Pain
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Alterations in amygdala activity are apparent in women who report a history of early life stress (ELS) and those diagnosed with chronic pain disorders. Chronic stress in adulthood induces visceral hypersensitivity by alterations in glucocorticoid receptor (GR) and corticotropin-releasing factor (CRF) expression within the central amygdala (CeA). Here, we hypothesized that unpredictable ELS, previously shown to induce visceral hypersensitivity in adult female rats, alters GR and CRF expression in the CeA. ⋯ Knockdown of GR increased visceral sensitivity in all rats but revealed an exaggerated visceral hypersensitivity in females with a history of predictable or unpredictable ELS compared with that of controls. Knockdown of CRF expression or antagonism of CRF1R in the CeA attenuated visceral hypersensitivity after unpredictable ELS. This study highlights a shift in GR and CRF regulation within the CeA after ELS that underlies the development of visceral hypersensitivity in adulthood.
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Recent studies suggest that longer durations of opioid use, independent of maximum morphine equivalent dose (MED) achieved, is associated with increased risk of new-onset depression (NOD). Conversely, other studies, not accounting for duration, found that higher MED increased probability of depressive symptoms. To determine whether rate of MED increase is associated with NOD, a retrospective cohort analysis of Veterans Health Administration data (2000-2012) was conducted. ⋯ Faster rates of MED escalation contribute to NOD, independent of maximum dose, pain, and total opioid duration. Dose escalation may be a proxy for loss of control or undetected abuse known to be associated with depression. Clinicians should avoid rapid dose increase when possible and discuss risk of depression with patients if dose increase is warranted for pain.
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Existing estimates of sociodemographic disparities in chronic pain in the United States are based on cross-sectional data, often treat pain as a binary construct, and rarely test for nonresponse or other types of bias. This study uses 7 biennial waves of national data from the Health and Retirement Study (1998-2010; n = 19,776) to describe long-term pain disparities among older (age 51+) American adults. It also investigates whether pain severity, reporting heterogeneity, survey nonresponse, and/or mortality selection might bias estimates of social disparities in pain. ⋯ No evidence of pain-related survey attrition is found, but surveys not accounting for pain severity and reporting heterogeneity are likely to underestimate socioeconomic disparities in pain. The lack of minority disadvantage (net of socioeconomic status) appears genuine. However, the age-related plateauing of pain observed cross-sectionally is not replicated longitudinally, and seems partially attributable to mortality selection, as well as to rising pain levels by birth cohort.
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Prior studies have documented an association of obesity with chronic pain, but the mechanism explaining the association remains unknown. This study evaluated the degree to which dietary intake of foods with anti-inflammatory effects mediates the relationship of body fat to body pain. Ninety-eight community-residing healthy adults (60% women; mean age = 43.2 ± 15.3 years; range: 20-78 years) participated in a home-based study of home environment, food-related behaviors, health, and adiposity. ⋯ Modeling in PROCESS revealed that Healthy Eating Index-2010 scores mediated the relationship between BMI and BP (bindirect = -0.34, 95% confidence interval = -0.68 to -0.13). The mediation model remained significant when controlling for biomechanical factors (arthritis/joint pain), medication use, psychological distress, age, and education, and models remained significant using the other 2 body fat measures. Thus, the data indicate that dietary intake of foods with anti-inflammatory effects mediates the relationship of body fat to body pain in healthy men and women.