Chronic Pain and Hypertension and Mediation Role of Inflammation and Depression

BACKGROUND: The association between chronic pain and incident hypertension is unclear. This study aimed to investigate the associations between different pain characteristics (pain type, location, and spread) and incident hypertension, and whether they were mediated by inflammation, depression, or medication. METHODS: In a cohort study of 206 963 UK Biobank participants, multivariable Cox-proportional regression was used to investigate the associations between pain at baseline, measured via a touchscreen questionnaire, and incident hypertension ascertained from linkage to health records. Mediation analysis was conducted to estimate the percentage of the association mediated by inflammation, depression, and medications. RESULTS: Over a median follow-up of 13.5 years, 19 911 (9.62%) participants developed hypertension. Compared with no pain, those with short-term pain (hazard ratio, 1.10 [95% CI, 1.03–1.17]), chronic localized pain (hazard ratio, 1.20 [95% CI, 1.14–1.26]), and chronic widespread pain (hazard ratio, 1.75 [95% CI, 1.52–2.00]) had an increased risk of hypertension. A dose-relationship also existed between the number of chronic pain sites and hypertension. Chronic headache, neck, back, abdominal, hip, and widespread pain were all associated with an increased risk of hypertension, as was chronic musculoskeletal pain. Together, depression (11.3%) and inflammation (0.4%), as measured by C-reactive protein, mediated 11.7% of the association between chronic pain and hypertension. CONCLUSIONS: People with chronic pain are at higher risk of developing hypertension, and this is partly explained by inflammation and depression. These findings reinforce the need for pain management, and the monitoring and early detection of hypertension.