ArticleEuropean journal of pain (London, England)2024
Familial effects account for association between chronic pain and past month smoking.
Article in European journal of pain (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors at 2 institutions in 1 country.
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Abstract
backgroundSmoking is associated with chronic pain, but it is not established whether smoking causes pain or if the link is due to familial effects. One proposed mechanism is that smoking strengthens maladaptive cortico-striatal connectivity, which contributes to pain chronification. We leveraged a twin design to assess direct effects of smoking on pain controlling for familial confounds, and whether cortico-striatal connectivity mediates this association.
methodsIn a population-based sample of 692 twins (age = 28.83 years), we assessed past-month smoking frequency (n = 132 used in the past month), presence and severity of a current pain episode (n = 179 yes), and resting-state functional connectivity of the nucleus accumbens and medial prefrontal cortex (NAc-mPFC).
resultsSmoking was significantly associated with pain, but the association was not significantly mediated by NAc-mPFC connectivity. In a co-twin control model, smoking predicted which families had more pain but could not distinguish pain between family members. Pain risk was 43% due to additive genetic (A) and 57% due to non-shared environmental (E) influences. Past-month smoking frequency was 71% genetic and 29% non-shared environmental. Smoking and pain significantly correlated phenotypically (r = 0.21, p = 0.001) and genetically (r
conclusionsPain and smoking are associated; however, the association appears to reflect shared familial risk factors, such as genetic risk, rather than being causal in nature. The connectivity strength of the reward pathway was not related to concurrent pain and smoking in this sample. SIGNIFICANCE: Smoking does not appear to directly cause chronic pain; rather, there may be shared biopsychosocial risk factors, including genetic influences, that explain their association. These findings can be integrated into future research to identify shared biological pathways of both chronic pain and smoking behaviours as a way to conceptualize pain chronification.
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