Osteoarthritis (OA) is one of the most common conditions with 1 in 5 people over 45 showing arthritic changes in at least one joint. It also accounts for 19% of the burden of disease from musculoskeletal conditions. As such, there is a huge focus on effective treatment of this often very painful condition. One of the key risk factors identified in OA is body weight (Felson & Chaisson, 1997). One explanation for this is the mechanical changes including the increased load, knee varus/valgus laxity and poor knee alignment (Felson et al., 2014; Sharma et al., 2000). However, given that people with high BMIs have a higher rate of OA in non-weight bearing joints mechanical stressors cannot be the sole factor (Wang & He, 2018). Researchers have suggested that the inflammatory response that is potentially caused by obesity impacts on the development of OA. This article will discuss whether this statement is accurate or whether there is an alternative explanation.
First, I’m going to talk a bit about the pathophysiology of the inflammation pathways involved in those with a high BMI and how this may impact the development of OA. Adipose tissue is involved in the production of inflammatory cytokines, chemokines and metabolically-active mediators known as adipokines. Two of the key adipokines are adiponectin and leptin have been linked with the inflammatory response in cartilage. Additionally, macrophages (which are derived from adipocytes) produce number of inflammatory cytokines that have been found in the synovial fluid, cartilage and subchondral bone indicating their role in OA pathophysiology (Wang & He, 2018).
So how does this impact on OA? OA was once thought to be a result of ‘wear and tear’ of the joints. However, it is now understood that cartilage metabolism is involved in the pathophysiology of OA (Sowers & Karvonen-Gutierrez, 2010). Thus the presence of higher levels of inflammatory cytokines in synovial fluid, cartilage and subchondral bone suggest that the inflammatory response to a high BMI may influence the inflammatory component to OA.
Conversely, I would like you to consider the fact that inflammation is also associated with weight cycling, that is the weight loss/weight regain cycle (Bacon & Aphramor, 2011). It is known that weight loss is unsustainable for the majority of people and there is no evidence that people can maintain the lifestyle factors (Bacon & Aphramor, 2011). For example, the women’s health initiative (which is the largest and longest RCT investigating a dietary intervention) tested a low-fat diet that reduced intake by an average of 360 calories per day and significantly increased their physical activity. Their final analysis showed that there was practically no change from their starting weight and abdominal fat actually increased. Attempts to lose weight are associated with weight cycling and these attempts to lose weight are more common in people with high BMIs (Kruger et al., 2004). Thus, people who have high BMIs are likely to have inflammation caused by weight-cycling. There is, therefore, an argument to be said that it is weight cycling and not a high BMI that leads to the inflammation associated with OA.
Furthermore, even if having a high BMI is associated with with a degree of inflammation, given that weight loss attempts lead to weight-cycling which in turn leads to increased inflammation are we not exacerbating one of the contributing factors to OA?
For the above reasons it is my belief that there is a compelling argument for weight-cycling being a risk factor for osteoarthritis as opposed to high BMI alone.
References
Bacon, L., Aphramor, L. Weight Science: Evaluating the Evidence for a Paradigm Shift. Nutr J 10, 9 (2011). https://doi.org/10.1186/1475-2891-10-9
Felson DT, Chaisson CE. Understanding the relationship between body weight and osteoarthritis. 1997; 114671-81. 10.3402/pba.v2i0.17470
Felson DT, Goggins J, Niu J, Zhang Y, Hunter DJ. The effect of body weight on progression of knee osteoarthritis is dependent on alignment. 2004; 50123904-9. 10.3402/pba.v2i0.17470
Kruger J, Galuska DA, Serdula MK, Jones DA: Attempting to lose weight: specific practices among U.S. adults. Am J Prev Med. 2004, 26: 402-406. 10.1016/j.amepre.2004.02.001
Sharma L, Lou C, Cahue S, Dunlop DD. The mechanism of the effect of obesity in knee osteoarthritis: the mediating role of malalignment. 2000; 433568-75. 10.3402/pba.v2i0.17470.
Sowers, M. R., & Karvonen-Gutierrez, C. A. (2010). The evolving role of obesity in knee osteoarthritis. Current opinion in rheumatology, 22(5), 533–537. https://doi.org/10.1097/BOR.0b013e32833b4682
Wang, T., & He, C. (2018). Pro-inflammatory cytokines: The link between obesity and osteoarthritis. Cytokine and Growth Factor Reviews, 44, 38–50. https://doi.org/10.1016/j.cytogfr.2018.10.002
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