Pain
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Chronic pain conditions frequently co-occur, suggesting common risks and paths to prevention and treatment. Previous studies have reported genetic correlations among specific groups of pain conditions and reported genetic risk for within-individual multisite pain counts (≤7). Here, we identified genetic risk for multiple distinct pain disorders across individuals using 24 chronic pain conditions and genomic structural equation modeling (Genomic SEM). ⋯ Annotation identified pathways associated with organogenesis, metabolism, transcription, and DNA repair, with overrepresentation of strongly associated genes exclusively in brain tissues. Cross-reference with previous GWASs showed genetic overlap with cognition, mood, and brain structure. These results identify common genetic risks and suggest neurobiological and psychosocial mechanisms that should be targeted to prevent and treat cross-condition chronic pain.
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Despite growing recognition of the importance of social, economic, and political contexts for population health and health inequalities, research on pain disparities relies heavily on individual-level data, while neglecting overarching macrolevel factors such as state-level policies and characteristics. Focusing on moderate or severe arthritis-attributable joint pain-a common form of pain that considerably harms individuals' quality of life-we (1) compared joint pain prevalence across US states; (2) estimated educational disparities in joint pain across states; and (3) assessed whether state sociopolitical contexts help explain these 2 forms of cross-state variation. We linked individual-level data on 407,938 adults (ages 25-80 years) from the 2017 Behavioral Risk Factor Surveillance System with state-level data on 6 measures (eg, the Supplemental Nutrition Assistance Program [SNAP], Earned Income Tax Credit, Gini index, and social cohesion index). ⋯ Educational gradients in joint pain exist in all states but vary substantially in magnitude, primarily due to variation in pain prevalence among the least educated. At all education levels, residents of states with greater educational disparities in pain are at a substantially higher risk of pain than peers in states with lower educational disparities. More generous SNAP programs (odds ratio [OR] = 0.925; 95% confidence interval [CI]: 0.963-0.957) and higher social cohesion (OR = 0.819; 95% CI: 0.748-0.896) predict lower overall pain prevalence, and state-level Gini predicts higher pain disparities by education.
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Endometriosis-related pain has been predominantly medically managed, which has hindered understanding of psychological factors involved in these pain experiences. Models of chronic pain highlight the biased interpretation of ambiguous information as health threat related (interpretation bias) as an important process in the development and maintenance of chronic pain. Whether interpretation bias may also be similarly implicated in endometriosis-related pain is unclear. ⋯ Within the endometriosis sample, interpretation bias was significantly associated with increases in pain-related interference, however, interpretation bias was not associated with any other pain outcomes and did not moderate the relationship between pain severity and pain interference. This study is the first to evidence biased interpretation styles among individuals with endometriosis and to show this bias is associated with pain interference. Whether interpretation bias varies over time and whether this bias can be modified through scalable and accessible interventions to alleviate pain-related interference are avenues for future research.
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Dorsal root ganglia (DRG) neurons have been well described for their role in driving both acute and chronic pain. Although nerve injury is known to cause transcriptional dysregulation, how this differs across neuronal subtypes and the impact of sex is unclear. Here, we study the deep transcriptional profiles of multiple murine DRG populations in early and late pain states while considering sex. ⋯ We see both stereotyped and unique subtype signatures in injured states after nerve injury at both an early and late timepoint. Although all populations contribute to a general injury signature, subtype enrichment changes can also be seen. Within populations, there is not a strong intersection of sex and injury, but previously unknown sex differences in naïve states-particularly in Aβ-RA + Aδ-low threshold mechanoreceptors-still contribute to differences in injured neurons.