Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Clin Ther. 2019 Jul;41(7):1323-1345. doi: 10.1016/j.clinthera.2019.04.021. Epub 2019 Jun 10.
Lifestyle may be important in the development of rheumatoid arthritis (RA). Therefore, changing behaviors may delay or even prevent RA onset. This article reviews the evidence basis for the associations of lifestyle factors with RA risk and considers future directions for possible interventions to reduce RA risk.
The literature was reviewed for cross-sectional studies, case-control studies, cohort studies, and clinical trials investigating potentially modifiable lifestyle factors and RA risk or surrogate outcomes on the path toward development such as RA-related autoimmunity or inflammatory arthritis. The evidence related to cigarette smoking, excess weight, dietary intake, physical activity, and dental health for RA risk were summarized.
Cigarette smoking has the strongest evidence base as a modifiable lifestyle behavior for increased seropositive RA risk. Smoking may increase seropositive RA risk through gene-environment interactions, increasing inflammation and citrullination locally in pulmonary/oral mucosa or systemically, thereby inducing RA-related autoimmunity. Prolonged smoking cessation may reduce seropositive RA risk. Evidence suggests that excess weight can increase RA risk, although this effect may differ according to sex, serologic status, and age at RA onset. TDietary intake may also affect RA risk: overall healthier patterns, high fish/omega-3 polyunsaturated fatty acid consumption, and moderate alcohol intake may reduce RA risk, whereas caffeine and sugar-sweetened soda consumption might increase RA risk. The impact of physical activity is less clear, but high levels may reduce RA risk. Periodontal disease might induce citrullination and RA-related autoimmunity, but the effect of dental hygiene behaviors on RA risk is unclear. Although the effect size estimates for these lifestyle factors on RA risk are generally modest, there may be relatively large public health benefits for targeted interventions given the high prevalence of these unhealthy behaviors. With the exception of smoking cessation, the impact of behavior change of these lifestyle factors on subsequent RA risk has not been established. Nearly all of the evidence for lifestyle factors and RA risk were derived from observational studies.
There are many potentially modifiable lifestyle factors that may affect RA risk. Improving health behaviors could have large public health benefits for RA risk given the high prevalence of many of the RA risk-related lifestyle factors. However, future research is needed to establish the effects of lifestyle changes on RA risk or surrogate outcomes such as RA-related autoimmunity or inflammatory arthritis.
生活方式可能在类风湿关节炎(RA)的发展中起重要作用。因此,改变行为可能会延迟甚至预防 RA 的发病。本文综述了生活方式因素与 RA 风险之间关联的证据基础,并考虑了可能的干预措施以降低 RA 风险的未来方向。
本文综述了横断面研究、病例对照研究、队列研究和临床试验,这些研究调查了潜在可改变的生活方式因素与 RA 风险或发病途径中的替代结局(如与 RA 相关的自身免疫或炎症性关节炎)之间的关系。总结了与 RA 风险相关的吸烟、超重、饮食摄入、身体活动和口腔健康等生活方式因素的证据。
吸烟是与 RA 阳性血清学相关的可改变生活方式行为中最具证据基础的因素,可增加 RA 阳性血清学风险。吸烟可能通过基因-环境相互作用增加 RA 阳性血清学风险,在肺部/口腔黏膜局部或全身增加炎症和瓜氨酸化,从而诱导与 RA 相关的自身免疫。长期戒烟可能会降低 RA 阳性血清学风险。有证据表明,超重会增加 RA 风险,但这种影响可能因性别、血清学状态和 RA 发病年龄而异。饮食摄入也可能影响 RA 风险:整体更健康的模式、高鱼类/ω-3 多不饱和脂肪酸摄入和适量饮酒可能降低 RA 风险,而咖啡因和含糖苏打水摄入可能会增加 RA 风险。身体活动的影响不太明确,但高水平的身体活动可能会降低 RA 风险。牙周病可能会诱导瓜氨酸化和与 RA 相关的自身免疫,但口腔卫生行为对 RA 风险的影响尚不清楚。尽管这些生活方式因素对 RA 风险的效应大小估计通常较小,但鉴于这些不健康行为的高患病率,针对这些行为进行干预可能会带来相对较大的公共卫生效益。除了戒烟外,这些生活方式因素对随后的 RA 风险的影响尚未确定。RA 风险相关生活方式因素的证据几乎都来自观察性研究。
有许多潜在的可改变的生活方式因素可能会影响 RA 的发病风险。鉴于许多与 RA 风险相关的生活方式因素的高患病率,改善健康行为可能会对 RA 风险产生重大的公共卫生效益。但是,需要进一步的研究来确定生活方式改变对 RA 风险或替代结局(如与 RA 相关的自身免疫或炎症性关节炎)的影响。