Cicuttini Flavia M, Proietto Joseph, Lim Yuan Z
School of Public Health and Preventive Medicine, Monash University, Melbourne, VIC, 3004, Australia.
Department of Medicine, The University of Melbourne, Melbourne, VIC, 3010, Australia.
Osteoarthr Cartil Open. 2023 Sep 9;5(4):100407. doi: 10.1016/j.ocarto.2023.100407. eCollection 2023 Dec.
Obesity is the major modifiable risk factor for osteoarthritis (OA). A major focus of management in OA is weight loss. Although we live in an obesogenic environment, obesity has a predominantly genetic and epigenetic basis. This explains a person's weight set point which is defended by biological mechanisms making weight loss difficult to achieve and maintain long term, regardless of the methods used. Significant weight regain occurs after weight loss, with weight tending to return to pre-treatment levels after cessation of interventions including the glucagon-like peptide-1 (GLP-1) agonists. An area that has received little attention is the slow, insidious weight creep of 0.5-1 kg/year over adulthood that sees individuals relentlessly increase weight. There is evidence that low intensity, personalised lifestyle interventions can prevent this weight creep, providing patients with achievable goals. In this narrative review, we examine the evidence for weight loss in OA, the biological mechanisms that make weight loss difficult to achieve and maintain and the potential negative impacts on patients. We review the evidence for preventing weight gain, the improvement in patient outcomes and the potential for significant healthcare savings through reduced knee replacements. We propose a combined approach of weight loss when indicated, together with targeting weight creep across adult years and the potential role of metformin. Implementing these combined approaches is likely to be more effective in improving patient related outcomes, reducing joint damage and healthcare costs, than our current focus on achieving weight loss in OA.
肥胖是骨关节炎(OA)主要的可改变风险因素。OA管理的一个主要重点是减重。尽管我们生活在一个致肥胖的环境中,但肥胖主要有遗传和表观遗传基础。这就解释了一个人的体重设定点,它受到生物机制的保护,使得无论采用何种方法,减重都难以实现且难以长期维持。减重后会出现显著的体重反弹,在包括胰高血糖素样肽-1(GLP-1)激动剂在内的干预措施停止后,体重往往会恢复到治疗前水平。一个很少受到关注的领域是成年人每年以0.5 - 1千克的速度缓慢、隐匿的体重增加,这使得个体体重持续上升。有证据表明,低强度、个性化的生活方式干预可以预防这种体重增加,为患者提供可实现的目标。在这篇叙述性综述中,我们研究了OA减重的证据、使减重难以实现和维持的生物学机制以及对患者的潜在负面影响。我们回顾了预防体重增加的证据、患者预后的改善以及通过减少膝关节置换手术实现显著医疗费用节省的可能性。我们提出一种联合方法,在有指征时进行减重,同时针对成年期的体重缓慢增加以及二甲双胍的潜在作用。与我们目前专注于OA减重相比,实施这些联合方法可能在改善患者相关预后、减少关节损伤和医疗成本方面更有效。