The Role of Nutrition in Osteoarthritis: Part 3

In which we conclude our examination by looking at the role that heavy metals and minerals play in the development and treatment of OA.




Certain minerals have proven to have an effect on OA, some showing a preventative or healing effect, and some a causative effect. The information in this section is all derived from one mega review of the literature on the subject (link to be found at the end of this section).


The long and short of it is, “boron, selenium, and copper increase cartilage matrix formation, enhance chondrocyte proliferation, and have anti-inflammatory and antioxidant effects, while other trace elements such as cadmium and iron may exacerbate OA pathogenesis and progression”.




Boron reduces inflammatory reactions in OA by downregulating certain enzyme activities at the site of inflammation, thus inhibiting the inflammatory response. As well, boron can help prevent the development of OA, “possibly by enhancing absorption of calcium, phosphorus, and magnesium, and retention of magnesium and calcium”. 


Furthermore, boron has been shown to repair “osteochondral defects”, which means it may be a valid treatment for cartilage injury in OA. (“An osteochondral defect refers to a focal area of damage that involves both the cartilage and a piece of underlying bone. These can occur from an acute traumatic injury to the knee or an underlying disorder of the bone.” )


(For more on boron see this older newsletter of mine.)




Copper is required to maintain the integrity and homeostasis of cartilage tissue, and “the disorder of copper metabolism is closely related to the pathogenesis of OA”. Therefore, it is no surprise that supplementing with copper has been found to reduce symptoms of osteochondrosis and cartilage lesions, perhaps by improving collagen cross-linking and synthesis of type II collagen in the body. (Osteochondrosis causes pieces of cartilage and thin layers of bone to separate from some of the bones within a person’s joints.”)


It is believed that copper may also prevent the breakdown of cartilage by inhibiting the release of nitric oxide, but there are those for whom copper supplementation is not a good idea. Those with “Wilson’s disease”, a disorder of copper metabolism that is genetic, have been found to develop early-onset OA due to their tendency to accumulate excessive copper in the body. Thus, like with many nutrients, the symptoms of deficiency are much like the symptoms of excess.


Others who should avoid copper are those who live in older houses with copper water pipes who drink their tap water unfiltered. This is a primary source of copper overload in people. (Also, copper IUDs in women can cause copper overload and zinc deficiency.)




Magnesium serves many functions that can help alleviate OA symptoms. It significantly reduces the degeneration of cartilage, and inhibits the expression of inflammatory compounds in the joints. As well, magnesium can increase the adhesion of synovial stem cells to osteochondral defects (similar to boron, as we saw above).




Manganese can slow down the degeneration of a particular form of cartilage and is beneficial for repairing this type of cartilage, known as articular cartilage. 


In one study, manganese was combined with the cartilage rebuilders glucosamine and chondroitin, and proved to relieve symptoms of OA and speed the healing of articular cartilage. And, of course, manganese deficiency is linked to a worsening of OA symptoms, in part because it is required for the synthesis of glycosaminoglycans in the body (which support collagen and elastin production).


Manganese also has powerful antioxidant properties and so “can reduce the oxidative stress of articular cartilage caused by inflammation and alleviate OA severity…and can serve as a promising approach for cartilage protection in OA”.


I had a closer look at the study that combined glucosamine and chondroitin with manganese just to get an idea of the amount of manganese used. Manganese, in excess, can easily function like a heavy metal and be counter productive. Subjects in this study received 1,000 mg of glucosamine, 800 mg of chondroitin, and 152 mg of manganese ascorbate, twice daily. (Original study). This at first struck me as a dangerous amount of manganese, but after digging more I found that manganese ascorbate only provides 20% elemental manganese. Therefore, subjects were actually receiving 30 mg of manganese twice daily.




Selenium deficiency results in articular cartilage degeneration, and selenium levels in patients with OA have been found to be significantly lower than that of normal controls. “It is apparent that selenium deficiency may be a potential risk factor for OA.” Selenium is an important part of our antioxidant system, so it also has significant anti-inflammatory properties.




Zinc is required by the body for the growth and maintenance of cartilage (and also improves the activity of vitamin D, further supporting its role in treating symptoms). 


Zinc has a particular role in cartilage maintenance due to it being required for the body to produce those stem cells which create chondrocytes. (“The cartilage is solely composed of cells known as chondrocytes. Surrounded by collagenous fibers, chondrocytes release substances to make cartilage strong yet flexible.” Source)


Zinc deficiency inhibits the production of chondrocytes, and studies “have demonstrated that a low dose of zinc can increase the cultured chondrocyte proliferation by 40–50%”. 




Iron is one mineral that can lead to the development of OA. As we age, too much iron can accumulate in the body particularly in cartilage. When a woman is still menstruating this is usually not a problem, as she has a way of eliminating excess iron from the body. Men and post-menopausal women do not have this mechanism to reduce iron, and as we age there also often is a reduction in blood circulation, which further allows iron accumulation in the articular cartilage.


Iron overload in the joints is directly linked to cartilage damage and degeneration, and to “the pathogenesis and progression of OA”.


It has been observed that, in patients with OA, high ferritin (stored iron) levels correlates with more severe knee cartilage pain and with narrower joint space. As well, OA is one of the most common ailments in people with hereditary hemochromatosis, an iron-overload disease. Furthermore, it is known that “the iron concentration in synovial fluid of patients with OA is significantly higher than that of patients with rheumatoid arthritis and age-matched healthy subjects”.


But, even with these clues and links between high iron and OA, research has yet to fully identify the mechanism by which iron causes this process of degeneration. However, we do know excess iron is linked to heart disease, some types of cancer, and non-alcoholic fatty liver disease. And we know that iron overload is associated with oxidative stress (i.e. free radical damage), which as we saw earlier, is a factor in the inflammation and pain associated with OA. (Source)


Those who think iron might be a problem should have their blood iron and ferritin levels checked to see if they appear too high. If you feel that iron may be a problem, avoid iron in supplements, don’t cook in cast iron pans, and avoid excessive red meat intake. Another good option for some of you is to donate blood once a month. This both gets rid of excess iron and helps the body by encouraging it to generate new red blood cells.




Another mineral linked to causing OA is cadmium. This metal is okay in trace amounts but functions as a detrimental heavy metal when ingested in high amounts. The main target of cadmium accumulation is the skeletal structure, but it also affects the kidneys, prostate and lungs. 


Though the relationship between OA and cadmium has not been studied much, it is known that the levels of blood cadmium is related to severity of OA, and those patients with OA do show high serum levels of cadmium.


Cadmium can reduce the content of proteoglycan and glycosaminoglycan and inhibit the expression of type II collagen and aggrecan in the extracellular matrix of articular cartilage.”


Those with excessive cadmium are usually smokers or former smokers, as the tobacco plant easily takes up cadmium from the environment. Workplace exposure is also a primary source of cadmium toxicity, found mostly in those mining cadmium-containing ores, or who have exposure to cadmium from paints and during work such as plating, soldering, and welding.


The non-smoking public, who do not work in the aforementioned industries, get their excessive cadmium from plant foods grown in soil high in cadmium. Unfortunately,  there is no way of knowing if a given food was grown in these soils. But there are certain areas of the world that have high industry and low environmental protection, in which the soil is more commonly contaminated with cadmium. For example, China: “Rapid industrialization in China during the last three decades has resulted in widespread contamination of Cd in agricultural soils. A considerable proportion of the rice grain grown in some areas of southern China has Cd concentrations exceeding the Chinese food limit.”  (Source)


Many synthetic fertilizers contain cadmium, so as with most foods, we want to avoid those grown in third world countries as there is little regulation designed to protect the ultimate consumer of foods grown there. A combination of illiterate farmers and unscrupulous salesmen can lead to much food contamination. 


Among the majority of foods eaten in the West, the two foods highest in cadmium are organ meats and shellfish, and high cadmium levels are often found in people who eat these foods frequently. Other foods to avoid are potato chips, french fries and chocolate. 


Basically, eat organic foods as much as possible to avoid undue cadmium exposure. Having adequate zinc stores in the body will prevent the uptake of cadmium, so here zinc serves a secondary function for helping us treat OA.


Removal of all heavy metals from the body is best done with infrared saunas and the use of Liposomal Glutathione.


(Primary Source for mineral information)




All of the beneficial minerals discussed are found in adequate levels for preventing deficiency, in our Mineral Mix product, and in the gender specific Pods (NutriPods for Men and NutriPods for Women). Original NutriPods would not be an ideal choice for our purposes here, as it does not contain boron and is lacking sufficient zinc for men. As well, none of these products would provide sufficient magnesium, nor vitamins C and D, they do however provide sufficient vitamin E (400 IU). Also, if one wanted to try manganese in a therapeutic amount, as discussed above, they would need to take an additional manganese product, as Pods only provide a maintenance dose of this mineral.

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