Familial effects account for association between chronic pain and past month smoking

Background Smoking 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...

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Bibliographic Details
Published in:European journal of pain 2024-08, Vol.28 (7), p.1144-1155
Main Authors: Rader, L., Reineberg, A. E., Petre, B., Wager, T. D., Friedman, N. P.
Format: Article
Language:English
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Summary:Background Smoking 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. Methods In 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). Results Smoking 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 (rg = 0.51, p 
ISSN:1090-3801
1532-2149
1532-2149
DOI:10.1002/ejp.2247