, (HR=2.78, 95% CI 2.02 – 3.86). After adjustment for the relevant covariates the survival disadvantage of AA persisted. Relative to Asians, Caucasians were 45% more likely to die (HR=1.45, 95% CI 1.10 – 1.93),while AA were more than two times as likely to die (HR=2.57, 95% CI 1.86 - 3.55). There were substantial racial/ethnic disparities in breast cancer survival among United States women. AA demonstrated survival disadvantage compared with either Caucasians or Asians, which persisted even after controlling factors known to influence breast cancer survivalLes disparités raciales/ethniques dans la survie du cancer du sein chez la femme persistent encore aux Etats-Unis. Néanmoins, l'on n'a pas encore évalué les disparités de manière comparative chez les Afro-Américains (AA), les Asiatiques et les Caucasiens. Nous avions comme objectif d'avancer les disparités dans la survie du cancer du sein et d'examiner les facteurs qui puissent expliquer la variabilité. Au total, on a diagnostiqué le cancer du sein chez 6951 femmes entre 1992 et 1998 qui ont été identifiées à travers la surveillance, l'épidémiologie et des listes des résultats définitifs de la tumeur. L'effet de la race / l'ethnie et les facteurs pronostiqués sur la survie ont été évalués à l'aide du modèle du danger proportionnel de Cox. L'AA a démontré un désavantage de la survie. Par rapport aux Asiatiques, les Caucasiens couraient un risque accru à74% de mourir (HR1, 74, 95% Cl = 1,31-2,33), alors que les AA avaient presque trois fois plus la possibilité de mourir que les Asiatiques (HR=2,78, 95%Cl 2,92-3,86). Après les ajustements pour arriver aux co-variables, le désavantage de la survie de l'AA a persisté. Par rapport aux Asiatiques, les Caucasiens avaient 45% plus la possibilité de mourir (HR=1,45, 95% CL 110-1,93), tandis que les AA avaient plus de deux fois la possibilité de mourir (HR=2,57, 95%CL 1,86-3,55). Il y avait beaucoup de disparités raciales/ethniques à l'égard de la survie du cancer du sein chez les femmes américaines. Les AA ont démontré un désavantage de la survie par rapport soit aux Caucasiens soit aux Asiatiques qui ont persisté même après avoir contrôlé les facteurs qui influent sur la survie du cancer du sei

Racial and Ethnic Heterogeneity in the Association Between Total Cholesterol and Pediatric Obesity

Publisher's PDFTotal cholesterol (TC) directly correlates with overweight/obesity, but it remains unclear if this association varies by race and ethnicity. We assessed the association as well as the racial/ethnic heterogeneity in this relationship. Data on 63,863 children were assessed using electronic medical records between 2010 and 2011. A cross-sectional design was utilized with log-binomial regression model and chi-squared statistic to examine the data. Overall, abnormal total cholesterol (ATC) was 7.5% (4812). Significant racial variability in ATC was observed: Black/African American (AA) (7.4%), White (7.0%), Asian (5.1%) and some other race (SOR) children (11.3%), 2 (5) = 141.5, p < 0.0001. Black/AA (34.7%) and SOR children (41.2%) were predominantly overweight/obese, unlike the Asian children, (25.8%), 2 (5) = 324.6, p < 0.0001. The BMI percentile was highest among SOR (69.0 28.6) and Black/AA children (65.2 29.1), but lowest among Asian children (55.7 31.5). A significant racial variability was also observed in weight, with the highest mean among Black/AA children (36.8kg 23.0) and the lowest among Asian children (28.7kg 16.8), f = 7.2, p < 0.001. Relative to normal TC, children with ATC were 2.6 times as likely to have abnormal BMI, relative risk (RR) =2.60, 99% CI, 2.54–2.68). Compared to non-Hispanic (RR = 2.62, 99% CI, 2.54–2.69), the risk was lower among Hispanics (RR = 2.34, 99%, 2.21–2.48). Among children with ATC, risk for abnormal BMI was highest among Asians, adjusted RR = 2.91, 99% CI, 2.34–3.62), intermediate among AA (ARR = 2.68, 99% CI, 2.59–2.77), but lowest among Whites (ARR = 2.40, 99% CI, 2.39–2.64), and SOR (ARR = 2.33, 99% CI, 2.19–2.50). In a large sample of children, total cholesterol directly correlates with BMI, with an observed racial and ethnic heterogeneity.University of Delaware. Department of Biological Sciences