Purine-Rich Foods

Diets high in protein and alcohol have long been thought to increase the risk of gout. Metabolic studies have shown that increased purified purine loads can raise serum uric acid concentration. For this reason, patients with gout have traditionally been encouraged to adhere to severely purine-restricted diets. Such diets can decrease the serum urate concentration by about 1 mg/dL but may be too impractical or unpalatable for long-term adherence. Conversely, modifications like those recommended for patients with insulin resistance, emphasizing caloric restriction and avoidance of saturated fat and refined carbohydrates, may be more palatable and have shown the ability both to decrease serum urate and to diminish the recurrence of gout. In a group of 13 men on such a diet, serum urate levels dropped an average of 1.7 mg/dL, and the number of monthly gout attacks decreased from 2.1 to 0.6. Weight loss and improved lipid profiles were other benefits.

These findings suggest dietary modification might be of value in preventing gout attacks but are limited by the small number of subjects and lack of data on specific foods. To elucidate the relationship between dietary risk factors and incident gout in more detail, the Health Professionals Follow-up Study (HPFS) followed 47,150 men with no baseline history of gout prospectively for 12 years. In that span, there were 730 incident cases of gout. Men in the highest quintile of meat intake (namely beef, pork, and lamb) were 41% more likely to develop gout than those in the lowest quintile, whereas those who consumed the most seafood (both fish and shellfish) had a 51% higher risk than those who consumed the least.

In addition to increasing incident gout risk, meat and seafood have also been shown to raise serum uric acid level. In the Third National Health and Nutrition Examination Survey (NHANES III), investigators surveyed the dietary habits of 14,809 participants and found that, after adjusting for age, the differences in uric acid levels between the top and bottom quintiles of consumption were 0.48 mg/dL (95% CI 0.34, 0.61; P <.001) for total meat and 0.16 mg/dL (95% CI 0.06, 0.27; P = .005) for seafood. After adjusting for several covariates, including age, sex, body mass index (BMI), serum creatinine, hypertension, alcohol use, and diuretic use, these differences remained statistically significant.

Vegetables and Dairy

Consumption of vegetable and dairy protein appears to confer a protective effect against gout. In the HPFS, those in the highest quintile of vegetable protein intake were 27% less likely to develop gout than those in the lowest quintile, whereas top consumers of dairy protein had a 48% lower risk compared with those in the bottom fifth. Foods rich in vegetable and dairy protein tend to be low in purines, but even purine-rich plant foods (peas, beans, lentils, spinach, mushrooms, oatmeal, and cauliflower) were not associated with an increased risk of gout. The protective effect of dairy was limited to low-fat dairy products, but high-fat dairy products also did nothing to increase gout risk.

In the NHANES III, those in the highest quintile of dairy consumption had a serum uric acid level 0.21 mg/dL lower than those in the lowest quintile (95% CI 0.04, 0.37; P = .02). Interestingly, those who consumed milk once or more per day had a lower serum uric acid level than those who did not (−0.25 mg/dL; 95% CI −0.40, −0.09 and P <.001), whereas those who consumed yogurt at least once every other day had a lower serum uric acid level than those who did not (−0.26 mg/dL; 95% CI −0.41, −0.12; P <.001). These findings closely parallel those in the HPFS and provide strong evidence for the observed trends in incident gout risk in that study.

Alcohol

The HPFS also demonstrated a strong association between alcohol intake and an increased risk of gout. The degree of association grew as the level of consumption increased and varied with the type of beverage. Specifically, consumption of beer showed the strongest link, with a relative risk of 1.49 (95% CI 1.32–1.70) per 12 ounce serving per day. Consumption of liquor was also significantly associated with gout, with a relative risk of 1.15 (95% CI 1.04–1.28) per drink or shot per day. Meanwhile, wine consumption was not associated with gout (relative risk 1.04; 95% CI 0.88–1.22).

Beer, wine, and liquor intake also affects serum uric acid level. After adjusting for other risk factors for hyperuricemia and consumption of the other alcoholic beverages surveyed, the NHANES III found that both beer (0.46 mg/dL per serving per day; 95% CI 0.32, 0.60) and liquor (0.29 mg/mL per serving per day; 95% CI 0.14, 0.45) increased serum uric acid level, whereas wine (0.04 mg/mL per serving per day; 95% CI −0.20, 0.11) did not. These findings corroborate earlier studies linking gout attacks to alcohol consumption but suggest that nonalcoholic components may play an important role. For instance, beer has a large purine content, whereas wine and liquor do not. The ingested purine in beer, in combination with the hyperuricemic effect of the alcohol itself, may account for its stronger association with gout. It is not known whether any protective effects of wine account for its lack of a demonstrable gout risk.

Fructose

Another dietary factor that deserves special mention given its widespread consumption is fructose. According to the HPFS, men who consume increased amounts of sugar-sweetened soft drinks and other sources of fructose, including fruit juice and fructose-rich fruits like apples or oranges, have an increased risk of gout. Specifically, those who consumed two or more servings of sugar-sweetened soft drinks per day were 85% more likely to develop gout than those who drank less than one per month. Diet drinks, by contrast, were not associated with any increased risk. Similarly, the NHANES III showed higher serum uric acid levels with increasing consumption of sugar-sweetened soft drinks. Drinking the equivalent of 0.5 to 0.9 servings per day increased serum uric acid level by 0.15 mg/dL, whereas drinking 1.0 to 3.9 servings per day increased the level by 0.33 mg/dL (95% CI 0.11, 0.73; P <.001 for trend). Consumption of diet soft drinks was not associated with any increase in serum uric acid levels.

Coffee and Tea

By contrast, coffee consumption is associated with a decreased risk of gout. As the number of daily cups of coffee increases, the risk of incident gout decreases. In the HPFS, the multivariate relative risk associated with drinking no cups per day was 1.00, whereas for one to three daily cups it was 0.92, and for four to five cups it was 0.60 (95% CI 0.41–0.87, P = .009). Decaffeinated coffee showed a modest inverse association with gout, whereas tea intake and total daily caffeine intake showed no protective effect. Serum uric acid level also decreases with increasing coffee intake, lower by 0.26 mg/dL (95% CI 0.11, 0.41) for those drinking four to five cups daily and 0.43 mg/dL (95% CI 0.23, 0.65) for those drinking six or more cups daily compared with those who do not drink coffee ( P <.001). Similarly, decaffeinated coffee intake has a modest inverse association with uric acid level, whereas tea and total caffeine intake have no effect. These findings suggest components of coffee other than caffeine may play a role in reducing the risk of hyperuricemia and gout. Potential mechanisms include a possible link between antioxidants in coffee and decreased insulin levels. Insulin decreases renal excretion of urate, and insulin resistance is associated with hyperuricemia.

Obesity

Common comorbidities should be considered in any discussion of lifestyle and dietary modifications for patients with gout. In addition to data on dietary risk factors, the HPFS reported findings linking gout to obesity. Those men with an elevated BMI had an increased relative risk of developing gout compared with those who were of normal weight. Those who had gained 30 or more pounds since age 21 were 1.99 times more likely to develop gout than those who maintained their weight (95% CI, 1.49–2.66). Meanwhile, losing 10 or more pounds during the course of the study had a protective effect (relative risk 0.61; 95% CI, 0.40–0.92). Other studies have linked gout and hyperuricemia to the metabolic syndrome with a prevalence of 63% among gout patients compared with 25% among patients without gout. Gout has also been linked with diabetes mellitus, cardiovascular disease, and even mortality. Given these findings, gout should itself be considered an important risk factor for metabolic diseases. Consequently, any lifestyle or dietary intervention for gout should simultaneously target these associated “lifestyle” diseases in an effort to minimize risk. Unfortunately, recent data indicate that patients with gout are not routinely following evidence-based dietary recommendations.

Summary

Gout is an inflammatory arthritis associated with several dietary and lifestyle risk factors. Meat, seafood, and sugar-sweetened beverages increase the risk of gout, as do beer and liquor, but not wine. By contrast, vegetable proteins, low-fat dairy products, and coffee decrease the risk of gout. Because gout is associated with important chronic lifestyle-related diseases, including diabetes mellitus and the metabolic syndrome, dietary and lifestyle changes should address the increased risk of those diseases. A reasonable approach should focus on daily exercise, weight control, and limiting intake of fructose and refined carbohydrates as in patients with diabetes mellitus. Excessive intake of beer and liquor should be avoided, and dairy and vegetable proteins should replace some of those derived from meat and fish. Large prospective trials of such a diet in patients with gout are needed to determine the ability of diet and lifestyle modification to prevent gout recurrence.

Which Diet?

There are a variety of “fad diets” targeted to the general population despite a lack of scientific studies to support their various claims. Energy restrictive diets result in significant initial loss of bodyweight but are associated with high dropout and relapse-rates over time. Low-fat diets yield minimal success with respect to weight loss but do result in significantly lower blood lipid levels. High-protein, low-carbohydrate diets are advertised as the most effective at reducing bodyweight, although there has been no study comparing them to low-calorie diets for long-term weight loss.

A study by Christensen and colleagues examined the effectiveness of a rapid, diet-induced weight loss intervention on overweight individuals with OA of the knee. Eighty patients with knee OA, 89% of whom were women, were randomized either to a low-energy diet (LED) intervention (3.4 MJ/d) or a control diet (5 MJ/d). The LED intervention consisted of a nutritional powder that met recommendations for daily intake of high-quality protein and was taken as six daily meals. The control intervention consisted of a traditional hypoenergetic, high-protein, low-calorie diet taken in the form of ordinary foods based on recommendations from a nutritional advice session. At study conclusion, the LED group had lost more weight and body fat than the control group. There was also a greater decrease in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores among the LED intervention group compared with the control group (mean between-groups difference 219.3 mm, P = .005). These results suggest that for OA patients a low-energy diet may be more beneficial than an ordinary diet because it yields more rapid weight loss and more significant loss of body fat.

The general recommendation for obese patients with OA is to adhere to a weight loss program with an initial goal of 10% body weight loss at a rate of 1 to 2 lb per week. This has been shown to provide symptomatic relief and improve function by an average of 28%. Regardless of the diet chosen, however, achieving and sustaining weight loss is difficult and requires a multidisciplinary team approach.

Inflammation and OA

Overweight individuals are at an increased risk of developing OA in weight-bearing joints. Although much of the risk is due to biomechanical factors, data suggest that other systemic effects may also play a role. A number of studies have shown that decreasing body fat is more important than overall weight loss in improving symptoms. Adipose tissue serves as an endocrine organ and secretes a number of inflammatory markers, including leptin, tumor necrosis factor-alpha, and cytokines, that may mediate symptoms in OA through chronic inflammation. Weight-loss programs for OA patients should therefore focus on loss of fat mass, particularly abdominal fat, while maintaining lean muscle mass.

Exercise Programs

In combination with diet, exercise is another effective tool for weight loss and symptom reduction in OA. The Arthritis, Diet, and Activity Promotion Trial (ADAPT) was a randomized, single-blind clinical trial lasting 18 months designed to determine whether long-term exercise and dietary weight loss are effective, either separately or in combination, at improving functional impairment, pain, and mobility in older overweight individuals with OA of the knee. Three hundred and sixteen adults with knee OA and a BMI of at least 28 kg/m2 were recruited and randomized to one of four interventions: healthy lifestyle (control), diet only, exercise only, or diet plus exercise. The primary outcome was self-reported physical function using the WOMAC index. Secondary outcomes included weight loss, 6-minute walk distance, stair-climb time, WOMAC pain and stiffness scores, and changes in joint space width on radiographs of the knees. At study conclusion, the combination of dietary weight loss and exercise resulted in greater overall improvement in function and pain compared with control and with either intervention alone.

Polyunsaturated Fatty Acids

Polyunsaturated fatty acids (PUFA) are classified as n-3, n-6, or n-9, depending on the position of the last double bond along the fatty acid chain. PUFAs are metabolized by cyclooxygenases (COX) and lipooxygenases (LOX) into different eicosanoids. The main dietary PUFAs are n-3-derived eicosanoids, which tend to be proinflammatory, and n-6-derived eicosanoids, which tend to be anti-inflammatory. Foods rich in omega-3 fatty acids include soybean, flaxseeds, walnuts, and fish and canola oils, whereas foods rich in omega-6 fatty acids include sunflower oil, soybean, safflower, corn, and meat. The modern Western diet is relatively low in n-3 PUFAs and high in n-6 PUFAs compared with the modern Eastern diet or the diet of preindustrial Western societies.

High n-3 intake correlates with a decreased incidence of cardiovascular disease, but the role of anti-inflammatory fatty acids in OA is less clear. A 24-week, double-blind, placebo-controlled trial of 10 mL daily cod liver oil supplementation (containing 786 mg of eicosapentaenoic acid) did not decrease the visual analog pain score or disability of 86 patients with a clinical diagnosis of OA. In vitro, however, n-3 PUFAs have anti-inflammatory and anticatabolic properties based on their ability to decrease expression of aggrecanase, COX-2, 5-LOX-activating protein (5-LOX), 5-lipoxygenase-activating protein (FLAP), interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-α, matrix metalloproteinase (MMP)-3, and MMP-13. At the same time, an imbalance of n-6 and n-3 may also be detrimental. Rats fed high doses of omega-3 fatty acids exhibited cartilage surface irregularities and localized proteoglycan depletion that may be similar to early changes seen in OA.

Avocado and Soybean Unsaponifiables

Avocado and soybean unsaponifiables (ASU) are nutritional supplements widely used in Europe but, until recently, unavailable in the United States. In vitro, ASUs have anabolic and anti-inflammatory effects on chondrocytes. A meta-analysis of four double-blind, randomized, placebo-controlled trials evaluated the effect of ASUs on knee and hip OA. Two 3-month trials showed that 300 mg of ASUs once daily decreased nonsteroidal anti-inflammatory drug (NSAID) intake compared with placebo. In a trial lasting 6 months, 300 mg of ASUs once daily showed an improved Lequesne functional index (LFI) compared with placebo. ASUs had a 2-month delayed onset of action with residual symptomatic effects up to 2 months after the end of treatment. Although treatment with ASUs may improve symptoms, they have not been shown to have disease modifying capabilities. In a 2-year randomized, controlled trial (RCT) on hip OA, 300 mg of ASUs once daily did not slow the rate of joint space narrowing. Furthermore, there was no effect on secondary endpoints (LFI, visual analog [VAS] of pain, NSAID intake, and patients’ and investigators’ global assessments) compared with placebo after 1 year. A post hoc analysis, however, did suggest that ASUs might decrease narrowing of joint space width in patients with severe hip OA. Thus, although some data suggest ASUs may be bring short-term symptomatic relief, their long-term effects and disease-modifying capabilities need further investigation.

Antioxidant Nutrients

Reactive oxygen species (ROS) play a crucial role in cartilage homeostasis through regulation of chondrocyte activities, including cell activation, proliferation, and matrix remodeling. When ROS are overproduced, as in OA, “oxidative stress” occurs, leading to structural and functional cartilage damage including cell death and matrix degradation. Vitamin supplements, which have antioxidant properties, may therefore be beneficial in OA.

Vitamin C, or ascorbic acid, is a water-soluble antioxidant vitamin found in citrus fruits, rose hips, black currants, strawberries, Brussels sprouts, broccoli, peppers, cabbage, potatoes, and parsley. The Framingham Osteoarthritis Cohort Study showed that a moderate intake of vitamin C (120–200 mg/d) was associated with a threefold reduction in risk of OA progression compared with low vitamin C intake. A multicenter, randomized, double-blind, placebo-controlled case-crossover study of 133 patients with hip or knee OA showed that 1 g of calcium ascorbate (containing 898 mg vitamin C) taken twice daily was more effective in decreasing pain than placebo. Determining the safety of using such high doses of vitamin C, however, requires further long-term data.

Vitamin E is found in vegetable and nut oils, safflower oil, nuts, sunflower seeds, and whole grains. Five randomized clinical trials have been conducted to assess the benefit of vitamin E in the symptomatic treatment of OA. Two trials concluded that Vitamin E was more effective than placebo in decreasing pain. A third suggested that Vitamin E was as effective as diclofenac. Two more recent studies performed over a longer period, however, showed no benefit. A 6-month double-blind RCT of 500 IU of vitamin E daily in 77 patients showed no improvement in pain, stiffness, or physical function compared with placebo. Similarly, a 2-year double-blind RCT of 500 IU of vitamin E daily in 136 patients showed no symptomatic or structure-modifying benefit over placebo. Thus, although vitamin E may be beneficial for short-term symptomatic relief of OA, its utility in long-term symptomatic treatment is less clear.

Summary

OA is a chronic degenerative disorder and a source of pain and functional impairment for millions of patients. Weight loss and exercise are the mainstays of treatment and, in combination, result in significant improvement of function and pain. Of the various dietary programs used by patients, diets focusing on the loss of fat mass are the most beneficial. Dietary supplements like ASUs and antioxidant nutrients have been shown to decrease pain in some, but not all, studies. More prospective clinical trials are needed to elucidate their role in the management of OA.

Which Diet?

There are a variety of “fad diets” targeted to the general population despite a lack of scientific studies to support their various claims. Energy restrictive diets result in significant initial loss of bodyweight but are associated with high dropout and relapse-rates over time. Low-fat diets yield minimal success with respect to weight loss but do result in significantly lower blood lipid levels. High-protein, low-carbohydrate diets are advertised as the most effective at reducing bodyweight, although there has been no study comparing them to low-calorie diets for long-term weight loss.

A study by Christensen and colleagues examined the effectiveness of a rapid, diet-induced weight loss intervention on overweight individuals with OA of the knee. Eighty patients with knee OA, 89% of whom were women, were randomized either to a low-energy diet (LED) intervention (3.4 MJ/d) or a control diet (5 MJ/d). The LED intervention consisted of a nutritional powder that met recommendations for daily intake of high-quality protein and was taken as six daily meals. The control intervention consisted of a traditional hypoenergetic, high-protein, low-calorie diet taken in the form of ordinary foods based on recommendations from a nutritional advice session. At study conclusion, the LED group had lost more weight and body fat than the control group. There was also a greater decrease in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores among the LED intervention group compared with the control group (mean between-groups difference 219.3 mm, P = .005). These results suggest that for OA patients a low-energy diet may be more beneficial than an ordinary diet because it yields more rapid weight loss and more significant loss of body fat.

The general recommendation for obese patients with OA is to adhere to a weight loss program with an initial goal of 10% body weight loss at a rate of 1 to 2 lb per week. This has been shown to provide symptomatic relief and improve function by an average of 28%. Regardless of the diet chosen, however, achieving and sustaining weight loss is difficult and requires a multidisciplinary team approach.

Inflammation and OA

Overweight individuals are at an increased risk of developing OA in weight-bearing joints. Although much of the risk is due to biomechanical factors, data suggest that other systemic effects may also play a role. A number of studies have shown that decreasing body fat is more important than overall weight loss in improving symptoms. Adipose tissue serves as an endocrine organ and secretes a number of inflammatory markers, including leptin, tumor necrosis factor-alpha, and cytokines, that may mediate symptoms in OA through chronic inflammation. Weight-loss programs for OA patients should therefore focus on loss of fat mass, particularly abdominal fat, while maintaining lean muscle mass.

Exercise Programs

In combination with diet, exercise is another effective tool for weight loss and symptom reduction in OA. The Arthritis, Diet, and Activity Promotion Trial (ADAPT) was a randomized, single-blind clinical trial lasting 18 months designed to determine whether long-term exercise and dietary weight loss are effective, either separately or in combination, at improving functional impairment, pain, and mobility in older overweight individuals with OA of the knee. Three hundred and sixteen adults with knee OA and a BMI of at least 28 kg/m2 were recruited and randomized to one of four interventions: healthy lifestyle (control), diet only, exercise only, or diet plus exercise. The primary outcome was self-reported physical function using the WOMAC index. Secondary outcomes included weight loss, 6-minute walk distance, stair-climb time, WOMAC pain and stiffness scores, and changes in joint space width on radiographs of the knees. At study conclusion, the combination of dietary weight loss and exercise resulted in greater overall improvement in function and pain compared with control and with either intervention alone.

Polyunsaturated Fatty Acids

Polyunsaturated fatty acids (PUFA) are classified as n-3, n-6, or n-9, depending on the position of the last double bond along the fatty acid chain. PUFAs are metabolized by cyclooxygenases (COX) and lipooxygenases (LOX) into different eicosanoids. The main dietary PUFAs are n-3-derived eicosanoids, which tend to be proinflammatory, and n-6-derived eicosanoids, which tend to be anti-inflammatory. Foods rich in omega-3 fatty acids include soybean, flaxseeds, walnuts, and fish and canola oils, whereas foods rich in omega-6 fatty acids include sunflower oil, soybean, safflower, corn, and meat. The modern Western diet is relatively low in n-3 PUFAs and high in n-6 PUFAs compared with the modern Eastern diet or the diet of preindustrial Western societies.

High n-3 intake correlates with a decreased incidence of cardiovascular disease, but the role of anti-inflammatory fatty acids in OA is less clear. A 24-week, double-blind, placebo-controlled trial of 10 mL daily cod liver oil supplementation (containing 786 mg of eicosapentaenoic acid) did not decrease the visual analog pain score or disability of 86 patients with a clinical diagnosis of OA. In vitro, however, n-3 PUFAs have anti-inflammatory and anticatabolic properties based on their ability to decrease expression of aggrecanase, COX-2, 5-LOX-activating protein (5-LOX), 5-lipoxygenase-activating protein (FLAP), interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-α, matrix metalloproteinase (MMP)-3, and MMP-13. At the same time, an imbalance of n-6 and n-3 may also be detrimental. Rats fed high doses of omega-3 fatty acids exhibited cartilage surface irregularities and localized proteoglycan depletion that may be similar to early changes seen in OA.

Avocado and Soybean Unsaponifiables

Avocado and soybean unsaponifiables (ASU) are nutritional supplements widely used in Europe but, until recently, unavailable in the United States. In vitro, ASUs have anabolic and anti-inflammatory effects on chondrocytes. A meta-analysis of four double-blind, randomized, placebo-controlled trials evaluated the effect of ASUs on knee and hip OA. Two 3-month trials showed that 300 mg of ASUs once daily decreased nonsteroidal anti-inflammatory drug (NSAID) intake compared with placebo. In a trial lasting 6 months, 300 mg of ASUs once daily showed an improved Lequesne functional index (LFI) compared with placebo. ASUs had a 2-month delayed onset of action with residual symptomatic effects up to 2 months after the end of treatment. Although treatment with ASUs may improve symptoms, they have not been shown to have disease modifying capabilities. In a 2-year randomized, controlled trial (RCT) on hip OA, 300 mg of ASUs once daily did not slow the rate of joint space narrowing. Furthermore, there was no effect on secondary endpoints (LFI, visual analog [VAS] of pain, NSAID intake, and patients’ and investigators’ global assessments) compared with placebo after 1 year. A post hoc analysis, however, did suggest that ASUs might decrease narrowing of joint space width in patients with severe hip OA. Thus, although some data suggest ASUs may be bring short-term symptomatic relief, their long-term effects and disease-modifying capabilities need further investigation.

Antioxidant Nutrients

Reactive oxygen species (ROS) play a crucial role in cartilage homeostasis through regulation of chondrocyte activities, including cell activation, proliferation, and matrix remodeling. When ROS are overproduced, as in OA, “oxidative stress” occurs, leading to structural and functional cartilage damage including cell death and matrix degradation. Vitamin supplements, which have antioxidant properties, may therefore be beneficial in OA.

Vitamin C, or ascorbic acid, is a water-soluble antioxidant vitamin found in citrus fruits, rose hips, black currants, strawberries, Brussels sprouts, broccoli, peppers, cabbage, potatoes, and parsley. The Framingham Osteoarthritis Cohort Study showed that a moderate intake of vitamin C (120–200 mg/d) was associated with a threefold reduction in risk of OA progression compared with low vitamin C intake. A multicenter, randomized, double-blind, placebo-controlled case-crossover study of 133 patients with hip or knee OA showed that 1 g of calcium ascorbate (containing 898 mg vitamin C) taken twice daily was more effective in decreasing pain than placebo. Determining the safety of using such high doses of vitamin C, however, requires further long-term data.

Vitamin E is found in vegetable and nut oils, safflower oil, nuts, sunflower seeds, and whole grains. Five randomized clinical trials have been conducted to assess the benefit of vitamin E in the symptomatic treatment of OA. Two trials concluded that Vitamin E was more effective than placebo in decreasing pain. A third suggested that Vitamin E was as effective as diclofenac. Two more recent studies performed over a longer period, however, showed no benefit. A 6-month double-blind RCT of 500 IU of vitamin E daily in 77 patients showed no improvement in pain, stiffness, or physical function compared with placebo. Similarly, a 2-year double-blind RCT of 500 IU of vitamin E daily in 136 patients showed no symptomatic or structure-modifying benefit over placebo. Thus, although vitamin E may be beneficial for short-term symptomatic relief of OA, its utility in long-term symptomatic treatment is less clear.

Summary

OA is a chronic degenerative disorder and a source of pain and functional impairment for millions of patients. Weight loss and exercise are the mainstays of treatment and, in combination, result in significant improvement of function and pain. Of the various dietary programs used by patients, diets focusing on the loss of fat mass are the most beneficial. Dietary supplements like ASUs and antioxidant nutrients have been shown to decrease pain in some, but not all, studies. More prospective clinical trials are needed to elucidate their role in the management of OA.