Your bag is
We’re active guys. We push ourselves to the limit. We chase excellence, and we strive for greatness. Our endeavors require a sharp, focused mind, and we expect peak physical performance from our bodies as well. This article is all about how you can use supernutrients from whole foods and certain supplements to make sure that you keep moving effectively, efficiently, and comfortably for the long haul.
You’re Not Getting Any Younger
Joint discomfort and stiffness impair mobility, adversely affect daily activities, and negatively impact quality of life.1,2 Simply put, tired, worn, and stiff joints can limit you from doing what you love to do and living the life of your dreams. Research shows that 43% of folks between the ages of 45 – 65 years old struggle with joint discomfort.3 Beyond that, it is estimated that 80% of the population will have radiographic (i.e., X-ray) evidence of significant joint breakdown by the age of 65.4
Researchers have found that two major risk factors associated with declining joint health and increased joint discomfort are age and overweight/obesity,5,6 and the degradation of joint tissue is thought to be precipitated by a number of factors, including oxidative and inflammatory stress.7–9
With regard to the latter, inflammatory stress can result from a number of factors, including excess body fat and poor diet. While it’s commonly viewed as a static depot for unwanted and unsightly body fat, adipose tissue is a dynamic tissue that secretes a large number of hormones and chemicals (e.g., cytokines)—many of which have a pro-inflammatory effect and favor an inflammatory environment.10–12 As a result, obesity is commonly recognized as a chronic, low-grade inflammatory state.
“These chemicals can influence the development of [joint discomfort],” says Dr. Jeffrey N. Katz, a professor of medicine and orthopaedic surgery at Harvard Medical School and Brigham and Women’s Hospital in Boston.
This effect can be seen in the numerous studies that have linked being overweight to joint discomfort in non-weight-bearing joints (e.g., hands). “Obviously, you don’t walk on your hands, so there may be something that is produced by fat cells in the body that causes the joint to break down more rapidly than it might otherwise,” says Dr. David Felson, a professor of medicine and epidemiology at Boston University School of Medicine.13
Of course, body weight has a direct impact on the amount of pressure placed on joints, and it’s estimated that a force of 3 – 6 times one’s body weight is exerted across the knee when walking. In other words, being just 10 pounds overweight can mean an additional 30 – 60 pounds of force on the knee with each step.14
While studies show that being overweight can increase joint discomfort, research suggests that even small amounts of weight loss can improve joint comfort.15,16 In fact, researchers have found that, for every 11-pound decrease in body weight, a woman’s risk of osteoarthritis decreases by a whopping 50%.
In addition to unnecessary body fat, excess calorie consumption (which is inherently associated with increasing body fat stores) and poor food choices (e.g., heavily processed and refined carbohydrates, low-quality, refined oils) also promote both acute and sustained inflammatory stress.17–19 This pattern of eating and its associated dietary composition lead to an overproduction of free radicals and pro-inflammatory cytokines, which result in oxidative stress and inflammatory stress. On the other hand, diets rich in fruits and vegetables—which are abundant in antioxidant phytonutrients—are inversely associated with inflammatory stress.20
While inflammation is a fashionable “buzzword,” it’s important to point out that inflammation is the normal, protective, and (usually) temporary response of the immune system to pathogens and injury. In other words, a normal, healthy, and acute inflammatory response is not only a good thing, it’s imperative to optimal human health and function. However, it’s when there’s recurrent stimuli or poor regulation of the system that chronic inflammation—and problems—ensue.
This also highlights the role that something referred to as pattern overload can also play in the breakdown of joint tissue and joint discomfort. According to Paul Chek, pattern overload “describes injury to soft tissues resulting from repetitive motion in one pattern of movement, or restricted movement in one or more planes of motion.”21 While it’s beyond the scope of this article to discuss movement assessments, mobility drills, and proper programming, it’s important to keep this in mind. Don’t just do something because you’re “supposed to” or because that’s how you’ve always done it. Be mindful and listen to your body.
While physiological aging (also referred to as senescence) is inevitable, researchers believe that age may be tied to declining joint health for a number of reasons. One factor that may lead to age-related changes in joint structures is the formation of advanced glycation end-products (AGEs). AGEs are the result of the addition of carbohydrates to proteins or lipids (i.e., fat), and they can be formed both inside and outside the body. For instance, AGEs can be created during cooking (especially high-heat cooking), and they can also be formed by the body after exposure to high levels of blood sugar, which results from regular consumption of simple sugars and refined carbohydrates, as well as poor insulin sensitivity and carbohydrate tolerance.22
AGEs can wreak havoc on the body’s tissues, including joint structures. For instance, AGEs can impact the mechanical properties of cartilage, and as a result, increase joint stiffness, increase joint fatigue, and inhibit the building of new, healthy joint tissue.6 What’s more, AGEs increase free radical formation, impair antioxidant defense systems, increase oxidative stress, and promote inflammation.23
Along those lines, excessive free radical production leads to oxidative stress, which is “a disturbance in the balance between the production of reactive oxygen species (ROS) and antioxidant defenses.”24 Oxidative stress has long been thought to play a central role in cellular senescence and the aging of various tissues, including joint structures.25,26 ROS (i.e., free radicals) appear to play an important role in joint tissue breakdown and promoting inflammatory stress, and as a result, supporting the body’s defense systems through increased antioxidant intake seems to be imperative to bolstering joint health.27
The Fabric of Body Armor
Currently, most people turn to options like acetaminophen and non-steroidal anti-inflammatory drugs (NSAIDs) to relieve joint discomfort, reduce stiffness, and improve physical function. While these tend to be effective in the short-term, regular, consistent use of NSAIDs has been found to be associated with a number of adverse health outcomes, including GI discomfort, enhanced risk for GI bleeding, hypertension, congestive heart failure, renal insufficiency, and more.28–30
With that said, more and more people are recognizing and seeking out the power of functional foods and nutraceuticals to help nourish joints. According to renowned joint health expert Dr. Jason Theodosakis (“Dr. Theo”), “We now know that certain foods can actually help ease and promote joint comfort.”31
Antioxidants play a tremendous role in fighting free radicals, and as mentioned above, excessive free radicals and oxidative stress may be damaging to joints and can contribute to joint discomfort. According to Dr. Theo, foods that contain vitamin A (e.g., beta-carotene), vitamin C, vitamin E, and/or selenium (collectively known as the “ACES”) are powerful weapons for combating free radicals and supporting superior joints.
Speaking of antioxidants, phytonutrients (e.g., flavonoids, anthocyanins, carotenoids, plant sterols, glucosinolates), which are found in an array plant-based foods, can have a prodigious impact on joint health by supporting the body’s antioxidant defense systems, reducing oxidative stress, and promoting a healthy inflammatory response. In addition, a number of other micronutrients (e.g., vitamin D, vitamin K, several B vitamins) may play a critical role in optimizing joint health and function.32
What’s more, certain fatty acids (e.g., omega-3 fatty acids) are protective by nature, promote a healthy inflammatory response, and ease joint discomfort.
With all of that in mind, I’d like to share with you a list of foods that can help nourish joints, support superior joint health, and promote joint comfort. Throughout, you’ll see a common theme of whole foods that are rich in potent antioxidants, support a healthy inflammatory response, and promote a robust immune system.
While the following sections highlight unique attributes of single foods, bear in mind that, in the grand scheme of things, how you look, feel, and perform are the product on your entire body of “nutrition work.” In other words, there’s no single magical food. Instead of viewing foods in isolation as “good” or “bad,” think about “deep health” as the result of practicing healthy eating habits, creating a positive food environment, and choosing high-quality nutritious foods in appropriate amounts regularly and consistently over time.
Going back to the “listen to your body” mantra, it’s also important to consider your own personal responses to foods. For instance, you might find that an otherwise perfectly healthy food (e.g., FODMAP-containing foods) might result in joint discomfort. While it’s beyond the scope of this article, identifying personal food sensitivities—defined as a negative physiological reaction to a food—can play a critical role in easing joint discomfort, as it’s not at all uncommon for specific foods (on an individual basis) to lead to joint flare-ups.
The rich red color of the flesh of cherries can be attributed to their rich concentration of anthocyanins, which have an antioxidant potential superior to vitamin E.33 These potent polyphenols promote a healthy inflammatory response by inhibiting the activity of a class of enzymes in the body called cyclooxygenase (COX). Inhibition of COX is a common target of NSAIDs to ease joint comfort and reduce stiffness, and the COX inhibitory activities of the anthocyanins from cherries have been shown to be comparable to that of commonly-used NSAIDs.34
Studies dating all the way back to the 1950s have suggested that cherry consumption may play a role in easing joint discomfort, and as a result, cherries have long had a reputation for supporting joint health.35 This long-standing belief was fortified in a study published in the Journal of Nutrition in which researchers found that the consumption of 45 cherries provoked a significant decrease in circulating levels of urate (i.e., uric acid) in women.36 When urate accumulates in joints, it is associated with discomfort, stiffness, and swelling.
Studies have also shown that regular consumption of cherries can significantly reduce circulating levels of a compound called C-reactive protein (CRP), a marker of systemic inflammation, and significantly reduce the risk of joint flare-ups.37,38 In recent years, tart cherry juice, which has been shown to decrease levels of urate and CRP, promote more restful sleep, soothe sore muscles, reduce joint stiffness, and improve physical function.39–42
Extra Virgin Olive Oil
Extra-virgin olive oil is naturally abundant in a polyphenol called oleocanthal, which has been shown to promote a healthy inflammatory response. Specifically, oleocanthal acts as a “natural anti-inflammtory compound” by inhibiting the activity of cyclooxygenase (COX) enzymes, a property it shares with the highly-recognizable NSAID ibuprofen.43,44
Not surprisingly, researchers have found that a Mediterranean diet, which is rich in olive oil, confers a number of health benefits, some of which seem to overlap with those attributed to NSAIDs.45,46 Mediterranean diets typically provide up to 40% of total calorie intake from fats—up 50% of which comes from monounsaturated fats (predominantly extra-virgin olive oil).47
In addition to oleocanthal, there are a number of other polyphenols (e.g., oleuropein, hydroxytyrosol) in extra-virgin olive oil that provide antioxidant activity and promote a healthy inflammatory response.48 In fact, Italian researchers have found that oleuropein, a compound that is similar in structure to oleocanthal, exerts anti-inflammatory effects and has the potential to mitigate joint degradation.49 Olive oil fortified with hydroxytyrosol has been shown to significantly improve the inflammatory response and reduce joint swelling in animals.50
It’s also important to choose the right type of olive oil. In one study, researchers divided healthy participants into three groups, each one receiving a meal with a different type of oil: Extra-virgin olive oil (EVOO), olive oil (OO), or corn oil (CO). The researchers found that only when the folks consumed meals with EVOO (not OO or CO), they experienced significant decreases in inflammatory markers (e.g., TXB2, LTB4) along with increases in markers of antioxidant capacity within two hours of the meal.51 While the EVOO and OO had nearly identical fatty acid compositions, the EVOO contained nearly 38 TIMES more health-promoting polyphenols.
Avocados are a rich source of antioxidant and anti-inflammatory compounds, including various vitamins (e.g., vitamins A, C, and E) and phytochemicals (e.g,. lutein, zeaxanthin, phytosterols, phenolics).52 In one study published in the American Journal of Clinical Nutrition, researchers from Oregon Health and Science University found that fruits and vegetables rich in lutein and zeaxanthin (the primary carotenoids in avocados) are associated with decreased risk of cartilage defects.53
A number of studies have demonstrated that supplementation with avocado-soybean unsaponifiables (ASU), which are concentrated extracts of these plants’ phytosterols, may promote joint comfort. Supplementation with ASU has been shown to lead to reduced NSAID usage, increased mobility, reduced joint discomfort and stiffness, and overall improved functional capacity.54,55 They phytosterols in avocados appear to work by reducing the production of multiple pro-inflammatory compounds (e.g., IL-1ß, TNF-α) and suppressing the activity of two key pro-inflammatory enzymes (i.e., COX-2, iNOS), which are tied to joint breakdown and discomfort.56
What’s more, the addition of avocado or avocado oil to other vegetables appears to promote greater absorption of their antioxidant phytonutrients. In a study published in the Journal of Nutrition, researchers found that when avocado or avocado oil was added to salsa, the absorption of fat-soluble carotenoids was up to four times higher than when the salsa was avocado-free, and when avocado was added to salads, the absorption of carotenoids was up to 15 times higher than when the salads were consumed avocado-free (i.e., fat-free).58
The skin of apples is rich in antioxidant phytonutrients, including anthocyanins and quercetin.59 Much like the former, quercetin has been shown to promote a healthy inflammatory response that is associated with easing joint discomfort.60 Researchers from La Trobe University in Australia also found that quercetin can prevent the loss of aggrecan, which is a key component of joint tissue structures.61
Not only that, quercetin has been shown to help promote healthy carbohydrate metabolism by inhibiting digestive enzymes like alpha-amylase and alpha-glucosidase, which are responsible for breaking down carbohydrates into absorbable sugars.62 This has implications on joint health because poor carbohydrate management is associated with AGE formation and increased joint discomfort, stiffness, and swelling.63
Regular apple consumption has also been shown to promote a healthy body weight and reduce levels of CRP, a marker of systemic inflammation that is commonly elevated in situations involving joint discomfort.64–66
Blueberries, Strawberries & Other Berries
Just like cherries, blueberries, strawberries, and other berries get their dark, deeply-colored hues from their concentrations of potent polyphenols called anthocyanins.67–69 Much like cherries, the anthocyanins found in berries have been shown to inhibit COX enzymes, thereby promoting a healthy inflammatory response and easing joint discomfort.34
A number of studies have shown that berry consumption has been associated with reduced markers of systemic inflammation. In one study, researchers found that folks who consumed two or more servings of strawberries per week (about 16 strawberries) were 14% less likely to have elevated levels of CRP, a marker of inflammatory stress that may be closely related to joint flare-ups.70 The polyphenols in blueberries have been shown to reduce the body’s ability to create new fat cells, increase anti-inflammatory molecules, reduce oxidative stress, accelerate recovery, and reduce soreness.71–73
Researchers from the Department of Food Science and Nutrition at Laval University in Quebec found that people who consumed a low-calorie cranberry juice cocktail daily for 4 – 12 weeks showed decreased levels of various markers of inflammation as well as a reduction in levels of matrix metalloproteinases (MMPs), which are enzymes involved in the breakdown of a variety of tissues in the body and are thought to play a pivotal role in joint degradation.74–76
Over the last several years, the health benefits of moderate red wine consumption have become increasingly clear, and among the myriad advantages appears to be joint protective effects. Like many of the other dark, rich-colored fruits already discussed, red wine is a rich source of antioxidant polyphenols, including anthocyanins.77
One of the best-known polyphenols found in red wine is resveratrol. A number of studies have demonstrated the anti-inflammatory activity of resveratrol and its ability to promote a healthy inflammatory response, mostly through inhibition of the COX enzymes.78,79 Resveratrol also seems to modulate the body’s inflammatory response by reducing both the production of inflammatory molecules as well as the formation of free radicals.80 What’s more, resveratrol has been shown to protect joints from cartilage damage associated with AGEs, which can reduce collagen synthesis and increase the activity of MMPs, leading to stiffness and joint tissue breakdown.81–83
While resveratrol seems to be the most popular antioxidant associated with red wine, the beneficial effects of red wine cannot be solely accounted for by it. Researchers from Hungary demonstrated that malvidin, the most abundant anthocyanin polyphenol in red wine, possesses potent antioxidant and anti-inflammatory activity, and the effects of malvidin “at least partially account for the positive effects of moderate red wine consumption.”84 Thus, moderate amounts of red wine—1 – 2 glasses per day for men—may be optimal. It’s important to note, however, that drinking alcohol in excess appears to increase the body’s production of pro-inflammatory molecules, according to researchers from the University of North Carolina.85
Coldwater fish (e.g., anchovy, herring, mackerel, sardine, salmon, trout, tuna) are abundant in the essential omega-3 fatty acids EPA and DHA, which the body cannot produce them and must be consumed through dietary sources. Unfortunately, the modern food supply is largely void of these important healthy fats and rife with omega-6 fatty acids.
Experts estimate that throughout human history the optimal ratio for consumption of omega-6 fatty acids (e.g., linoleic acid) to omega-3 fatty acids (e.g., alpha linolenic acid, DHA, EPA) was about 2:1 or 1:1.86 With the contemporary diet, this ratio has shifted dramatically in favor omega-6 fatty acids to 20:1.87 While there are multiple explanations (reductions in healthful seafood consumption), researchers attribute this in large part to the ubiquity of vegetable oils (e.g., soybean oil) present in the Western diet.88 Excessive consumption of omega-6 fatty acids coupled with a deficiency of omega-3 fats is connected to an increase in all conditions characterized by inflammatory stress, including joint discomfort and poor joint health.86,89
This is important for a number of reasons, especially when it comes to promoting a healthy inflammatory response. For example, omega-3 fatty acids have anti-inflammatory effects (e.g., suppress IL-1ß, TNF-α, and IL-6) whereas omega-6 fatty acids do not.90 In fact, studies show that omega-6 fats promote inflammation, particularly when they are consumed in excess of omega-3 fats.91 The omega-3 fatty acids EPA and DHA appear to help ease joint discomfort through their actions on promoting a healthy inflammatory response.92
Studies have shown that diet interventions designed to decrease the ratio of omega-6 to omega-3 fats results in various favorable effects on metabolic and inflammatory profiles (e.g., reductions in IL-1ß, TNF-α).93 When reviewing the body of evidence, researchers from Harvard Medical School have concluded that supplementation with omega-3 fatty acids significantly reduces joint discomfort and stiffness.94
Broccoli and Other Cruciferous Veggies
Broccoli (along with other cruciferous vegetables) is rich in a compound called sulforaphane, which has been shown to promote a healthy inflammatory response and support joint health.95 Sulforaphane blocks the action of enzymes (i.e., MMPs) that result in joint tissue breakdown and provides superior joint protection by promoting a healthy inflammatory response.96–98
In addition to sulforaphane, broccoli is an excellent source of vitamin C. In fact, among the cruciferous family, which also includes cauliflower, Brussels sprouts, kale, cabbage, and bok choy, broccoli is the most concentrated source of this potent antioxidant, providing over 100% of the daily Dietary Reference Intake (DRI) in single one-cup serving. Epidemiological studies have shown that folks with the highest intake of vitamin C showed the greatest joint protective effects and lowest incidence of knee discomfort.99 While vitamin C is typically viewed simply as an antioxidant, it’s important to note that vitamin C plays a significant role in the synthesis of collagen, a major component of many connective tissues including cartilage and bone.100
On top of these joint protective nutrients, broccoli is also an excellent source of vitamin K, providing over 200% of the DRI in a one-cup serving. Vitamin K plays an important role in bone and cartilage mineralization (i.e., the process of creating new bone and cartilage), and several studies have found a link between low levels of vitamin K, poor joint health, and joint discomfort.101–103
Brazil Nuts and Other Nuts
Brazil nuts are one of the most concentrated sources of the micronutrient selenium, which serves a critical role in the body’s antioxidant defense systems, and studies have shown that Brazil nut consumption can significantly improve antioxidant status and increase the activity of glutathione peroxidase, a family of enzymes whose main task is to reduce oxidative stress.104–106 Researchers from the University of North Carolina have also found that there may be a direct connection between low selenium intake, poor joint health, and the severity of joint discomfort.107
In addition to Brazil nuts, walnuts and pecans are among the plant-based foods with the highest content of total antioxidants.108 Nuts (especially walnuts and pistachios) are among the best sources of vitamin E, and research has shown a connection between vitamin E intake and joint health.99 Walnuts are also one of the better plant-based sources of omega-3 fatty acids, specifically alpha linolenic acid (ALA), which is considered to be the “parent” omega-3 fatty acid to the aforementioned EPA and DHA. Cashews are an excellent source of copper, which is necessary for the synthesis of elastin and collagen, proteins that provide the framework for healthy joint structures; studies have linked low copper intake to joint discomfort and declining joint health.109,110
Dairy, Yogurt, and Other Fermented Foods
There’s a common misconception that dairy products may lead to joint discomfort and stiffness. However, the body of evidence suggests otherwise; in fact, there’s a robust body of research to suggest that dairy may ease joint discomfort and reduce joint flare-ups. This really shouldn’t come as much of a surprise, as higher intakes of specific nutrients from dairy (e.g., calcium, B vitamins, protein, magnesium, vitamin D) are linked to improved bone health and muscle function, which may enhance joint protection.111,112
Not only that, studies show that dairy intake is inversely associated with body fat percentage, abdominal fat, body mass index, waist circumference, and hip circumference.113 Studies find that folks who regularly consume dairy experience less joint discomfort, fewer joint flare-ups, and decreased joint tissue breakdown over time.114–116 Observational studies have also shown that dairy consumption is associated with lower concentrations of uric acid.117
While dairy may help ease joint discomfort and promote joint health, fermented dairy (e.g., yogurt, kefir) and other traditionally-fermented foods rich (e.g., sauerkraut, pickles, miso, tempeh) in healthy bacteria may provide even greater benefit. As has been discussed, there are a number of factors (e.g., oxidative stress, inflammation, overweight/obesity, AGEs, aging) that may contribute to declining joint health and joint discomfort, and more and more researchers are beginning to speculate that the gut microbiome may also play a role.
In fact, Dr. Jose Scher, a rheumatologist at New York University, has published a number of studies showing that the gut microbiome of folks who regularly experience joint discomfort and flare-ups is characterized by dysbiosis.118,119 Dysbiosis refers to microbial imbalances on or within the body. In other words, dysbiosis describes the state of an unhealthy imbalance of bacteria in the gut flora, characterized by excessive levels of pathogenic bacteria, inadequate amounts of commensal and probiotic bacteria, and/or reduced bacterial diversity.
This connection between gut dysbiosis and joint discomfort makes sense, as healthy bacteria serve a wide array of functions in the body, including regulating and supporting a healthy immune system and promoting a healthy inflammatory response by producing anti-inflammatory cytokines (and down-regulating pro-inflammatory cytokines).120,121 Supplementation with a probiotic (Lactobacillus casei) daily for 8 weeks has been shown to significantly improve joint health, reduce the production of several inflammatory chemicals (e.g,. TNF-α, IL-6, IL-12), and improve overall inflammatory status.122
Superfoods for Superior Joints
As highlighted above, there are a number of factors that appear to contribute to declining joint health and joint discomfort, and the great news is that research shows that many of these can be managed through dietary choices and lifestyle behaviors. In other words, promoting joint health, supporting joint comfort, improving physical function, reducing joint stiffness, and decreasing joint flare-ups may be well within your control, starting with the food choices that you make.
The superfoods outlined above are nutrient-dense, and they are rife with vitamins, minerals, antioxidant phytochemicals, anti-inflammatory nutrients, healthy bacteria, and more. Consider adding more of these whole foods, which support a strong antioxidant defense system, a healthy inflammatory response, and a robust immune system, to your nutrition arsenal to bolster joint health. Also, pay close attention to how your body responds to your overall diet to help identify if specific foods lead you to experience joint discomfort, flare-ups, and stiffness.
Tim lives with his beautiful wife Amie in Austin, Texas, and he is the Director of Nutrition and Exercise with BioTRUST Nutrition, which develops and distributes a line of premium, scientifically-backed nutrition supplements. Tim earned his Master’s degree in Exercise Physiology from the University of Texas, he is a NSCA Certified Strength and Conditioning Specialist, and he is a Precision Nutrition Level 2 nutrition coach. You can read other articles written by Tim at his blog, and he can be reached by e-mail at tskwiat@BioTRUST.com.
1. Liikavainio T, Lyytinen T, Tyrväinen E, Sipilä S, Arokoski JP. Physical function and properties of quadriceps femoris muscle in men with knee osteoarthritis. Arch Phys Med Rehabil. 2008;89(11):2185-2194. doi:10.1016/j.apmr.2008.04.012.
2. Phillips S, Dow L. Impact of impaired morning function on quality of life in rheumatoid arthritis: results of an exploratory patient survey. Int J Clin Rheumatol. 2012;7(6):597-606. doi:10.2217/ijr.12.62.
3. Health, United States, 2011: With Special Feature on Socioeconomic Status and Health. National Center for Health Statistics.; 2012. http://www.cdc.gov/nchs/data/hus/hus11.pdf.
4. Green GA. Understanding NSAIDs: from aspirin to COX-2. Clin Cornerstone. 2001;3(5):50-60.
5. Richmond SA, Fukuchi RK, Ezzat A, Schneider K, Schneider G, Emery CA. Are joint injury, sport activity, physical activity, obesity, or occupational activities predictors for osteoarthritis? A systematic review. J Orthop Sports Phys Ther. 2013;43(8):515-B19. doi:10.2519/jospt.2013.4796.
6. Shane Anderson A, Loeser RF. Why is osteoarthritis an age-related disease? Best Pract Res Clin Rheumatol. 2010;24(1):15-26. doi:10.1016/j.berh.2009.08.006.
7. Jacques C, Gosset M, Berenbaum F, Gabay C. The role of IL-1 and IL-1Ra in joint inflammation and cartilage degradation. Vitam Horm. 2006;74:371-403. doi:10.1016/S0083-6729(06)74016-X.
8. Goldring MB, Berenbaum F. The regulation of chondrocyte function by proinflammatory mediators: prostaglandins and nitric oxide. Clin Orthop. 2004;(427 Suppl):S37-S46.
9. van der Kraan PM, van den Berg WB. Anabolic and destructive mediators in osteoarthritis. Curr Opin Clin Nutr Metab Care. 2000;3(3):205-211.
10. Hajer GR, van Haeften TW, Visseren FLJ. Adipose tissue dysfunction in obesity, diabetes, and vascular diseases. Eur Heart J. 2008;29(24):2959-2971. doi:10.1093/eurheartj/ehn387.
11. Hummasti S, Hotamisligil GS. Endoplasmic reticulum stress and inflammation in obesity and diabetes. Circ Res. 2010;107(5):579-591. doi:10.1161/CIRCRESAHA.110.225698.
12. Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol. 2011;29:415-445. doi:10.1146/annurev-immunol-031210-101322.
13. Kane A. How Fat Affects Arthritis. Arthritis Found. http://www.arthritis.org/living-with-arthritis/comorbidities/obesity-arthritis/fat-and-arthritis.php.
14. Felson DT. Weight and osteoarthritis. J Rheumatol Suppl. 1995;43:7-9.
15. Anderson JJ, Felson DT. Factors associated with osteoarthritis of the knee in the first national Health and Nutrition Examination Survey (HANES I). Evidence for an association with overweight, race, and physical demands of work. Am J Epidemiol. 1988;128(1):179-189.
16. Felson DT, Zhang Y, Hannan MT, et al. Risk factors for incident radiographic knee osteoarthritis in the elderly: the Framingham Study. Arthritis Rheum. 1997;40(4):728-733. doi:10.1002/1529-0131(199704)40:4<728::AID-ART19>3.0.CO;2-D.
17. Patel C, Ghanim H, Ravishankar S, et al. Prolonged reactive oxygen species generation and nuclear factor-kappaB activation after a high-fat, high-carbohydrate meal in the obese. J Clin Endocrinol Metab. 2007;92(11):4476-4479. doi:10.1210/jc.2007-0778.
18. Aljada A, Mohanty P, Ghanim H, et al. Increase in intranuclear nuclear factor kappaB and decrease in inhibitor kappaB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect. Am J Clin Nutr. 2004;79(4):682-690.
19. Aljada A, Friedman J, Ghanim H, et al. Glucose ingestion induces an increase in intranuclear nuclear factor kappaB, a fall in cellular inhibitor kappaB, and an increase in tumor necrosis factor alpha messenger RNA by mononuclear cells in healthy human subjects. Metabolism. 2006;55(9):1177-1185. doi:10.1016/j.metabol.2006.04.016.
20. Calder PC, Ahluwalia N, Brouns F, et al. Dietary factors and low-grade inflammation in relation to overweight and obesity. Br J Nutr. 2011;106 Suppl 3:S5-S78. doi:10.1017/S0007114511005460.
21. Chek P. Pattern Overload. N Z Fit. December 2006. http://chekdocs.s3.amazonaws.com/Pattern_Overload.pdf.
22. Goldin A. Advanced Glycation End Products: Sparking the Development of Diabetic Vascular Injury. Circulation. 2006;114(6):597-605. doi:10.1161/CIRCULATIONAHA.106.621854.
23. Nowotny K, Jung T, Höhn A, Weber D, Grune T. Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus. Biomolecules. 2015;5(1):194-222. doi:10.3390/biom5010194.
24. Betteridge DJ. What is oxidative stress? Metabolism. 2000;49(2 Suppl 1):3-8.
25. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956;11(3):298-300.
26. Finkel T, Holbrook NJ. Oxidants, oxidative stress and the biology of ageing. Nature. 2000;408(6809):239-247. doi:10.1038/35041687.
27. Henrotin YE, Bruckner P, Pujol J-PL. The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthr Cartil OARS Osteoarthr Res Soc. 2003;11(10):747-755.
28. Singh G. Recent considerations in nonsteroidal anti-inflammatory drug gastropathy. Am J Med. 1998;105(1B):31S - 38S.
29. Griffin MR. Epidemiology of nonsteroidal anti-inflammatory drug-associated gastrointestinal injury. Am J Med. 1998;104(3A):23S - 29S; discussion 41S - 42S.
30. Wright JM. The double-edged sword of COX-2 selective NSAIDs. CMAJ Can Med Assoc J J Assoc Medicale Can. 2002;167(10):1131-1137.
31. Theodosakis J, Buff S. The Arthritis Cure: The Medical Miracle That Can Halt, Reverse, and May Even Cure Osteoarthritis. New York: St. Martin’s Press; 2004.
32. Green JA, Hirst-Jones KL, Davidson RK, et al. The potential for dietary factors to prevent or treat osteoarthritis. Proc Nutr Soc. 2014;73(02):278-288. doi:10.1017/S0029665113003935.
33. Wang H, Nair MG, Strasburg GM, et al. Antioxidant and antiinflammatory activities of anthocyanins and their aglycon, cyanidin, from tart cherries. J Nat Prod. 1999;62(2):294-296. doi:10.1021/np980501m.
34. Seeram N. Cyclooxygenase inhibitory and antioxidant cyanidin glycosides in cherries and berries. Phytomedicine. 2001;8(5):362-369. doi:10.1078/0944-7113-00053.
35. Blau LW. Cherry diet control for gout and arthritis. Tex Rep Biol Med. 1950;8(3):309-311.
36. Jacob RA, Spinozzi GM, Simon VA, et al. Consumption of cherries lowers plasma urate in healthy women. J Nutr. 2003;133(6):1826-1829.
37. Kelley DS, Rasooly R, Jacob RA, Kader AA, Mackey BE. Consumption of Bing sweet cherries lowers circulating concentrations of inflammation markers in healthy men and women. J Nutr. 2006;136(4):981-986.
38. Zhang Y, Neogi T, Chen C, Chaisson C, Hunter DJ, Choi HK. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis Rheum. 2012;64(12):4004-4011. doi:10.1002/art.34677.
39. Bell PG, Gaze DC, Davison GW, George TW, Scotter MJ, Howatson G. Montmorency tart cherry (Prunus cerasus L.) concentrate lowers uric acid, independent of plasma cyanidin-3-O-glucosiderutinoside. J Funct Foods. 2014;11:82-90. doi:10.1016/j.jff.2014.09.004.
40. Schumacher HR, Pullman-Mooar S, Gupta SR, Dinnella JE, Kim R, McHugh MP. Randomized double-blind crossover study of the efficacy of a tart cherry juice blend in treatment of osteoarthritis (OA) of the knee. Osteoarthritis Cartilage. 2013;21(8):1035-1041. doi:10.1016/j.joca.2013.05.009.
41. Howatson G, Bell PG, Tallent J, Middleton B, McHugh MP, Ellis J. Effect of tart cherry juice (Prunus cerasus) on melatonin levels and enhanced sleep quality. Eur J Nutr. 2012;51(8):909-916. doi:10.1007/s00394-011-0263-7.
42. Kuehl KS, Perrier ET, Elliot DL, Chesnutt JC. Efficacy of tart cherry juice in reducing muscle pain during running: a randomized controlled trial. J Int Soc Sports Nutr. 2010;7(1):17. doi:10.1186/1550-2783-7-17.
43. Beauchamp GK, Keast RSJ, Morel D, et al. Phytochemistry: ibuprofen-like activity in extra-virgin olive oil. Nature. 2005;437(7055):45-46. doi:10.1038/437045a.
44. Vane JR, Botting RM. New insights into the mode of action of anti-inflammatory drugs. Inflamm Res Off J Eur Histamine Res Soc Al. 1995;44(1):1-10.
45. Togna GI, Togna AR, Franconi M, Marra C, Guiso M. Olive oil isochromans inhibit human platelet reactivity. J Nutr. 2003;133(8):2532-2536.
46. Chrysohoou C, Panagiotakos DB, Pitsavos C, Das UN, Stefanadis C. Adherence to the Mediterranean diet attenuates inflammation and coagulation process in healthy adults: The ATTICA Study. J Am Coll Cardiol. 2004;44(1):152-158. doi:10.1016/j.jacc.2004.03.039.
47. Brehm BJ, Lattin BL, Summer SS, et al. One-Year Comparison of a High-Monounsaturated Fat Diet With a High-Carbohydrate Diet in Type 2 Diabetes. Diabetes Care. 2009;32(2):215-220. doi:10.2337/dc08-0687.
48. Bulotta S, Celano M, Lepore SM, Montalcini T, Pujia A, Russo D. Beneficial effects of the olive oil phenolic components oleuropein and hydroxytyrosol: focus on protection against cardiovascular and metabolic diseases. J Transl Med. 2014;12:219. doi:10.1186/s12967-014-0219-9.
49. Impellizzeri D, Esposito E, Mazzon E, et al. Oleuropein aglycone, an olive oil compound, ameliorates development of arthritis caused by injection of collagen type II in mice. J Pharmacol Exp Ther. 2011;339(3):859-869. doi:10.1124/jpet.111.182808.
50. Silva S, Sepodes B, Rocha J, et al. Protective effects of hydroxytyrosol-supplemented refined olive oil in animal models of acute inflammation and rheumatoid arthritis. J Nutr Biochem. 2015;26(4):360-368. doi:10.1016/j.jnutbio.2014.11.011.
51. Bogani P, Galli C, Villa M, Visioli F. Postprandial anti-inflammatory and antioxidant effects of extra virgin olive oil. Atherosclerosis. 2007;190(1):181-186. doi:10.1016/j.atherosclerosis.2006.01.011.
52. Dreher ML, Davenport AJ. Hass Avocado Composition and Potential Health Effects. Crit Rev Food Sci Nutr. 2013;53(7):738-750. doi:10.1080/10408398.2011.556759.
53. Wang W, Connor SL, Johnson EJ, Klein ML, Hughes S, Connor WE. Effect of dietary lutein and zeaxanthin on plasma carotenoids and their transport in lipoproteins in age-related macular degeneration. Am J Clin Nutr. 2007;85(3):762-769.
54. Blotman F, Maheu E, Wulwik A, Caspard H, Lopez A. Efficacy and safety of avocado/soybean unsaponifiables in the treatment of symptomatic osteoarthritis of the knee and hip. A prospective, multicenter, three-month, randomized, double-blind, placebo-controlled trial. Rev Rhum Engl Ed. 1997;64(12):825-834.
55. Maheu E, Mazières B, Valat JP, et al. Symptomatic efficacy of avocado/soybean unsaponifiables in the treatment of osteoarthritis of the knee and hip: a prospective, randomized, double-blind, placebo-controlled, multicenter clinical trial with a six-month treatment period and a two-month followup demonstrating a persistent effect. Arthritis Rheum. 1998;41(1):81-91. doi:10.1002/1529-0131(199801)41:1<81::AID-ART11>3.0.CO;2-9.
56. Au RY, Al-Talib TK, Au AY, Phan PV, Frondoza CG. Avocado soybean unsaponifiables (ASU) suppress TNF-α, IL-1β, COX-2, iNOS gene expression, and prostaglandin E2 and nitric oxide production in articular chondrocytes and monocyte/macrophages. Osteoarthritis Cartilage. 2007;15(11):1249-1255. doi:10.1016/j.joca.2007.07.009.
57. Cameron M, Chrubasik S. Oral herbal therapies for treating osteoarthritis. In: The Cochrane Collaboration, ed. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2014. http://doi.wiley.com/10.1002/14651858.CD002947.pub2. Accessed October 22, 2015.
58. Unlu NZ, Bohn T, Clinton SK, Schwartz SJ. Carotenoid absorption from salad and salsa by humans is enhanced by the addition of avocado or avocado oil. J Nutr. 2005;135(3):431-436.
59. Boyer J, Liu RH. Apple phytochemicals and their health benefits. Nutr J. 2004;3:5. doi:10.1186/1475-2891-3-5.
60. Jackson JK, Higo T, Hunter WL, Burt HM. The antioxidants curcumin and quercetin inhibit inflammatory processes associated with arthritis. Inflamm Res Off J Eur Histamine Res Soc Al. 2006;55(4):168-175. doi:10.1007/s00011-006-0067-z.
61. Lay E, Samiric T, Handley CJ, Ilic MZ. Short- and long-term exposure of articular cartilage to curcumin or quercetin inhibits aggrecan loss. J Nutr Biochem. 2012;23(2):106-112. doi:10.1016/j.jnutbio.2010.11.004.
62. S. A. H, A. A, T. O. M, T. A. A. Quercetin Dampens Postprandial Hyperglycemia in Type 2 Diabetic Patients Challenged with Carbohydrates Load. Int J Diabetes Res. 2012;1(3):32-35. doi:10.5923/j.diabetes.20120103.01.
63. Diabetes and Your Joints. Clin Diabetes. 2001;19(3):136-136. doi:10.2337/diaclin.19.3.136.
64. Chai SC, Hooshmand S, Saadat RL, Payton ME, Brummel-Smith K, Arjmandi BH. Daily apple versus dried plum: impact on cardiovascular disease risk factors in postmenopausal women. J Acad Nutr Diet. 2012;112(8):1158-1168. doi:10.1016/j.jand.2012.05.005.
65. Tishler M, Caspi D, Yaron M. C-reactive protein levels in patients with rheumatoid arthritis: the impact of therapy. Clin Rheumatol. 1985;4(3):321-324.
66. Otterness IG. The value of C-reactive protein measurement in rheumatoid arthritis. Semin Arthritis Rheum. 1994;24(2):91-104.
67. Del Rio D, Borges G, Crozier A. Berry flavonoids and phenolics: bioavailability and evidence of protective effects. Br J Nutr. 2010;104(S3):S67-S90. doi:10.1017/S0007114510003958.
68. Felgines C, Talavéra S, Gonthier M-P, et al. Strawberry anthocyanins are recovered in urine as glucuro- and sulfoconjugates in humans. J Nutr. 2003;133(5):1296-1301.
69. Norberto S, Silva S, Meireles M, Faria A, Pintado M, Calhau C. Blueberry anthocyanins in health promotion: A metabolic overview. J Funct Foods. 2013;5(4):1518-1528. doi:10.1016/j.jff.2013.08.015.
70. Sesso HD, Gaziano JM, Jenkins DJA, Buring JE. Strawberry intake, lipids, C-reactive protein, and the risk of cardiovascular disease in women. J Am Coll Nutr. 2007;26(4):303-310.
71. Moghe SS, Juma S, Imrhan V, Vijayagopal P. Effect of blueberry polyphenols on 3T3-F442A preadipocyte differentiation. J Med Food. 2012;15(5):448-452. doi:10.1089/jmf.2011.0234.
72. McAnulty LS, Nieman DC, Dumke CL, et al. Effect of blueberry ingestion on natural killer cell counts, oxidative stress, and inflammation prior to and after 2.5 h of running. Appl Physiol Nutr Metab Physiol Appliquée Nutr Métabolisme. 2011;36(6):976-984. doi:10.1139/h11-120.
73. McLeay Y, Barnes MJ, Mundel T, Hurst SM, Hurst RD, Stannard SR. Effect of New Zealand blueberry consumption on recovery from eccentric exercise-induced muscle damage. J Int Soc Sports Nutr. 2012;9(1):19. doi:10.1186/1550-2783-9-19.
74. Ruel G, Pomerleau S, Couture P, Lemieux S, Lamarche B, Couillard C. Low-calorie cranberry juice supplementation reduces plasma oxidized LDL and cell adhesion molecule concentrations in men. Br J Nutr. 2008;99(2):352-359. doi:10.1017/S0007114507811986.
75. Ruel G, Pomerleau S, Couture P, Lemieux S, Lamarche B, Couillard C. Plasma matrix metalloproteinase (MMP)-9 levels are reduced following low-calorie cranberry juice supplementation in men. J Am Coll Nutr. 2009;28(6):694-701.
76. Itoh T, Matsuda H, Tanioka M, Kuwabara K, Itohara S, Suzuki R. The role of matrix metalloproteinase-2 and matrix metalloproteinase-9 in antibody-induced arthritis. J Immunol Baltim Md 1950. 2002;169(5):2643-2647.
77. Bitsch R, Netzel M, Frank T, Strass G, Bitsch I. Bioavailability and Biokinetics of Anthocyanins From Red Grape Juice and Red Wine. J Biomed Biotechnol. 2004;2004(5):293-298. doi:10.1155/S1110724304403106.
78. de la Lastra CA, Villegas I. Resveratrol as an anti-inflammatory and anti-aging agent: mechanisms and clinical implications. Mol Nutr Food Res. 2005;49(5):405-430. doi:10.1002/mnfr.200500022.
79. Udenigwe CC, Ramprasath VR, Aluko RE, Jones PJH. Potential of resveratrol in anticancer and anti-inflammatory therapy. Nutr Rev. 2008;66(8):445-454. doi:10.1111/j.1753-4887.2008.00076.x.
80. Candelario-Jalil E, de Oliveira ACP, Gräf S, et al. Resveratrol potently reduces prostaglandin E2 production and free radical formation in lipopolysaccharide-activated primary rat microglia. J Neuroinflammation. 2007;4:25. doi:10.1186/1742-2094-4-25.
81. Verzijl N, DeGroot J, Ben ZC, et al. Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis. Arthritis Rheum. 2002;46(1):114-123. doi:10.1002/1529-0131(200201)46:1<114::AID-ART10025>3.0.CO;2-P.
82. Yammani RR, Carlson CS, Bresnick AR, Loeser RF. Increase in production of matrix metalloproteinase 13 by human articular chondrocytes due to stimulation with S100A4: Role of the receptor for advanced glycation end products. Arthritis Rheum. 2006;54(9):2901-2911. doi:10.1002/art.22042.
83. Liu F-C, Hung L-F, Wu W-L, et al. Chondroprotective effects and mechanisms of resveratrol in advanced glycation end products-stimulated chondrocytes. Arthritis Res Ther. 2010;12(5):R167. doi:10.1186/ar3127.
84. Bognar E, Sarszegi Z, Szabo A, et al. Antioxidant and anti-inflammatory effects in RAW264.7 macrophages of malvidin, a major red wine polyphenol. PloS One. 2013;8(6):e65355. doi:10.1371/journal.pone.0065355.
85. Crews FT, Bechara R, Brown LA, et al. Cytokines and alcohol. Alcohol Clin Exp Res. 2006;30(4):720-730. doi:10.1111/j.1530-0277.2006.00084.x.
86. Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med Maywood NJ. 2008;233(6):674-688. doi:10.3181/0711-MR-311.
87. Simopoulos AP. Overview of evolutionary aspects of omega 3 fatty acids in the diet. World Rev Nutr Diet. 1998;83:1-11.
88. Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011;93(5):950-962. doi:10.3945/ajcn.110.006643.
89. Hibbeln JR, Nieminen LRG, Blasbalg TL, Riggs JA, Lands WEM. Healthy intakes of n-3 and n-6 fatty acids: estimations considering worldwide diversity. Am J Clin Nutr. 2006;83(6 Suppl):1483S - 1493S.
90. Simopoulos AP. Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases. Biomed Pharmacother Bioméd Pharmacothérapie. 2006;60(9):502-507. doi:10.1016/j.biopha.2006.07.080.
91. Bosma-den Boer MM, van Wetten M-L, Pruimboom L. Chronic inflammatory diseases are stimulated by current lifestyle: how diet, stress levels and medication prevent our body from recovering. Nutr Metab. 2012;9(1):32. doi:10.1186/1743-7075-9-32.
92. James MJ, Cleland LG. Dietary n-3 fatty acids and therapy for rheumatoid arthritis. Semin Arthritis Rheum. 1997;27(2):85-97.
93. Guebre-Egziabher F, Rabasa-Lhoret R, Bonnet F, et al. Nutritional intervention to reduce the n-6/n-3 fatty acid ratio increases adiponectin concentration and fatty acid oxidation in healthy subjects. Eur J Clin Nutr. 2008;62(11):1287-1293. doi:10.1038/sj.ejcn.1602857.
94. Fortin PR, Lew RA, Liang MH, et al. Validation of a meta-analysis: The effects of fish oil in rheumatoid arthritis. J Clin Epidemiol. 1995;48(11):1379-1390. doi:10.1016/0895-4356(95)00028-3.
95. Juge N, Mithen RF, Traka M. Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cell Mol Life Sci CMLS. 2007;64(9):1105-1127. doi:10.1007/s00018-007-6484-5.
96. Davidson RK, Jupp O, de Ferrars R, et al. Sulforaphane represses matrix-degrading proteases and protects cartilage from destruction in vitro and in vivo. Arthritis Rheum. 2013;65(12):3130-3140. doi:10.1002/art.38133.
97. Ah Kim H, Yeo Y, Kim W-U, Kim S. Phase 2 enzyme inducer sulphoraphane blocks matrix metalloproteinase production in articular chondrocytes. Rheumatology. 2009;48(8):932-938. doi:10.1093/rheumatology/kep132.
98. Kim H-A, Yeo Y, Jung HA, Jung YO, Park SJ, Kim SJ. Phase 2 enzyme inducer sulphoraphane blocks prostaglandin and nitric oxide synthesis in human articular chondrocytes and inhibits cartilage matrix degradation. Rheumatol Oxf Engl. 2012;51(6):1006-1016. doi:10.1093/rheumatology/ker525.
99. McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum. 1996;39(4):648-656.
100. Clark AG, Rohrbaugh AL, Otterness I, Kraus VB. The effects of ascorbic acid on cartilage metabolism in guinea pig articular cartilage explants. Matrix Biol J Int Soc Matrix Biol. 2002;21(2):175-184.
101. Neogi T, Booth SL, Zhang YQ, et al. Low vitamin K status is associated with osteoarthritis in the hand and knee. Arthritis Rheum. 2006;54(4):1255-1261. doi:10.1002/art.21735.
102. Oka H, Akune T, Muraki S, et al. Association of low dietary vitamin K intake with radiographic knee osteoarthritis in the Japanese elderly population: dietary survey in a population-based cohort of the ROAD study. J Orthop Sci Off J Jpn Orthop Assoc. 2009;14(6):687-692. doi:10.1007/s00776-009-1395-y.
103. Misra D, Booth SL, Tolstykh I, et al. Vitamin K Deficiency Is Associated with Incident Knee Osteoarthritis. Am J Med. 2013;126(3):243-248. doi:10.1016/j.amjmed.2012.10.011.
104. Tapiero H, Townsend DM, Tew KD. The antioxidant role of selenium and seleno-compounds. Biomed Pharmacother Bioméd Pharmacothérapie. 2003;57(3-4):134-144.
105. Tinggi U. Selenium: its role as antioxidant in human health. Environ Health Prev Med. 2008;13(2):102-108. doi:10.1007/s12199-007-0019-4.
106. Huguenin GVB, Oliveira GMM, Moreira ASB, et al. Improvement of antioxidant status after Brazil nut intake in hypertensive and dyslipidemic subjects. Nutr J. 2015;14(1). doi:10.1186/s12937-015-0043-y.
107. Jordan JM. An Ongoing Assessment of Osteoarthritis in African Americans and Caucasians in North Carolina: The Johnston County Osteoarthritis Project. Trans Am Clin Climatol Assoc. 2015;126:77-86.
108. Blomhoff R, Carlsen MH, Andersen LF, Jacobs DR. Health benefits of nuts: potential role of antioxidants. Br J Nutr. 2006;96 Suppl 2:S52-S60.
109. Harris ED, Rayton JK, Balthrop JE, DiSilvestro RA, Garcia-de-Quevedo M. Copper and the synthesis of elastin and collagen. Ciba Found Symp. 1980;79:163-182.
110. Kremer JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol. 1996;23(6):990-994.
111. Houston DK, Nicklas BJ, Ding J, et al. Dietary protein intake is associated with lean mass change in older, community-dwelling adults: the Health, Aging, and Body Composition (Health ABC) Study. Am J Clin Nutr. 2008;87(1):150-155.
112. Janssen HCJP, Samson MM, Verhaar HJJ. Vitamin D deficiency, muscle function, and falls in elderly people. Am J Clin Nutr. 2002;75(4):611-615.
113. Murphy K, Crichton G, Dyer K, et al. Dairy Foods and Dairy Protein Consumption Is Inversely Related to Markers of Adiposity in Obese Men and Women. Nutrients. 2013;5(11):4665-4684. doi:10.3390/nu5114665.
114. Kaçar C, Gilgil E, Tuncer T, et al. The association of milk consumption with the occurrence of symptomatic knee osteoarthritis. Clin Exp Rheumatol. 2004;22(4):473-476.
115. Lu B, Driban JB, Duryea J, McAlindon T, Lapane KL, Eaton CB. Milk Consumption and Progression of Medial Tibiofemoral Knee Osteoarthritis: Data From the Osteoarthritis Initiative: Association of Milk Consumption With Progression of Knee OA. Arthritis Care Res. 2014;66(6):802-809. doi:10.1002/acr.22297.
116. Dalbeth N, Ames R, Gamble GD, et al. Effects of skim milk powder enriched with glycomacropeptide and G600 milk fat extract on frequency of gout flares: a proof-of-concept randomised controlled trial. Ann Rheum Dis. 2012;71(6):929-934. doi:10.1136/annrheumdis-2011-200156.
117. Choi HK, Liu S, Curhan G. Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2005;52(1):283-289. doi:10.1002/art.20761.
118. Scher JU, Sczesnak A, Longman RS, et al. Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis. eLife. 2013;2:e01202. doi:10.7554/eLife.01202.
119. Scher JU, Ubeda C, Artacho A, et al. Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis Rheumatol Hoboken NJ. 2015;67(1):128-139. doi:10.1002/art.38892.
120. Bahrami B, Macfarlane S, Macfarlane GT. Induction of cytokine formation by human intestinal bacteria in gut epithelial cell lines. J Appl Microbiol. 2011;110(1):353-363. doi:10.1111/j.1365-2672.2010.04889.x.
121. Menard S. Lactic acid bacteria secrete metabolites retaining anti-inflammatory properties after intestinal transport. Gut. 2004;53(6):821-828. doi:10.1136/gut.2003.026252.
122. Vaghef-Mehrabany E, Alipour B, Homayouni-Rad A, Sharif S-K, Asghari-Jafarabadi M, Zavvari S. Probiotic supplementation improves inflammatory status in patients with rheumatoid arthritis. Nutr Burbank Los Angel Cty Calif. 2014;30(4):430-435. doi:10.1016/j.nut.2013.09.007.