Reducing weight reduces likelihood of knee and hip replacement.
To examine the association between body mass index (BMI) trajectories from early adulthood to late midlife and risk of total knee arthroplasty (TKA) for osteoarthritis.
Trajectories of body mass index from early adulthood to late midlife and incidence of total knee arthroplasty for osteoarthritis: findings from a prospective cohort study
Summary
Objective
To examine the association between body mass index (BMI) trajectories from early adulthood to late midlife and risk of total knee arthroplasty (TKA) for osteoarthritis.
Methods
24,368 participants from the Melbourne Collaborative Cohort Study with weight collected during 1990–1994, 1995–1998, and 2003–2007, recalled weight at age 18–21 years, and height measured during 1990–1994 were included. Incident TKA from 2003 to 2007 to December 2018 was determined by linking cohort records to the National Joint Replacement Registry.
Results
Using group-based trajectory modelling, six distinct trajectories (TR) of BMI from early adulthood (age 18–21 years) to late midlife (approximately 62 years) were identified: lower normal to normal BMI (TR1; 19.7% population), normal BMI to borderline overweight (TR2; 36.7%), normal BMI to overweight (TR3; 26.8%), overweight to borderline obese (TR4; 3.5%), normal BMI to class 1 obesity (TR5; 10.1%), overweight to class 2 obesity (TR6; 3.2%). Over 12.4 years, 1,328 (5.4%) had TKA. The hazard ratios for TKA increased in all TR compared to TR1 [from TR2: 2.03 (95% CI 1.64–2.52) to TR6: 8.59 (6.44–11.46)]. 28.4% of TKA could be prevented if individuals followed the trajectory one lower, an average weight reduction of 8–12 kg from early adulthood to late midlife, saving $AUS 373 million/year. Most reduction would occur in TR2 (population attributable fraction 37.9%, 95% CI 26.7–47.3%) and TR3 (26.8%, 20.0–31.2%).
Conclusions
Prevention of weight gain from young adulthood to late midlife in order to reduce overweight/obesity has the potential to significantly reduce the cost and burden of TKA.
Introduction
Obesity is the most important modifiable risk factor for knee osteoarthritis (OA). However meta-analyses of randomized controlled trials have shown limited effects of intensive exercise- and diet-based weight loss programs on knee pain and structure structural outcomes1, despite weight loss of 5–10%. Achieving substantial weight loss is possible but challenging2, and long-term maintenance of lost weight is even more difficult3.
Weight tends to steadily increase from the age of 18–50 years4 (0.5 kg/year in Australia5 and 0.5–1.0 kg/year in the USA4) so the population slowly transits to higher obesity categories6. Obesity affects the knee over the life course with obesity-related structural changes demonstrated early in the course of the disease before any clinical disease is detected7. This may explain why weight loss has only a modest effect on knee joint health once significant OA is present (evidenced by structural damage)8.
Understanding the effect of weight gain at different stages of adult life on knee OA has the potential to inform more effective approaches to tackling obesity in the prevention and treatment of this disease. Examining weight or body mass index (BMI) at one or two time points may not capture the effect of different patterns of weight accumulation or obesity on the development and progression of knee OA. These differences in risk can be examined using trajectory analysis9,10, which enables the examination of the relationship between different patterns of change in BMI over the life course (i.e., different BMI trajectories) and risk of OA9,10.
To date, only a few studies have examined BMI trajectories (TR) and knee OA11,12. One study identified three BMI trajectories over 30 months and reported an increased progression of synovitis in the weight gain trajectory compared with those of stable weight11. This study was limited by the small sample size and post-hoc analysis of a randomized controlled trial of weight loss, thus limiting its generalizability to community-based populations. The other examining the British Birth cohort showed elevated risk of knee OA from exposure to a high BMI through adulthood from 26 to 43 years12. This study compared the BMI trajectories between participants with knee OA and those without. Thus, the effect of patterns of BMI change identified by BMI trajectories on knee OA in community-based populations remains unknown. Using data from a large cohort study with BMI assessed at multiple timepoints, we examined the association between BMI trajectories across early adulthood to late midlife and incidence of total knee arthroplasty (TKA) for OA, as a measure of severe OA. Furthermore, we calculated the potential health system savings related to preventable TKAs if individuals followed the trajectory that was one lower.
Section snippets
Study population and setting
The Melbourne Collaborative Cohort Study (MCCS) is a prospective cohort study of 41,513 participants (24,469 women) aged 27–75 years (99.3% were aged 40–69 years). Participants were recruited via the electoral roll, advertisements and community announcements in local media in 1990–199413. The purpose of this study was to prospectively investigate the role of diet and other lifestyle factors in the development of common chronic diseases14. Southern European migrants to Australia were
Results
Six distinct trajectories (TR) of BMI were identified and named according to their patterns in relation to the WHO classification of BMI31 (Fig. 2). A summary of each BMI trajectory is presented in Table I. From early adulthood (18–21 years) to late mid adulthood (median age 62 years, IQR 49–76 years), participants in TR1 (19.7%) had a lower normal to normal BMI, TR2 (36.7%) had BMI increased from normal to borderline overweight, TR3 (26.8%) started with a normal BMI and became overweight
Discussion
In this large cohort study of well-characterised community-based adults, we identified six distinct BMI trajectories from early adulthood (age 18–21 years) through to late midlife (median age 62 years): lower normal to normal BMI (TR1), normal BMI to borderline overweight (TR2), normal BMI to overweight (TR3), overweight to borderline obese (TR4), normal BMI to class 1 obese (TR5), and overweight to class 2 obese (TR6). Most participants (93.3%) had a normal BMI in early adulthood but only
Authors’ contributions
SMH: Conceptualization, Formal Analysis, Investigation, Writing – original draft. INA: Economic analysis, Writing – original draft. YW, DRE, AEW, GGG: Data curation, Investigation, Writing – original draft. FC: Data curation, Investigation, Methodology, Supervision, Writing – original draft. All authors were involved in writing (review and editing). All authors had full access to all of the data in the study. FMC (flavia.cicuttini@monash.edu) is the guarantor.
Declaration of competing interest
The authors declare that they have no conflict of interest.
Role of funding sources
The recruitment of the Melbourne Collaborative Cohort Study was funded by VicHealth and Cancer Council Victoria. This study was funded by grants from the National Health and Medical Research Council (NHMRC; 209057, 251533, 396414, 623208), and was further supported by infrastructure provided by Cancer Council Victoria. SMH is the recipient of NHMRC Early Career Fellowship (APP1142198), YW is the recipient of NHMRC Translating Research Into Practice Fellowship (APP1168185), and FMC is the
Acknowledgements
The Melbourne Collaborative Cohort Study was made possible by the contribution of many people, including the original investigators and the diligent team who recruited the participants and who continue working on follow up. We would like to express our gratitude to the many thousands of Melbourne residents who participated in the study. For the data linkage, we would especially like to thank the Managing and Research Director of the registry Professor Stephen E. Graves, the Registry coordinator