Obesity is associated with a range of disabling musculoskeletal conditions in adults. As the prevalence of obesity increases, the societal burden of these chronic musculosketelal conditions, in terms of disability, health-related quality of life, and health-care costs, also increases. Research exploring the nature and strength of the associations between obesity and musculoskeletal conditions is accumulating, providing a better understanding of underlying mechanisms. Weight reduction is important in ameliorating some of the manifestations of musculoskeletal disease and improving function.
Obesity represents a major public health problem and carries with it the risk of developing significant medical problems. The global burden of obesity is rising at an alarming rate. The World Health Organization estimates that more than one billion people are overweight and of these, 300 million are obese.1 In Australia, about 20% of the population is obese (approximately 2.6 million).2 In addition, the levels of extreme obesity (obesity grade 3, body mass index (BMI) ⩾40) are also escalating.3 Recently, McTigue et al.3 reported that weight-related health risk, specifically all-cause mortality, varies with degree of excess weight with those in the obesity grade 3 range faring significantly worse than individuals of normal weight or a lower grade of obesity.3
Concurrently, in part due to the aging population, the burden of arthritis and musculoskeletal conditions as causes of pain and disability continues to increase. In Australia, these conditions have been identified as the third largest contributor to direct health expenditure (behind cardiovascular disease and neurological disorders).4 ‘Arthritis and related disorders’ were the most common cause of disability in Australia in a recent population survey,5 the second most common reason for general practitioner (GP) visits and also the cause of a large number of hospital separations.6 In an analysis of the direct costs of obesity, it was estimated that the cost of osteoarthritis (some $300 million) was second only to the cost of diabetes in obesity-associated conditions.
There is a significant positive association between musculoskeletal disorders and the level of obesity.7 The Centre for Disease Control recently reported that in the United States, more than 31% of obese adults reported a doctor diagnosis of arthritis compared to only 16% of non-obese people.8 The nature and extent of the impact of obesity on the musculoskeletal system and the spectrum of conditions implicated is not well appreciated. This is surprising considering the high prevalence of chronic musculoskeletal conditions in a rapidly aging population and the associated significant societal burden of lost productivity and direct health-care costs. In addition, the chronic pain and disability associated with musculoskeletal conditions not only significantly affect an individual's quality of life but often result in the early uptake of a sedentary lifestyle associated with various serious comorbidities.
Obesity has been implicated in the development or progression of a wide variety of musculoskeletal conditions. These are summarized in Table 1. Obesity is also associated with increased operative risks in the surgical management of some of these conditions.9 The aim of this study is to provide a comprehensive overview of the specific musculoskeletal conditions associated with obesity and present the evidence underpinning the association between obesity and these musculoskeletal conditions. The possible impact of obesity on therapy is also explored. A literature search (Medline and Pubmed) was conducted from January 1966 to December 2006. Articles assessing the effect of obesity or weight loss on musculoskeletal conditions were reviewed.
Osteoarthritis (OA) is the most common form of arthritis and the leading cause of chronic disability among older people. Large longitudinal studies10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23 have demonstrated that obesity is a significant risk factor for both the development and progression of tibio-femoral knee OA (both symptomatic and radiographic). An association, though modest, has also been demonstrated between obesity and OA at other sites such as the hip, hand and patello-femoral joint, suggesting that both mechanical and metabolic factors may be responsible for the link between OA and obesity.
Prospective data from the Framingham population demonstrated that obesity predates the development of knee OA, and that obesity is an independent risk factor for incident radiographic OA. The odds ratio (OR) per 5-U BMI increase was 1.6.10 In the Chingford study of over 1000 women, obesity was classified as the upper tertile of BMI (the boundaries of the middle tertile were 23.4 and 26.4 kg m−2).24 The age-adjusted OR of unilateral and bilateral radiological knee OA comparing the high and low tertiles of BMI were 6.2 and 18, respectively, and the risk was 8.6 times higher for symptomatic disease. In the recent MOST cohort, those with highest obesity were again at highest risk of developing symptomatic and radiological knee OA at 15 months (OR 3.4).25 A recent study on ambulatory loads in overweight and obese subjects indicated that cartilage thickness at the knee joint responds to loading during gait in a similar manner to OA patients. These findings suggest the possibility that increased weight initiates a pathway of cartilage degeneration prior to the emergence of OA symptoms.26
In a controlled study with twins, Cicuttini et al.19 showed that each kilogram increase in body weight was associated with an increased risk of radiographic features of OA at the knee and carpometacarpal joint. The strong association between high BMI and knee OA was confirmed in another twin study and this association was found not likely to be mediated by shared genetic factors.27 Obese patients with knee OA have more joint space narrowing in the medial and lateral tibio-femoral compartments than non-obese patients.28
Obesity is also an important risk factor for the progression of knee OA17 and has long-term detrimental effects on the knee joint.29 Sharma et al.30 looked at the role of mechanical factors, specifically malalignment, in mediating knee OA severity or progression. In patients with knee OA, there was a relationship between BMI and radiographic severity in those with varus malalignment, but not in those with valgus malalignment. BMI correlated positively with varus malalignment. However, the partial correlation between BMI and medial joint space width was reduced from 0.24 to 0.04 after adjustment for malalignment, due to the strong positive association between medial joint space width and varus malalignment. It was found that varus malalignment may explain, in part, the uniquely strong association between BMI and OA at the knee compared to other lower extremity sites. However, given the cross-sectional nature of the study, it cannot be established whether varus malalignment is causal or consequential in the relationship between obesity and OA. Nevertheless, varus malalignment is an important mediating factor in knee OA in the obese individual. Felson et al.31 also found that the adverse effect of high BMI on knee OA progression was limited to those patients with moderate malalignment.
Although the strong association between knee OA and obesity has been demonstrated, the factors underlying the mechanism of the effect have not been entirely elucidated. Age, serum lipids, serum uric acid, blood glucose or diabetes, body fat distribution, blood pressure, smoking, chondrocalcinosis, hysterectomy or estrogen replacement therapy have not been found to affect the obesity–OA relationship.30 However, being overweight is associated with increase in cartilage turnover biomarkers. Cartilage oligomeric matrix protein and collagen type 2 degradation products were increased in those with high BMI.32, 33
Another study examined the effects of measures of body composition on the longitudinal change in tibial cartilage volume using magnetic resonance imaging (MRI).34 Eighty-six healthy adults underwent assessment of body composition using dual X-ray absorptiometry and MRI at baseline and 2 years. A strong positive association was found between muscle mass in the lower limbs, muscle mass in all limbs, and muscle mass in the total body and medial tibial cartilage volume after adjustment for confounders such as age, sex, BMI, medial tibial bone size and physical activity. Importantly, in the longitudinal analysis, increased muscle mass was also associated with a reduction in the rate of loss of both medial and lateral tibial cartilage volume. In contrast, body fat was not associated with medial or lateral tibial cartilage volumes or loss in adjusted analysis. This finding was confirmed in a recent larger study suggesting that apparent gender difference in articular cartilage volumes (men demonstrating higher cartilage volume) may be largely explained by fat-free muscle mass.35 However, another study reported that increased muscle mass may predispose to lateral patello-femoral OA progression in women,36 whereas in another, greater quadriceps strength was found to have no effect on cartilage loss at the tibio-femoral joint, even in malaligned knees.37
The association between knee structural alteration and BMI was evaluated in a cross-sectional convenience sample of 372 largely healthy subjects.38 Apart from the lateral tibio-femoral compartment, BMI was significantly associated with knee cartilage defect scores such that obese subjects had higher cartilage defect severity and prevalence. BMI was also positively associated with tibial bone area but there was no significant change in cartilage volume or thickness compared to those with normal weight. This study shows that increasing BMI may induce cartilage defects even in those with no radiographic OA. The reasons for this remain to be elucidated.
There is some evidence suggesting that knee bone size may be important in the development of knee OA. Knee bone size is under strong genetic control and is higher in the offspring of those with severe OA.38 The authors propose that a greater BMI can induce larger knee subchondral bone size or that knee subchondral bone may respond to higher loads by expansion of the joint surface area. In this study, knee bone size mediated, in part, the associations between BMI and knee cartilage defects, because these associations were attenuated after adjustment for bone size and vice versa.
Higher BMI is also associated with increased risk of degenerative meniscal lesions.39 However, it is not certain if degenerative meniscal lesions have an etiological role in the development of knee OA.
The First National Health and Nutrition Examination Survey data show that obesity was more closely associated with bilateral hip OA than with unilateral hip OA.40 A systematic review found moderate evidence for a positive association between obesity and the occurrence of hip OA (OR ∼2).41 The associations between obesity and hip OA were stronger when the diagnosis included clinical as well as radiological criteria.
The association between obesity and hand OA is less certain with some studies suggesting a link and others showing conflicting results.16, 42, 43, 44, 45, 46, 47. In a large Finnish study, BMI was found to be directly proportional to the prevalence of thumb carpo-metacarpal OA in both sexes.48 The adjusted OR was 1.29 per 5 kg m−2 increment in BMI.
In the recent Rotterdam study, overweight showed a significant association with hand OA independent of other metabolic factors (OR 1.4).49 An association between overweight and hand OA infers other underlying mechanisms apart from increased load across weight-bearing joints. In this study, no intermediate effect of metabolic factors on the association of overweight with hand OA was found. Leptin may have an important role in the metabolic influence of overweight on OA. Serum leptin, the product of the obese (ob) gene, is involved in energy regulation at the level of the hypothalamus and recent evidence suggests that leptin may act locally in joint tissues.50 Leptin has been detected in synovial fluid samples obtained from OA patients and levels of leptin have been found to correlate with BMI.51 Leptin has also been strongly overexpressed in human OA cartilage and in osteophytes.
Normal weight is associated with a decreased risk incidence and progression of OA.15, 52 Both the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) recommend weight loss and exercise for obese patients with knee OA.53, 54
In the Framingham study, evaluation of 800 women showed a decrease in BMI of ⩾2 kg m−2 in the preceding 10 years decreased the odds of developing symptomatic OA by >50%.11 It has also been suggested that if all overweight and obese people reduced their weight by 5 kg or until their BMI was within the normal recommended range, 24% of the surgical cases for knee OA might be avoided.55
Until recently, only a few nonrandomized clinical trials have examined the effect of weight loss on pain and function in knee OA, suggesting that the combination of dietary weight loss plus exercise is effective.56, 57, 58 Recently, a large clinical trial, the ADAPT study, randomized 316 overweight or obese older subjects with knee OA to exercise only (combined aerobic and strengthening), dietary weight loss only, exercise plus dietary weight loss or a healthy lifestyle control group. After 18 months, despite only modest reductions in body weight, significant improvements in pain and physical function were seen in the diet plus exercise group compared to the healthy lifestyle group, but not for the weight loss or exercise-only allocations.59
A subset of the ADAPT study cohort underwent biomechanical analysis testing over an 18-month period.60 There was a significant relationship between weight loss and reduction in compressive knee-joint loads, with a four-pound reduction in knee-joint load per step for every 1 pound weight loss. To date, there are no longitudinal studies evaluating if weight loss slows the progression of knee OA but this effect would appear to be clinically plausible. In the ADAPT study, no changes in joint space narrowing were noted between the different groups.61 However, the study was probably underpowered to detect differences in joint space narrowing over an 18-month period. MRI possibly allows a more sensitive measure of joint space loss compared with radiography, but thus far, no studies have looked at MRI outcomes in subjects undergoing weight loss.
A second recent randomized clinical trial, evaluating a rapid weight loss diet among 80 patients with knee OA, found that a weight reduction of 10% improved function by 28%. The authors found that less than four patients (95% confidence interval 2–9 patients) would need to be treated with a low-energy diet for one patient to achieve a ⩾50% improvement in the WOMAC score (a measure of joint pain, stiffness and function) when compared to a control diet.62
The effects of weight loss and exercise interventions on serum leptin were also assessed in the ADAPT cohort.63 In the ADAPT cohort, serum leptin was significantly reduced by a long-term diet (weight loss) intervention with modest weight loss of 5–6%. Serum leptin was also related to self-reported physical function with higher leptin concentrations related to greater impairments in physical function. The authors also found that initial baseline leptin levels were a predictor for subsequent weight loss, with lower baseline levels of leptin predicting greater weight loss.
The need for joint replacement surgery has been escalating with the increased burden of OA in the community. In Australia, orthopedic surgery had the second longest median waiting time in 2003–2004.64 With the increasing prevalence of obesity, the proportion of joint replacements performed in obese patients is likely to increase dramatically, with estimates suggesting over a third of all total hip and knee replacements are performed in the obese.65, 66, 67, 68 A frequency-matched case–control study found that very obese females (BMI >40) were more likely to face joint surgery compared with matched normal weight females in either the hips (OR=4) or knees (OR=19).69 Similarly, obese males were more likely to undergo joint replacement surgery compared with non-obese males.
A recent review discussed the decision by three primary care trusts in the United Kingdom to not entitle patients with BMI >30 to hip and knee replacement surgery, and evaluated the current evidence for outcomes in obese patients for both total knee and hip replacement surgery.9 In the midterm, outcomes of knee replacement in the obese (BMI >30) are probably comparable to the non-obese but larger, prospective studies are needed to ascertain long-term outcomes. However, there is some evidence that outcomes in the morbidly obese (BMI >40) are consistently poor.9 Similar data are not available for the effect of morbid obesity in hip replacement.
Obesity may not be a contraindication to simultaneous bilateral total knee replacement surgery.70 However, a BMI >32 predicted failure in those undergoing minimally invasive medial unicompartmental knee arthroplasty in a retrospective series.71 Obesity is a risk factor for patients undergoing high tibial osteotomy for the treatment of unicompartmental knee OA in the presence of malalignment.72 Outcomes relating to quality of life and satisfaction following arthroscopic debridement of the knee were also poorer in overweight women than the normal weight group.73
Low back pain
Low back pain from degenerative disc disease of the lumbar spine, spinal canal stenosis and zygo-apophyseal joint disease is a very common problem in the community resulting in significant morbidity.74 This has important consequences in terms of productivity at work and utilization of health services. The association between obesity and lower back pain is conflicting.75, 76, 77, 78, 79 A recent review describes the lack of a clear dose–response relationship between BMI and low back pain.80
However, compared with non-obese patients, obese patients were more likely to have radicular pain and neurologic signs.81 Obesity was a significant, independent determinant of chronicity in a prospective cohort study in workers claiming compensation for lower back pain.82 In morbidly obese subjects with lower back pain undergoing bariatric surgery, weight loss significantly improved the degree of functional disability,83 and resulted in less frequent lower back pain and the use of reduced doses of medications.84
In a population-based study of 129 middle-aged working men comprising machine drivers, construction carpenters and office workers, persistent overweight was strongly associated with decreased signal intensity of the nucleus pulposus at follow-up MRI (adjusted OR 4.3).85 However, it is not known whether these MRI findings correlate with clinical symptoms. Spinal epidural lipomatosis is also associated with obesity.86 Here, there is hypertrophy of the epidural adipose tissue, causing a narrowing of the spinal canal and compression of neural structures.
The relationship between ambulation and obesity in older individuals with and without low back pain was assessed in a retrospective study. BMI had a significant inverse relationship with ambulatory measurements in terms of distance walked, steps taken and walking velocity.87
A retrospective study assessing outcomes of sciatica found that obesity was associated with adverse 6-month outcomes.88 Being overweight and obese is also a risk factor (OR 1.83) for postoperative meralgia paraesthetica after posterior thoracolumbar surgery.89 However, outcome assessment in elderly patients undergoing lumbar spinal surgery did not find any difference in the obese group suggesting that surgery in the elderly obese with appropriate symptoms would be reasonable.90
Diffuse idiopathic skeletal hyperostosis
Diffuse idiopathic skeletal hyperostosis (DISH) or Forestier's disease, a chronic age-related condition, is characterized by new bone growth especially at the entheses. DISH affects many skeletal structures but typically affects the thoracic spine. It is associated with obesity, diabetes mellitus, hyperinsulinemia and hyperlipidemia.91, 92 In an age- and gender-matched case–control study, patients with DISH were more likely to have elevated BMI than controls without DISH.93 A study examining the role of leptin in the ossification of spinal ligaments found that serum leptin levels were significantly elevated in subjects compared to controls.94 The daughters of subjects who were severely obese also had high serum leptin levels although they had not developed the condition. Leptin may thus be genetically and indirectly associated with the pathogenesis of the ossification of spinal ligaments in female patients. The role of obesity in the pathogenesis of DISH is yet to be clearly defined and the effect of weight reduction in reversing/slowing progression of disease has not been studied.
Obesity is also associated with structural and functional limitations95 with impairment of normal gait,96 flattening of the foot arches97, 98, 99 and pronation of the ankles. In a pilot study, body composition was found to influence arch index values in overweight and obese subjects.100 Obesity increases rearfoot motion during walking and causes the forefoot to abduct significantly more than in normal weight individuals.101
Excess weight is associated with increases in the amount of force across a weight-bearing joint.30, 102 A study assessing postural instability in extremely obese individuals found these individuals had inadequate postural instability as measured by time of balance maintenance and medial-lateral sway of the trunk.103 After a 3-week body weight reduction program and specific balance training, postural stability could be improved which has the potential to reduce the propensity of overweight individuals to fall while performing everyday activities. In another study, obesity was associated with attenuated dynamic balance performance.104 Poorer balance was found to be associated with higher pain scores in t he presence of weaker knees.
Morbidly obese subjects also walk significantly slower than their obese and lean counterparts.105 BMI was one of the factors affecting the variance in walking distance. The effects of obesity on gait need to be further understood as an important part of management would include incorporating an appropriate exercise program.
Soft tissue complaints
There is a high prevalence of pain in the neck (10–19%), shoulder (18–26%), elbow (8–12%) and wrist/hand (9–17%) at any given time in the community.106 Obesity is consistently a significant risk factor associated with the occurrence of these complaints. Obesity was also found to predict those who were likely to develop upper extremity tendonitis associated with work activity in a prospective cohort study over 5 years.107 In another prospective survey of upper-limb work-related musculoskeletal disorders in repetitive work, obesity again increased the risk of ulnar entrapment at the elbow.108
A recent study assessed the point prevalence of painful musculosketelal conditions in obese subjects before and after weight loss following bariatric surgery.109 There was an increased prevalence of these conditions at baseline compared to the general population. There was a significant decrease in pain at most sites following weight loss and physical activity after 6–12 months, in particular the cervical and lumbar spine, and foot.
Carpal tunnel syndrome is a common condition in the community. In a large case–control study using the UK General Practice Database, obesity was a significant risk factor associated with carpal tunnel syndrome (OR=2.06).110 Obesity has been shown to be an independent risk factor for carpel tunnel syndrome in a number of studies.111, 112 There is also an association between obesity and shoulder repair surgery for rotator cuff and other conditions, suggesting that increasing BMI is a risk factor for rotator cuff tendonitis and related conditions.113
Plantar fasciitis is a common soft-tissue disorder of the foot. Obesity is a risk factor for developing unilateral plantar fasciitis (OR 5.6 compared to normal BMI).114 Obesity is also associated with chronic plantar heel pain.115 The link between obesity and plantar heel pain is, however, not well understood. Arch biomechanics are thought to play a role in etiology but this has not been conclusive.116 Obesity is also a risk factor for trochanteric bursitis, a frequent cause of lateral hip pain in middle-aged and elderly individuals.117
A number of studies have demonstrated that body weight is closely correlated with bone mineral density (BMD).118, 119, 120 In cross-sectional studies, a 10 kg increase in body weight is associated with approximately a 1% increase in BMD. This relationship has been demonstrated for both women and men and across cultures but the effect of weight on BMD appears to be stronger in women than in men,121, 122, 123 and more in postmenopausal than premenopausal women.124, 125
Several mechanisms have been proposed to explain the effect of weight on bone density. Firstly, it could be due to the amount of adipose tissue, which is the major site of conversion of androgens to estrogen in both elderly men and women. If estrogen has a greater role in preservation of bone mass in women than men, this may explain why the effect of weight is greater in women than men. This may also explain why shortly after menopause, obese women do not lose bone as rapidly as their non-obese counterparts.126, 127 A second mechanism relates to the increased mechanical load that heavier individuals place on weight-bearing bones. This is supported by some data suggesting that body size is a better determinant in weight bearing rather than non-weight-bearing sites.123 Although it is often considered that obese subjects are at lower risk of osteoporosis, there is evidence that changes in bone marrow fat with ageing may adversely affect skeletal strength. Visceral fat may have a protective effect on BMD128 through biochemical factors such as adiponectin. The latter is an adipocyte-derived hormone that regulates insulin sensitivity and energy homeostasis.
There is still controversy over the relative importance of fat versus lean mass in the determination of BMD. Reid129 concluded that while both fat and lean mass are related to bone measures, the effect of fat mass becomes more important in postmenopausal women and that the relationship between lean mass and bone density was substantially accounted for by body size. Only a few studies have investigated the association of bone mineral measures with body composition components adjusted for body size or their distribution (such as centrality indices).130
However, recent research suggests that obesity may accelerate bone loss.131 Deng et al. showed, in two large population samples, that the bone strengthening effects of a heavy body were not due to fat but to elevated muscle mass, which increases bone density.131 The authors report that increased fat mass is associated with decreased bone mass, when the mechanical loading effect of body weight on bone mass is adjusted for. The risk of fracture in the obese is not clear with conflicting associations being reported.132, 133
There is also evidence from longitudinal studies that weight loss is a risk factor for rapid bone loss in men and women,134, 135, 136 although methodological differences between machines in relation to measurement of BMD due to changes in fat distribution may affect results. Another study showed that overweight postmenopausal women may be more susceptible to bone loss with weight reduction. Weight loss correlated with BMD loss at the trochanter but not at the femoral neck in the group receiving normal calcium intake daily compared to high calcium intake.137 Weight loss due to caloric restriction appears to induce rapid bone loss at clinically important sites of fracture, unlike exercise-induced weight loss.138 In addition, the rapid increase in obesity has led to an escalation in the uptake of surgical techniques to control weight. Procedures that involve duodenal bypassing place individuals at risk for osteoporosis as this is the primary site for calcium absorption.139 Obesity is also a risk factor for vitamin D deficiency.140
Gout is the most common form of crystal-induced arthritis and in the United States affects more than 1% of adults.141 It results from the deposition of monosodium urate crystals. Obesity is a well-known modifiable risk factor in the pathogenesis of gout and serum uric acid is positively associated with BMI.142 The size of the visceral fat area is the strongest contributor to elevated serum uric acid concentration, decreased uric acid clearance and increased urinary uric acid/creatinine ratio.143 Weight loss is advocated in the overall management of gout but no study has assessed the effect of weight reduction on uric acid levels or attacks of gout.
Fibromyalgia is a complex disorder resulting in pain, disturbed sleep and altered mood. A number of risk factors are associated with this condition and obesity also plays a role.144 In a pilot study of overweight and obese women with fibromyalgia, the relationship between BMI and fibromyalgia symptoms were assessed after a 20-week behavioral weight loss treatment.145 Participants lost, on average, 4.4% of their initial weight, and weight loss predicted a reduction in fibromyalgia symptoms, pain interference, body satisfaction and quality of life. In a study of obese subjects undergoing bariatric surgery, there was a significant reduction in fibromyalgia syndrome at follow-up 6–12 months later.109
Connective tissue disorders
Rheumatoid arthritis (RA) is the most common chronic inflammatory joint disease. Obesity has been identified as a risk factor for RA.146 Two population-based cohort studies have shown an association between obesity and the development of RA,147, 148 whereas one149 did not. The association appears to be a threshold effect with no relationship between BMI and the risk for RA below a BMI of 30. Paradoxically, one study in a cohort of 779 RA patients found that BMI was inversely associated with mortality independent of methotrexate use. Corticosteroid use was not tabulated. Interestingly, an interaction was found between BMI and erythrocyte sedimentation rate and BMI was protective only if the erythrocyte sedimentation rate was low.150 However, obesity was also recently found to be independently associated with impaired quality of life in patients with RA.151 A marked increase in plasma levels of adipocytokines (leptin, adiponectin and visfastin) have been noted in patients with RA suggesting a role in the modulation of the inflammatory environment in these patients.152
In systemic lupus erythematosus, obesity is a strong predictor of preeclampsia.153 Obesity is common in the lupus population, 36% prevalence in one urban university clinic.154 However, obesity was not associated with hypertension and diabetes in this cohort and contrary to expectation, overweight systemic lupus erythematosus patients appeared to register the highest quality of life on questioning.
Hypoandrogenicity in males is common in obesity and in chronic inflammatory conditions such as systemic lupus erythematosus and RA.155 Leptin, as well reflecting adipose tissue mass, is stimulated by tumor necrosis factor and is associated with hypoandrogenicity in non-inflammatory conditions. Leptin has been found to correlate negatively with adrenal androgen concentrations in patients with systemic lupus erythematosus and RA, suggesting that leptin may be an important link between chronic inflammation and the hypoandrogenic state.155
Disability/quality of life
It is increasingly being recognized that obesity impacts on health-related quality of life and disability. Obesity increases the risk of disability among people who have arthritis.156, 157, 158, 159 Obesity is also associated with disability in those without self-reported arthritis.159, 160 People who have disabilities are 2.5 times more likely to be obese than those who do not have disabilities.161 In the ADAPT cohort, exercise and dietary weight loss improved mobility-related self-efficacy and self-reported pain.162 In cross-sectional data from the 1998 Quebec Health Survey, being overweight was significantly associated with short- and long-term activity limitation related to musculoskeletal disease.163
Obesity is also consistently associated with lower limb joint pain (hip and knee)164, 165, 166 and back pain.167 Osteoarticular pain (knee and hip pain) is a major predictor of poor health-related quality of life in obese subjects168 and obesity is linked with knee pain severity and disability among older knee pain sufferers in the general population.169 Population-based surveys have confirmed J-shaped associations between BMI and health-related quality of life, with obese individuals significantly more likely to report fair or poor general health status.170, 171
Exercise capacity is decreased in obesity, both at submaximal and peak intensity, and during recovery.172 Importantly, weight reduction was found to have positive short-term effects on musculoskeletal pain, perceived disability, and observed functional limitations.173 A recent systematic review also provides category 1a evidence that weight reduction reduces pain and disability in knee OA patients.174
Obesity is also significantly associated with the frailty syndrome. Frailty indicators include weakness, slowness and low physical activity, and predisposes to loss of independence. Physical frailty is common in community-dwelling obese elderly men and women.175, 176 In home-dwelling elders, obesity was again one of the primary predictors of decreased quality of life.177
Clearly, obesity has an important impact on health-care costs due to direct and indirect costs. Obesity cost Australians $21 billion in 2005, double the cost of Medicare in Australia. Lost tax revenue, welfare and other government payouts incurred by obesity sufferers was estimated at $358 million.178 In a Dutch case–control study among self-employed insured farmers, neck, shoulder, upper extremity and back disorders accounted for 30% of claims for sick leave of less than 1 year. Multivariate analysis assessing risk factors showed that BMI>27 was two times more likely to result in musculoskeletal disorders as a cause of sick leave.179 Obese subjects were found to have more work-restricting musculoskeletal pain than the general population in a Swedish study.180 In a large cross-sectional study of patients with spinal disease, obese patients had more comorbidities and were more likely to be receiving worker's compensation.81
Obesity also results in significantly higher primary care drug prescribing in most drug categories including musculoskeletal and joint disease as noted in a recent retrospective review in the United Kingdom.181 There is also a positive relationship between musculoskeletal disorders and the consumption of disability products.182 Moreover, there is an association between obesity and being on the disability pension. A linear relationship was identified between BMI and disabling knee OA.183 In Swedish 5 birth-year cohorts, there was a J-shaped relationship between BMI and incidence of disability pension (RR in obese subjects 2.8) and musculoskeletal disorders were one of the primary reasons.184 This is corroborated in a Finnish study.185
The increasing prevalence of obesity among patients and caregivers can also lead to more frequent and serious musculoskeletal injuries among caregivers.186 The ramifications include the need to utilize safe and appropriate equipment to cope with obese individuals which inevitably requires extra care and resources.
Obesity is associated with a number of musculoskeletal conditions and is responsible for significant disability and impaired quality of life. The global obesity epidemic has significant consequences for both the individual and the community in terms of direct and indirect health-care costs. Further studies prospectively evaluating these conditions in the obese population are imperative to define better the mechanisms by which obesity mediates musculoskeletal disorders, and to determine the effects of moderate to large weight loss on these conditions. This has important ramifications in both the prevention and development of appropriate treatment strategies in the ongoing management of these conditions.
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Ananthila Anandacoomarasamy holds a National Health and Medical Research Council Medical Postgraduate Research Scholarship (ID number 402901).
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Anandacoomarasamy, A., Caterson, I., Sambrook, P. et al. The impact of obesity on the musculoskeletal system. Int J Obes 32, 211–222 (2008). https://doi.org/10.1038/sj.ijo.0803715
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