医学
相对风险
慢性疼痛
人口
内科学
队列研究
物理疗法
置信区间
环境卫生
作者
Anders Pedersen Årnes,Mats Kirkeby Fjeld,Hein Stigum,Christopher Sivert Nielsen,Audun Stubhaug,Aslak Johansen,Laila Arnesdatter Hopstock,Bente Morseth,Tom Wilsgaard,Ólöf Anna Steingrímsdóttir
出处
期刊:Pain
[Ovid Technologies (Wolters Kluwer)]
日期:2024-03-05
卷期号:165 (9): 2011-2023
被引量:1
标识
DOI:10.1097/j.pain.0000000000003209
摘要
Abstract Knowledge is needed regarding mechanisms acting between physical activity (PA) and chronic pain. We investigated whether cold pain tolerance mediates an effect of leisure-time physical activity on the risk of chronic pain 7 to 8 years later using consecutive surveys of the population-based Tromsø Study. We included participants with information on baseline leisure-time PA (LTPA) and the level of cold pressor–assessed cold pain tolerance, who reported chronic pain status at follow-up as any of the following: chronic pain for ≥3 months, widespread chronic pain, moderate-to-severe chronic pain, or widespread moderate-to-severe chronic pain. We included 6834 participants (52% women; mean age, 55 years) in counterfactual mediation analyses. Prevalence decreased with severity, for example, 60% for chronic pain vs 5% for widespread moderate-to-severe chronic pain. People with one level higher LTPA rating (light to moderate or moderate to vigorous) at baseline had lower relative risk (RR) of 4 chronic pain states 7 to 8 years later. Total RR effect of a 1-level LTPA increase was 0.95 (0.91-1.00), that is, −5% decreased risk. Total effect RR for widespread chronic pain was 0.84 (0.73-0.97). Indirect effect for moderate-to-severe chronic pain was statistically significant at RR 0.993 (0.988-0.999); total effect RR was 0.91 (0.83-0.98). Statistically significantly mediated RR for widespread moderate-to-severe chronic pain was 0.988 (0.977-0.999); total effect RR was 0.77 (0.64-0.94). This shows small mediation of the effect of LTPA through pain tolerance on 2 moderate-to-severe chronic pain types. This suggests pain tolerance to be one possible mechanism through which PA modifies the risk of moderate-to-severe chronic pain types with and without widespread pain.
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