Most guidelines recommending weight loss for hip osteoarthritis are based on research on knee osteoarthritis. Prior studies found no association between weight loss and hip osteoarthritis, but no previous studies have targeted older adults. Therefore, we aimed to determine whether there is any clear benefit of weight loss for radiographic hip osteoarthritis in older adults because weight loss is associated with health risks in older adults.We used data from white female participants aged ≥65 years from the Study of Osteoporotic Fractures. Our exposure of interest was weight change from baseline to follow-up at 8 years. Our outcomes were the development of radiographic hip osteoarthritis (RHOA) and the progression of RHOA over 8 years. Generalized estimating equations (clustering of 2 hips per participant) were used to investigate the association between exposure and outcomes adjusted for major covariates.There was a total of 11,018 hips from 5509 participants. There was no associated benefit of weight loss for either of our outcomes. The odds ratios  for the development and progression of RHOA were 0.99 (0.92–1.07) and 0.97 (0.86–1.09) for each 5% weight loss, respectively. The results were consistent in sensitivity analyses where participants were limited to those who reported trying to lose weight and who also had a body mass index in the overweight or obese range.Our findings suggest no associated benefit of weight loss in older female adults in the structure of the hip joint as assessed by radiography. As the hip joint is less sensitive to obesity and weight change than the knee joint,13 perhaps related to its ball-and-socket anatomy where mechanical forces are diffused across the joint in comparison to the hinge anatomy of the knee joint,15 it may be the case that weight loss has no or little benefit for the hip. Indeed, observational studies22 have not suggested any apparent benefit of weight loss for hip osteoarthritis.For the management of hip osteoarthritis, most guidelines around the world recommend weight loss for people with the condition and concurrent overweight or obesity.22 specifically investigated the effect of weight loss on hip osteoarthritis in older adults, as they involved adults aged between 18 and 79 years. If weight loss has no clear benefit for hip osteoarthritis in older adults, guidelines recommending weight loss for this condition may introduce unnecessary health risks in older adults, for whom weight loss is associated with problems such as increased hip fracture,24 mortality,25 functional impairment, and incident disability.26 Therefore, this current study aimed to determine whether weight loss is associated with benefits for structural defects of hip osteoarthritis in older women, using data from the Study of Osteoporotic Fractures (SOF).None of the above-mentioned observational studies27 To be eligible, participants needed to be female, aged 65 years or older at recruitment, and able to walk without assistance, with the exclusion of non-white participants or those who had undergone a bilateral total hip replacement. Ethical approval was obtained by the institutions undertaking the original SOF study, and all participants provided written informed consent.The SOF is a prospective cohort study of risk factors for osteoporosis and fractures that initially enrolled 9704 white female participants recruited from a population-based listing in four areas of the United States of America.28); hip fracture at or before baseline; under-weight body mass index (BMI < 18.5 kg/m2) at baseline or at any time point during follow-up (not only at the 8-year follow-up); missing weight data at baseline or at the 8-year follow-up. By excluding participants with missing weight data at the 8-year follow-up visit, we automatically excluded those participants who died before the 8-year follow-up visit (1296 participants). Finally, we excluded hips with missing radiography data at either baseline or the 8-year follow-up visit  and the 8-year follow-up (January 1995–June 1996). We then excluded participants with the following characteristics: rheumatoid arthritis at baseline (as assessed by radiographyup visit .Our exposure of interest was weight change between baseline and the follow-up visit at 8 years (mean [SD] time between baseline and the 8-year follow-up visit was 7.9 [0.4] years), expressed as a percent of baseline weight. Weight change was calculated from the weight of participants which was measured in clinics using balance beam scales.30 The modified Croft grade was rated 0–4 .31 Development of RHOA was defined as a hip having RHOA at the 8-year follow-up visit while not having it at baseline. Progression of RHOA was defined as a hip that had RHOA at baseline having an increase in modified Croft grade ≥1 between baseline and the 8-year follow-up visit.We had two primary outcomes related to structural defects of the overall hip as assessed by radiography, as well as nine secondary outcomes related to defects of individual structural features of the hip as assessed by radiography. Our two primary outcomes were the development of radiographic hip osteoarthritis (RHOA) and the progression of RHOA. RHOA was defined as a hip having a modified Croft grade ≥2.32 due to the high frequency of JSN in the medial compartment in the SOF cohort30); or an increase of 1 grade for subchondral cysts, subchondral sclerosis, and femoral head deformity (when it had been grade 0 at baseline).Our nine secondary outcomes related to defects of individual structural features of the hip were: joint space narrowing (JSN) in the lateral compartment; JSN in the medial compartment; osteophytes on the lateral acetabular surface; osteophytes on the inferior acetabular surface; osteophytes on the lateral femoral surface; osteophytes on the inferior femoral surface; subchondral cysts; subchondral sclerosis; and femoral head deformity. Each defect of an individual structural feature of the hip was rated in one of the following 3 ways: JSN, 0–4; osteophytes, 0–3; and subchondral cysts, subchondral sclerosis, and femoral head deformity, 0 (absent) or 1 (present). Our secondary outcomes were ‘degeneration’ of each of the nine defects of individual structural features of the hip, defined as a change in grade from baseline to the 8-year follow-up visit in one of the following ways: increase in ≥1 grade for JSN in the lateral compartment or osteophytes; increase in ≥2 grades for JSN in the medial compartment , and the ‘RHOA progression cohort’ (consisting of hips that had RHOA at baseline) . Our ninWe used generalized estimating equations with a logistic link function  to estimate the odds ratios (ORs) and 95% confidence intervals (CI) for the association of weight change with our outcomes. Univariate (unadjusted) and multivariable (adjusted) analyses were performed. The multivariable analyses were adjusted for the baseline values of the following 6 variables: age; weight; calcaneal bone mineral density (BMD); use of nonsteroidal anti-inflammatory drugs (NSAIDs); smoking status ; and physical activity. In addition, we also adjusted for ‘baseline severity of hip osteoarthritis as assessed by radiography’ . These variables were selected because of their association with hip osteoarthritis, as shown in the literature.33 There was no violation of this assumption of linearity. We calculated and reported odds ratios for our outcomes based on each 5% weight loss from baseline to the 8-year follow-up visit. We reported the odds ratios based on each 5% weight loss because previous studies suggest that this degree of weight loss is clinically relevant.34 While we report the odds ratios based on each 5% weight loss, we reported the descriptive statistics  stratified by the following three weight change groups of: weight loss (5% or more from baseline to the 8-year follow-up visit); stable weight (less than 5% weight change from baseline to the 8-year follow-up visit); and weight gain (5% or more from baseline to the 8-year follow-up visit).In our analyses, weight change was treated as a continuous variable. The assumption of linearity in the association between weight change and our outcomes was tested using the Box-Tidwell method.2—were consistent with our findings when restricted to only those participants who reported trying to lose weight at the 6-year follow-up visit and who also had a BMI ≥25 kg/m2 at baseline . To this end, we created a sub-cohort from the RHOA development cohort and a sub-cohort from the RHOA progression cohort, with each sub-cohort including only participants who answered ‘yes’ to the question of “In the past year, or since you last completed a questionnaire for the study, have you been trying to lose weight?” which was asked at the 6-year follow-up visit, and who also had overweight or obesity at baseline. We then determined the association between weight loss and our outcomes in these 2 sub-cohorts, and compared the results with our main analyses.We did not differentiate between participants who were intentionally trying to lose weight or not, due to the unavailability of this data at baseline. However, data about whether or not participants were intentionally trying to lose weight—regardless of whether or not they did lose weight—was available at the 6-year follow-up visit, and we performed a sensitivity analysis using this data. Here, we explored whether our findings from our main analyses—which included participants with any BMI ≥18.5 kg/mp value of less than 0.05.We used STATA/BE 17.0 for Windows (64-bit x86–64) for our analyses. We set our threshold for statistical significance as a two-tailed 2, 59.5% of participants in the RHOA development cohort, and 55.2% of participants in the RHOA progression cohort)   and 2.About a third of participants in both cohorts (31.0% in the RHOA development cohort and 32.0% in the RHOA progression cohort) reported that they were trying to lose weight at the 6-year follow-up visit . About aOf the 9285 hips in the RHOA development cohort , 292 (3.1%) developed RHOA by the 8-year follow-up visit . In neitOf the 697 hips in the RHOA progression cohort , 146 (21.0%) had progression of RHOA by the 8-year follow-up visit . In neitThe results showed no association of weight loss with the odds of degeneration of any of the nine individual structural features of the hip by the 8-year follow-up visit in the RHOA development cohort or the RHOA progression cohort .2 at baseline. In the sub-cohort from the RHOA development cohort, 67 (3.1%) of the total of 2176 participants developed RHOA by the 8-year follow-up, while in the sub-cohort from the RHOA progression cohort, 34 (19.3%) of the total of 176 participants had progression of RHOA by the 8-year follow-up. The results of our sensitivity analyses were similar to those from our main analyses, where we included participants regardless of their intention to lose weight and who had a BMI ≥18.5 kg/m2 . Of the 4 studies that investigated hip replacement,21 only one study,20 involving participants from the Osteoarthritis Initiative (OAI), followed up over 8 years, showed an association of weight loss with decreased risk of hip replacement, but only in participants who had hip pain at baseline. However, two of the 4 studies that investigated hip replacement21 included the same OAI cohort in their analyses and did not find any evidence of an association between weight loss and the risk of hip replacement. Of the 7 studies22 that investigated the association of weight loss with hip osteoarthritis, 3 studies18 that investigated hip pain showed mixed results, with one17 finding a reduction in self-reported hip pain after weight loss, but lacking a control group and a small sample size. None of these seven observational studies22 specifically investigated the effect of weight loss on hip osteoarthritis in older adults, as they included adults aged between 18 and 79 years. Our current study of older female adults (65 years and older) found no association between weight loss and hip joint structure as assessed by radiography.These findings add to growing evidence that weight loss has no benefit for hip osteoarthritis. We do not know of any randomized controlled trials that have investigated the effect of weight loss on hip osteoarthritis, but we know of 7 observational studies35 A notable exception is those from the Osteoarthritis Research Society International guidelines (OARSI),36 which cite a lack of clinical trials as a reason for not recommending weight loss for hip osteoarthritis. As mentioned in the 11 and other aspects of health,38 it is associated with increased health risks in older adults.26 Recommending weight loss for people with hip osteoarthritis is sensible if hip osteoarthritis coexists with knee osteoarthritis. However, the guidelines for managing hip osteoarthritis do not specify the requirement of coexistence with knee osteoarthritis. It should be noted that the prevalence of the co-existence of knee and hip osteoarthritis is lower than that of isolated hip osteoarthritis. For example, data from the Canadian Longitudinal Study on Aging (CLSA)39 showed that of 1334 people with hip osteoarthritis, 925 (69.3%) had hip osteoarthritis only and 409 (30.7%) had a coexistence of knee and hip osteoarthritis. Given the high prevalence of isolated hip osteoarthritis, combined with the evidence for increased health risks due to weight loss, and no association of weight loss with apparent benefit for hip osteoarthritis, a review of the recommendation of weight loss for the management of hip osteoarthritis in older women who are free of knee osteoarthritis is warranted.While there is no apparent benefit of weight loss for hip osteoarthritis, weight loss is recommended for managing hip osteoarthritis in 6 different health guidelines worldwide.42 we cannot rule out the possibility that weight loss achieved through these means would have a positive impact on hip osteoarthritis in older adults. As a sixth limitation, as hip osteoarthritis typically occurs in middle-aged to older adults,45 our cohort of female adults aged ≥65 years might have been subject to the selection bias of ‘depletion of susceptibles.’46 This bias arises when people most susceptible to outcomes of interest  are excluded or unavailable for the study. For example, in the SOF study, people who could not walk without assistance or who had bilateral total hip replacement were excluded. Therefore, our cohort might have consisted of people less susceptible to osteoarthritis, which might have biased our estimates toward the null. As a seventh limitation, this analysis included participants who had to have data on weight and the outcomes of hip osteoarthritis available at the 8-year follow-up and therefore must have survived to the 8-year follow-up. We could not investigate the outcomes for shorter follow-up periods because there was no radiography data at less than an 8-year follow-up. Thus, we can conclude that weight loss is not associated with radiographic hip osteoarthritis among older female adults who survive until an 8-year follow-up. In the general population of older adults, mortality may compete with weight loss with respect to the outcomes of hip osteoarthritis that were investigated in this study. The final limitation of this study is the use of data that was collected over 37 years ago, with baseline data being collected between 1986 and 1988, with an 8-year follow-up. The age of this data may raise concerns about its relevance today due to factors such as changes in medical practices and patient demographics. However, the method used at that time—and in the SOF study—for visualization of hip joint structure  is the most commonly-used method today.47This study has several limitations. Firstly, our findings are associative due to the nature of observational studies. Secondly, there were possibly latent confounders that were not captured in our analyses or the SOF cohort from which we sourced the data for this study. Thirdly, while it is a strength that we studied older adults, our participants were all white, and all female, therefore generalizability of the findings from this study is limited to this population. As a fourth limitation, we measured weight change between baseline and the 8-year follow-up visit, but weight can fluctuate markedly during that time, and we did not capture the possible impact of weight fluctuations on the outcomes in this study. As a fifth limitation, we had no data available to determine whether weight loss was achieved through severe dietary energy restriction or an unbalanced diet that leads to nutritional deficiencies, or whether it was achieved through a balanced diet plus exercise. Given that a balanced diet plus exercise are beneficial for bone health,In conclusion, there was no associated benefit of weight loss for the structure of the hip as assessed by radiography over 8 years in older adult females. Because previous research has shown potential health risks of weight loss for older adults, our findings call for a review of the recommendation for weight loss for managing hip osteoarthritis for older women who are free of knee osteoarthritis.Supplementary materialSupplementary Figure A. Histogram of percent weight change from baseline that hips were exposed to in the RHOA development cohort.Supplementary Figure B. Histogram of percent weight change from baseline that hips were exposed to in the RHOA progression cohort.Supplementary Figure C. Outcomes of degeneration of individual structural features of the hip in univariate and multivariable analyses.Supplementary Table S1. Characteristics of the RHOA development cohort and the RHOA progression cohort during follow-up, stratified by weight loss (5% or more from baseline), stable weight (less than 5% weight change from baseline), and weight gain (5% or more from baseline).Supplementary Table S2. Sensitivity Analyses. Association of weight loss with the odds of development and progression of RHOA by the 8-year follow-up visit in people who had the intention to lose weight and had overweight or obesity, as shown in univariate and multivariable analyses.Supplementary STROBE Statement. Checklist of items that should be included in reports of observational studies.