Pain
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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.
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Patients with neuropathic pain are heterogeneous in etiology, pathophysiology, and clinical appearance. They exhibit a variety of pain-related sensory symptoms and signs (sensory profile). Different sensory profiles might indicate different classes of neurobiological mechanisms, and hence subgroups with different sensory profiles might respond differently to treatment. ⋯ All clusters occurred across etiologies but frequencies differed. We present a new approach of subgrouping patients with peripheral neuropathic pain of different etiologies according to intrinsic sensory profiles. These 3 profiles may be related to pathophysiological mechanisms and may be useful in clinical trial design to enrich the study population for treatment responders.
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We aimed to evaluate the effect of pain education on opioid prescribing by early-career general practitioners. A brief training workshop was delivered to general practice registrars of a single regional training provider. The workshop significantly reduced "hypothetical" opioid prescribing (in response to paper-based vignettes) in an earlier evaluation. ⋯ There was some evidence of a reduction in initial opioid prescriptions in the training group (interaction odds ratio: 0.74; 95% CI: 0.48-1.16; P value 0.19). This brief training package failed to increase overall opioid cessation. The inconsistency of these actual prescribing results with "hypothetical" prescribing behavior suggests that reducing opioid prescribing in chronic noncancer pain requires more than changing knowledge and attitudes.
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Multicenter Study
Genetic variant rs3750625 in the 3'UTR of ADRA2A affects stress-dependent acute pain severity after trauma and alters a microRNA-34a regulatory site.
α2A adrenergic receptor (α2A-AR) activation has been shown in animal models to play an important role in regulating the balance of acute pain inhibition vs facilitation after both physical and psychological stress. To our knowledge, the influence of genetic variants in the gene encoding α2A-AR, ADRA2A, on acute pain outcomes in humans experiencing traumatic stress has not been assessed. In this study, we tested whether a genetic variant in the 3'UTR of ADRA2A, rs3750625, is associated with acute musculoskeletal pain (MSP) severity following motor vehicle collision (MVC, n = 948) and sexual assault (n = 84), and whether this influence was affected by stress severity. ⋯ In both cohorts, the minor allele at rs3750625 was associated with increased musculoskeletal pain in distressed individuals (stress*rs3750625 P = 0.043 for MVC cohort and P = 0.007 for sexual assault cohort). We further found that (1) miR-34a binds the 3'UTR of ADRA2A, (2) the amount of repression is greater when the minor (risk) allele is present, (3) miR-34a in the IMR-32 adrenergic neuroblastoma cell line affects ADRA2A expression, (4) miR-34a and ADRA2A are expressed in tissues known to play a role in pain and stress, (5) following forced swim stress exposure, rat peripheral nerve tissue expression changes are consistent with miR-34a regulation of ADRA2A. Together, these results suggest that ADRA2A rs3750625 contributes to poststress musculoskeletal pain severity by modulating miR-34a regulation.