Declines in body mass index (BMI) were linked with slower worsening of knee osteoarthritis (OA), according to data from three large longitudinal cohort studies.
With more than 6,000 knees evaluated for OA progression and 4 to 5 years of follow-up, “each 1-unit decrease in BMI was associated with a 4.76% reduction … in the odds of the incidence and progression of the overall structural defects of knee osteoarthritis” as assessed under the Kellgren-Lawrence grading system, reported Zubeyir Salis, BEng, of the University of New South Wales in Kensington, Australia, and colleagues in Arthritis & Rheumatology.
While such a relationship seems obvious, it has evaded firm proof, the researchers noted. Earlier studies had tied body weight to risk of OA development and the likelihood of progression and end-stage outcomes such as total joint replacement. But whether losing or gaining weight alters the trajectory over time is another matter.
Salis and colleagues identified just one previous attempt to address the question directly: patients already showing joint degeneration who lost around 10 kg (22 lb) on average in a randomized diet-and-exercise trial showed no less progression than a control group with little weight loss, but follow-up only lasted 18 months. (A number of other studies had lumped patients without structural damage at baseline together with those with established degeneration, and they had mixed results.)
For the current analyses, Salis and colleagues combined data from three independent cohort studies from the U.S. and the Netherlands: the Osteoarthritis Initiative (OAI), which was also the basis for some of the above-mentioned studies; the Multicenter Osteoarthritis Study (MOST); and the Cohort Hip and Cohort Knee (CHECK) study. These data covered 9,683 knees (5,774 individual patients) for assessing the incidence of structural knee degeneration (i.e., no evidence of joint damage at baseline) and 6,074 knees (3,988 individuals) for progression of established degeneration.
Structural joint parameters were measured with x-rays at baseline and at follow-up, which was 4 years in the OAI and 5 years in the other two cohorts. Changes in these parameters (medial and lateral joint space narrowing and femoral and tibial surface osteophytes) were correlated against changes in BMI.
For patients included in the evaluation of new-onset structural damage, mean age at baseline was 60; about 40% were men and 88% were white. BMI at baseline averaged 28.2, with 33% of participants classified as obese (BMI ≥30). A total of 1,101 participants in this analysis saw BMI declines of at least 1 unit during follow-up, whereas 1,611 had increases of 1 or more units.
Patients’ baseline characteristics in the study of progression were similar. Baseline BMI was a bit higher on average (30.4), and 48% were obese. BMI declines of 1 or more units were seen in 798 participants, while 1,008 had increases.
Salis and colleagues found a significant association between BMI changes and the risk of developing structural damage, with an odds ratio of 1.05 (95% CI 1.02-1.09) for each 1-unit increment in BMI. This value was nearly identical to that seen for risk of progression in patients with damage at baseline (OR 1.05, 95% CI 1.01-1.09). In both analyses, joint space narrowing in the medial area largely drove the overall findings, with odds ratios in both cases of 1.08 per 1-unit BMI increment.
However, the results suggested that weight loss was far from the only factor at play in governing joint-damage incidence and progression. The researchers estimated population-attributable fractions of the total risk accounted for by weight loss at 13% for incidence and 10% for progression.
In addition, the investigators stopped short of asserting that the findings prove that weight loss slows OA disease progression, saying they “showed evidence of association, not causality.” But the researchers did argue that “people with overweight or obesity — and potentially also those of normal weight — may benefit from a decrease in BMI to prevent, delay or slow the structural defects in knee osteoarthritis.”
This study was supported by the Australian government; the individual cohort studies each had their own funding sources, none of which were commercial entities.
Salis and one co-author were co-owners of a company dedicated to education around weight management. Two co-authors also reported relationships with multiple pharmaceutical companies.