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      Could epigenetics help explain racial disparities in chronic pain?

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          Abstract

          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.

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          Most cited references 56

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          Epigenetic programming by maternal behavior.

          Here we report that increased pup licking and grooming (LG) and arched-back nursing (ABN) by rat mothers altered the offspring epigenome at a glucocorticoid receptor (GR) gene promoter in the hippocampus. Offspring of mothers that showed high levels of LG and ABN were found to have differences in DNA methylation, as compared to offspring of 'low-LG-ABN' mothers. These differences emerged over the first week of life, were reversed with cross-fostering, persisted into adulthood and were associated with altered histone acetylation and transcription factor (NGFI-A) binding to the GR promoter. Central infusion of a histone deacetylase inhibitor removed the group differences in histone acetylation, DNA methylation, NGFI-A binding, GR expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, suggesting a causal relation among epigenomic state, GR expression and the maternal effect on stress responses in the offspring. Thus we show that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible.
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            Reversal of maternal programming of stress responses in adult offspring through methyl supplementation: altering epigenetic marking later in life.

            Stress responses in the adult rat are programmed early in life by maternal care and associated with epigenomic marking of the hippocampal exon 1(7) glucocorticoid receptor (GR) promoter. To examine whether such epigenetic programming is reversible in adult life, we centrally infused the adult offspring with the essential amino acid L-methionine, a precursor to S-adenosyl-methionine that serves as the donor of methyl groups for DNA methylation. Here we report that methionine infusion reverses the effect of maternal behavior on DNA methylation, nerve growth factor-inducible protein-A binding to the exon 1(7) promoter, GR expression, and hypothalamic-pituitary-adrenal and behavioral responses to stress, suggesting a causal relationship among epigenomic state, GR expression, and stress responses in the adult offspring. These results demonstrate that, despite the inherent stability of the epigenomic marks established early in life through behavioral programming, they are potentially reversible in the adult brain.
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              Race and unhealthy behaviors: chronic stress, the HPA axis, and physical and mental health disparities over the life course.

              We sought to determine whether unhealthy behaviors play a stress-buffering role in observed racial disparities in physical and mental health. We conducted logistic regressions by race on data from the first 2 waves of the Americans' Changing Lives Survey to determine whether unhealthy behaviors had buffering effects on the relationship between major stressors and chronic health conditions, and on the relationship between major stressors and meeting the criteria for major depression. Among Whites, unhealthy behaviors strengthened the relationship between stressors and meeting major-depression criteria. Among Blacks, however, the relationship between stressors and meeting major-depression criteria was stronger among those who had not engaged in unhealthy behaviors than among those who had. Among both race groups there was a positive association between stressors and chronic health conditions. Among Blacks there was an additional positive association between number of unhealthy behaviors and number of chronic conditions. Those who live in chronically stressful environments often cope with stressors by engaging in unhealthy behaviors that may have protective mental-health effects. However, such unhealthy behaviors can combine with negative environmental conditions to eventually contribute to morbidity and mortality disparities among social groups.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2019
                18 February 2019
                : 12
                : 701-710
                Affiliations
                [1 ]School of Nursing, University of Alabama at Birmingham, Birmingham, AL, USA, earoke@ 123456uab.edu
                [2 ]Sensory Science and Metabolism Unit (SenSMet), Division of Intramural Research, National Institute of Nursing Research, National Institute of Health, DHHS, Bethesda, MD, USA
                [3 ]Department of Psychology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA
                [4 ]Department of Biology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA
                Author notes
                Correspondence: Edwin N Aroke, School of Nursing, University of Alabama at Birmingham, University Boulevard, Birmingham, AL 35294, USA, Tel +1 205 975 75700, Fax +1 205 996 9165, Email earoke@ 123456uab.edu
                Article
                jpr-12-701
                10.2147/JPR.S191848
                6388771
                © 2019 Aroke et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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