Antioxidant supplements for joint health -
For instance, men who eat plenty of the antioxidant lycopene found in red fruits and vegetables such as tomatoes, apricots, pink grapefruit and watermelon may be less likely than other men to develop prostate cancer. Lycopene has also been linked to reduced risk of developing type 2 diabetes mellitus.
Lutein, found in spinach and corn, has been linked to a lower incidence of eye lens degeneration and associated vision loss in the elderly.
Research also suggests that dietary lutein may improve memory and prevent cognitive decline. Studies show that flavonoid-rich foods prevent some diseases, including metabolic-related diseases and cancer.
Apples, grapes, citrus fruits, berries, tea, onions, olive oil and red wine are the most common sources of flavonoids. Plant foods are rich sources of antioxidants.
They are most abundant in fruits and vegetables, as well as other foods including nuts, wholegrains and some meats, poultry and fish.
Good sources of specific antioxidants include:. There is increasing evidence that antioxidants are more effective when obtained from whole foods, rather than isolated from a food and presented in tablet form.
Research shows that some vitamin supplements can increase our cancer risk. For example, vitamin A beta-carotene has been associated with a reduced risk of certain cancers, but an increase in others — such as lung cancer in smokers if vitamin A is purified from foodstuffs.
A study examining the effects of vitamin E found that it did not offer the same benefits when taken as a supplement. A well-balanced diet, which includes consuming antioxidants from whole foods, is best.
If you need to take a supplement, seek advice from your doctor or dietitian and choose supplements that contain all nutrients at the recommended levels. Research is divided over whether antioxidant supplements offer the same health benefits as antioxidants in foods.
To achieve a healthy and well-balanced diet , it is recommended we eat a wide variety from the main 5 food groups every day:. To meet your nutritional needs, as a minimum try to consume a serve of fruit and vegetables daily.
Although serving sizes vary depending on gender, age and stage of life, this is roughly a medium-sized piece of fruit or a half-cup of cooked vegetables.
The Australian Dietary Guidelines External Link has more information on recommended servings and portions for specific ages, life stage and gender. It is also thought antioxidants and other protective constituents from vegetables, legumes and fruit need to be consumed regularly from early life to be effective.
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Skip to main content. Healthy eating. Home Healthy eating. Participants for this current study were recruited from MCCS.
A further exclusion criterion was a contraindication to MRI including pacemaker, metal sutures, the presence of shrapnel or iron filings in the eye, or claustrophobia. We invited subjects who fulfilled our inclusion criteria and attended the first year of round-three follow-up of the MCCS, which commenced in We used quota sampling whereby recruitment ceased when our target sample of approximately subjects was achieved.
By the end of , eligible subjects were recruited into the current study. The study was approved by The Cancer Council Victoria's Human Research Ethics Committee and by the Standing Committee on Ethics in Research Involving Humans of Monash University.
All participants gave written informed consent. Extensive information was collected at MCCS baseline — using questionnaires and physical measurements. Questionnaires covered demographic data and diet — via a item food frequency questionnaire developed from a study of weighed food records [ 20 ].
Nutrient intakes were calculated from the food frequency questionnaire using Australian food composition data [ 21 ], and using the US Department of Agriculture database for carotenoids α-carotene, β-carotene, β-cryptoxanthin, lutein and zeaxanthin, lycopene [ 22 ].
All nutrient intakes reflect those from food only without supplements. Fruits and vegetables are important food sources of vitamin C, vitamin E, and carotenoids [ 6 , 23 ]; they were therefore chosen as potentially influential foods, and their intakes were assessed from the food frequency questionnaire [ 20 ].
Participant weight was measured using electronic scales with bulky clothing removed. Their height was measured using a stadiometer with shoes removed. During —, each subject had an MRI scan performed on the dominant knee defined as the lower limb the subject used to step off when walking.
Knees were imaged on a 1. The tibial cartilage volume was determined by image processing on an independent workstation using Osiris software Geneva, Switzerland as previously described [ 11 , 12 ].
The measurement was performed by two independent trained observers. One observer measured all subjects, and the other observer carried out cross-checks; that is, measured randomly selected subjects, choosing one out of five subjects, in a blinded fashion.
The coefficients of variation for cartilage volume measures were 2. The tibial plateau cross-sectional area was used as a measure of tibial bone size from images reformatted in the axial plane using Osiris software, as previously described [ 12 , 15 ].
Using this technique, osteophytes, if present, are not included in the area of interest. The coefficients of variation for the medial tibial and the lateral tibial plateau areas were 2. Cartilage defects were graded on the magnetic resonance images with a classification system previously described [ 13 , 14 ], for the medial and lateral tibial and femoral cartilages.
The measurement was carried out by a single trained observer, who measured all images in duplicate on separate occasions. A cartilage defect was identified as present if there was any irregularity on the cartilage surface or the cartilage bottom with a loss of cartilage thickness on at least two consecutive slices at any site of that compartment.
The intraobserver reliability and interobserver reliability assessed in 50 magnetic resonance images expressed as the intraclass correlation coefficient were 0.
Bone marrow lesions were defined as areas of increased signal intensity adjacent to subcortical bone in either the distal femur or the proximal tibia [ 16 , 17 ]. A lesion was identified as present if it appeared on two or more adjacent slices in either tibiofemoral compartment [ 16 , 17 ].
Two trained observers, who were blinded to the characteristics of subjects, together assessed the presence of lesions for each subject. The outcomes were the tibial cartilage volume, the tibial plateau bone area, and the presence of tibiofemoral cartilage defects and bone marrow lesions.
The first two outcomes were initially assessed for normality before being regressed against intakes of food and nutrients. They showed a normal distribution, and thus linear regression was used.
Multivariate regression models were constructed to explore the relationship between food or antioxidant intake and the knee structure elements, adjusting for potential confounders of age, gender, body mass index, and energy intake. Food intakes were divided into quartiles and assigned the median value for the quartile; hence the odds ratios reflect the odds associated with an increase of one serving per day in intake.
Dietary antioxidants were standardized so that the coefficients represent the effect of a one-standard-deviation increment in intake.
All analyses were performed using the SPSS statistical package standard version Two hundred and ninety-seven participants entered the study. The vitamin C intake was not significantly associated with tibial cartilage volume or the presence of cartilage defects.
There was no significant association between vitamin E intake and knee cartilage or bone measures Table 2. These marginal significances disappeared after vitamin C intake was added to the models. There was no significant association between the intake of other carotenoids and knee cartilage or bone measures in the multivariate analyses Table 3.
Fruit intake was not significantly associated with the tibial cartilage volume or with the presence of cartilage defects. Vegetable intake was not significantly associated with knee cartilage or bone measures Table 4.
Adding lifestyle factors such as physical activity, education level, smoking, and alcohol consumption to the multivariate models did not alter the results data not shown.
In this population of healthy, middle-aged people with no clinical knee OA, vitamin C intake was inversely associated with the tibial plateau bone area and with the presence of bone marrow lesions, both of which are important in the pathogenesis of knee OA. Consistent with fruit being an important source of vitamin C, fruit intake was also found to be inversely associated with the tibial plateau bone area and with the presence of bone marrow lesions.
These data suggest a beneficial effect of vitamin C and fruit on bone structure. The lutein and zeaxanthin intake was associated with a decreased risk of cartilage defects independent of vitamin C intake, and β-cryptoxanthin intake was associated with decreased tibial plateau bone area independent of vitamin E intake, suggesting a beneficial effect of these carotenoids on knee cartilage and bone.
The vitamin E intake, however, tended to be positively associated with the tibial plateau bone area independent of vitamin C intake, which is a negative effect on the bone.
There is conflicting evidence on the role of vitamin C and vitamin E with regard to the risk of knee OA. The Framingham OA Cohort Study showed that vitamin C intake reduced the risk of progression of knee OA, and that vitamin E intake reduced the risk of OA progression in men only [ 7 ].
In contrast, ascorbic acid supplementation worsened spontaneous OA in a guinea pig model [ 24 ], and we previously showed no effect of supplementary vitamin E on the change in knee cartilage volume in a randomized placebo-controlled trial during 2 years in subjects with knee OA [ 8 ].
All data available to date have been in patients with established OA. No previous studies have examined the relationship between vitamin C and vitamin E intake and knee structure in healthy subjects.
In our current study performed on healthy subjects free of clinical knee OA, we found a negative association between vitamin C intake and the tibial plateau bone area and the presence of bone marrow lesions. This suggests a protective effect of vitamin C on the risk of knee OA since previous studies have suggested that an increase in bone size is a very early response of the knee to known risk factors for knee OA [ 25 , 26 ].
For example, changes of bone expansion are seen in response to increased adductor moment [ 25 ] and obesity [ 26 ] even before changes are seen in cartilage. Moreover, the bone area is increased in patients with OA compared with those without OA [ 27 ], and the area increases over time in those with OA [ 15 ].
This cannot be explained by osteophytes which were not included in the bone area measurements. In addition, bone marrow lesions have been shown to be associated with pain and progressive joint space loss in knee OA [ 16 , 17 ]. These findings may explain the mechanism by which vitamin C effects the previously reported reduction in the risk of knee OA [ 7 ].
Vitamin E intake, however, was shown to be associated with an increased tibial plateau bone area, which is thought to be an adverse finding in terms of knee structure in OA [ 15 ].
The evidence regarding the effect of carotenoids on the risk of knee OA is limited. The Framingham OA Cohort Study showed that β-carotene intake reduced the risk of progression of knee OA [ 7 ]. A case—control study performed by De Roos and colleagues, however, found that those in the highest tertile of serum lutein or β-cryptoxanthin were less likely to have knee OA than controls, and those in the highest tertile of serum β-carotene or zeaxanthin were more likely to have knee OA [ 28 ].
In contrast, our study found that the lutein and zeaxanthin intake was associated with a decreased risk of cartilage defects, and that β-cryptoxanthin intake was associated with a decreased tibial plateau bone area — both suggesting a beneficial effect on the knee.
There was no significant association between any other carotenoids and knee cartilage or bone. This discrepancy may partly be explained by the different methods used to measure exposure. The Framingham OA Cohort Study and our study assessed dietary intake rather than serum levels. Although serum measures reflect the dietary intake of the carotenoids, they also reflect differences in interindividual absorption and metabolism.
Moreover, when examining the effect of carotenoid intake on the knee, we used a more sensitive method of assessing knee structure than the Framingham study and De Roos and colleagues' study, which used radiographic assessment of the knee joint [ 7 , 28 ].
The present study has a number of limitations. We were able to measure dietary nutrients in a valid fashion [ 29 ]. A single measure of nutrient intakes 10 years earlier, however, was used as the exposure measure in our study, which may not reflect more recent and perhaps relevant intake, if intervening illness or other life changes affected the intake.
While not all studies have shown dietary stability in adults, there is some evidence that the nutrient intake is relatively stable and tends to be more stable with increasing age [ 30 , 31 ].
We have no way of knowing what the situation is in the MCCS cohort. Longitudinal studies have suggested that individuals may move toward a more healthy diet over time [ 32 , 33 ]. The participants in our study are likely to represent the more healthy and health conscious of all those who were initially recruited into the MCCS, since they were selected from those who took part in the first year of the follow-up.
They may have already adopted a healthy diet and thus be less likely to change in this direction. While selection bias towards healthier subjects may have affected the estimates of nutrient intake and knee structure measures, it is unlikely that this would modify the relationships between nutrient intakes and knee structure.
Although nutritional data collected 10 years earlier may have resulted in some misclassification of exposure, such misclassification is likely to be nondifferential in relation to knee structure, since only subjects with no history of knee symptoms or injury were included.
Nondifferential misclassification tends to underestimate the strength of any observed associations. The prospective design is also a potential strength of our study since a substantial period of time has elapsed between the ascertainment of exposure to nutritional factors and the development of outcomes cartilage and bone measures.
Another limitation of this study is that no information on dietary supplements was available, and we were therefore unable to adjust the effect of these supplements in the statistical analyses.
Articular cartilage and bone health is dependent upon the regular provision of nutrients, and it has been suggested that diets deficient in nutrients may lead to arthropathy [ 3 ].
The effect of foods and nutrients on knee structure is likely to be complex. Our study suggests that the direct effect of vitamin C is on bone rather than on cartilage. Although vitamin C and vitamin E are known potent antioxidants, given that different effects of vitamin C and vitamin E were found on the bone area in the present study, the mechanism of action in this situation may not be via an antioxidant effect.
Vitamin C is a cofactor in the hydroxylation of lysine and proline, and therefore is required in the cross-linking of collagen fibrils in bone.
Vitamin C stimulates alkaline phosphatase activity, a marker for osteoblast formation. Several studies have reported a beneficial effect of vitamin C intake on the bone mineral density [ 34 , 35 ].
A higher bone mineral density is associated with greater rigidity and strength of the bone. Bone may therefore expand less in relation to factors such as increased loading on the bone. This may provide an explanation of the association of higher vitamin C intake with decreased bone area and the risk of bone marrow lesions.
The emerging evidence of structural change in OA and pre-OA suggests that bony changes occur early and that cartilage defects predate changes in the cartilage volume, which in turn occur before any radiological change is evident.
This continuum acknowledges that bone plays an important role in early OA. Recent work has suggested that the well described risk factors for OA, including obesity and the knee adduction moment, may act through an effect on tibial bone before any effect on cartilage occurs [ 25 , 26 ].
The enlargement of the tibial plateau bone may attenuate the tibial cartilage, and this attenuation may play a role in the pathogenesis of OA [ 15 ]. The present study suggests a beneficial effect of vitamin C intake on the reduction in bone size and the number of bone marrow lesions, both of which are important in the pathogenesis of knee OA.
Our study also suggests benefits for bone health from fruit consumption, consistent with fruit being an important source of vitamin C. These observations support the dietary recommendation for eating more fruit. While our findings need to be confirmed by larger longitudinal studies, they do highlight the potential of diet to modify the risk of OA.
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