Carballo-Casla Adrián, García-Esquinas Esther, Lopez-Garcia Esther, Donat-Vargas Carolina, Banegas José R, Rodríguez-Artalejo Fernando, Ortolá Rosario
Department of Preventive Medicine and Public Health, Universidad Autónoma de Madrid/Idipaz, and CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain.
IMDEA Food Institute, CEI UAM+CSIC, Madrid, Spain.
J Gerontol A Biol Sci Med Sci. 2023 Feb 24;78(2):267-276. doi: 10.1093/gerona/glac103.
Despite its importance, evidence regarding pain prevention is inadequate. Leveraging the growing knowledge on how diet regulates inflammation, we examined the association of 3-year changes in the inflammatory potential of diet with pain incidence over the subsequent 3 years.
We used data from 819 individuals aged ≥60 years and free of pain in 2012, drawn from the Spanish Seniors-ENRICA-1 cohort. The inflammatory potential of diet was estimated via a validated diet history and 2 indices: the dietary inflammatory index (DII) and the empirical dietary inflammatory index (EDII). The frequency, severity, and number of locations of incident pain were combined into a scale that classified participants as suffering from no pain, intermediate pain, or highest pain.
Shifting the diet toward a higher inflammatory potential was associated with subsequent increased risk of highest pain (fully-adjusted relative risk ratio [95% confidence interval] per 1-standard deviation increment in the DII and the EDII = 1.45 [1.16,1.80] and 1.21 [0.98,1.49], respectively) and intermediate pain (0.99 [0.75,1.31] and 1.37 [1.05,1.79]). The 3 components of the pain scale followed similar trends, the most consistent one being pain severity (moderate-to-severe pain: DII = 1.39 [1.11,1.74]; EDII = 1.35 [1.08,1.70]). The association of increasing DII with highest incident pain was only apparent among the less physically active participants (2.08 [1.53,2.83] vs 1.02 [0.76,1.37]; p-interaction = .002).
An increase in the inflammatory potential of diet was associated with higher pain incidence over the following years, especially among the less physically active participants. Future studies in older adults should assess the efficacy of pain prevention interventions targeting the inflammatory potential of diet.
尽管疼痛预防很重要,但相关证据并不充分。利用饮食如何调节炎症方面日益增长的知识,我们研究了饮食炎症潜能的3年变化与随后3年疼痛发生率之间的关联。
我们使用了来自西班牙老年人ENRICA-1队列中819名年龄≥60岁且在2012年无疼痛的个体的数据。通过经过验证的饮食史和2个指标来估计饮食的炎症潜能:饮食炎症指数(DII)和经验性饮食炎症指数(EDII)。将新发疼痛的频率、严重程度和部位数量合并为一个量表,将参与者分类为无疼痛、中度疼痛或重度疼痛。
饮食炎症潜能升高与随后重度疼痛风险增加相关(DII和EDII每增加1个标准差的完全调整相对风险比[95%置信区间]分别为1.45[1.16,1.80]和1.21[0.98,1.49])以及中度疼痛(0.99[0.75,1.31]和1.37[1.05,1.79])。疼痛量表的3个组成部分呈现相似趋势,最一致的是疼痛严重程度(中度至重度疼痛:DII = 1.39[1.11,1.74];EDII = 1.35[1.08,1.70])。DII升高与重度新发疼痛之间的关联仅在身体活动较少的参与者中明显(2.08[1.53,2.83]对1.02[0.76,1.37];交互作用P值 = 0.002)。
饮食炎症潜能增加与随后几年较高的疼痛发生率相关,尤其是在身体活动较少的参与者中。未来针对老年人的研究应评估针对饮食炎症潜能的疼痛预防干预措施的效果。