The Role of Nutrition in Osteoarthritis: Part Two
In which we continue our examination of nutrients germane to osteoarthritis (OA).
Of course we must touch on vitamin D for, as I often claim, “there is not a disease known to man that is not somehow linked to vitamin D”.
Since it is well established that vitamin D is essential for bone, teeth, and muscle health, in part by enhancing intestinal calcium and phosphorus absorption, this suggests that vitamin D metabolites “may affect OA cartilage directly”, as well as possibly “influencing healthy cartilage indirectly through the endocrine system”.
However, reviews of the literature on vitamin D and OA seem to indicate that only those with suboptimal vitamin D levels find pain relief when supplementing with it. Correspondingly, those with lower than ideal levels of vitamin D have been found to be at an increased risk of a worsening of OA knee pain.
The results of one detailed study on the subject “suggest there is a small but statistically significant clinical benefit to vitamin D treatment in patients with knee OA, although we recommend a long-term study to determine whether these changes are clinically important and whether they will be sustained with time”.
In this study vitamin D insufficiency was set at ≤ 50 nmol/L, and the group that received vitamin D (as opposed to the placebo group) were given a healthy dose. They received “60,000 IU per day for 10 days followed by 60,000 IU once a month for 12 months”. (Source)
In my opinion, while the mega dose for ten days should have easily brought those with inadequate levels back into range, the follow up dose for the rest of the year only amounts to 2,000 IU daily. This I would consider to be too low for any real benefits to manifest, in the long run.
An overview of studies on OA and vitamin K determined that “a sufficient level of vitamin K is associated with a lower risk of OA and pathological joint features”.
It appears that vitamin K, as well as having some anti-inflammatory properties, activates what are known as “matrix gla proteins”, a potent inhibitor of calcification that can prevent calcification of cartilage. “Although the current data are insufficient to establish the optimal dose of vitamin K to prevent OA, ensuring sufficient dietary intake seems to protect the elderly from OA.” (Source)
Antioxidants counteract oxidative stress by scavenging and neutralising free radicals, and this mechanism can be helpful in reducing symptoms of OA. Particularly, vitamins C and E have been shown to be of value here, along with curcumin. (Source)
Many animal studies have demonstrated a benefit in reducing OA symptoms when the lab animals were given vitamin C, either as a dietary supplement or when injected directly into the joints. In these studies vitamin C also protected the joints from further deterioration.
Given that some of the science on the subject was inconclusive, perhaps due to certain flaws in the studies, researchers feel that “more randomized placebo-controlled trials in humans are desperately needed in order to fully understand whether vitamin C therapy is efficacious in treating and/or preventing OA”. (Source)
In one rodent study, simply adding vitamin C to the diet led to a reduction in cartilage loss and OA symptoms. However, in this study the optimal dose of vitamin C was 100 mg per kilogram of bodyweight, and a higher amount proved to be less efficient. From a human perspective, if one weighed 150 lbs (68 kilograms) this would amount to 6,800 mg of vitamin C per day, far more than most of us take. (Source)
However, even though higher levels of vitamin C were not of value for rats, we have to remember that these creatures are able to synthesize their own vitamin C internally, whereas we are not. Therefore, a higher intake of vitamin C may be more suitable for humans than rats.
Now, 6.8 grams of vitamin C could create a laxative effect in some people. One way around this is to use Liposomal Vitamin C which will not have this effect and, being far more absorbable than regular vitamin C, will prove effective at a much lower dose.
Another option to avoid a laxative effect would be to use a “buffered” vitamin C, which is ascorbic acid reacted with a mineral to produce a non-acidic ascorbate form. The only thing to be aware of is that, when using calcium ascorbate, if one took 6.8 grams they would also get about 600 mg of calcium, which can be too much for many people. So, ideally one would use a magnesium or sodium ascorbate, or a multi-mineral ascorbate, rather than just calcium ascorbate.
Since vitamin E is both a powerful antioxidant and has anti-inflammatory effects, it has been studied for its ability to help treat OA. However, results of vitamin E studies, like vitamin C, are considered controversial as studies have provided mixed results. But, we must consider that most of this type of research is done on animals, where they induce OA symptoms in the creatures. So not an ideal representation of what real OA is in a human being. Nonetheless, “animal studies suggested that vitamin E treatment prevented cartilage degeneration and improved oxidative status in animal models of osteoarthritis”.
And, human studies have “observed low circulating or synovial vitamin E in human osteoarthritic patients compared to healthy controls”. As a result of such studies the current scientific perspective is that “vitamin E may retard the progression of osteoarthritis by ameliorating oxidative stress and inflammation of the joint”. (Source)
Finally, I have one good human study designed to evaluate the beneficial effects of vitamin E in the plasma, synovial fluid, and synovial tissue of patients with osteoarthritis of the knee.
One study looked at 72 subjects scheduled for knee surgery. For two months before undergoing surgery the patients were given either a placebo or 400 IU of vitamin E (alpha tocopherol) daily. The conclusion was positive: “Vitamin E is an effective antioxidant that can improve clinical symptoms and reduce oxidative stress conditions in patients with late-stage knee osteoarthritis.” (Source)
Human studies have found curcumin (turmeric extract) to be effective in alleviating knee OA symptoms. A trademarked turmeric product was tested by giving patients 400 mg twice daily (containing 80 mg curcumin each). This dose “was found to be effective and safe in alleviating symptoms in patients suffering from knee osteoarthritis when administered for 90 days”. (Source)
Another study, using a different trademarked product, gave 139 patients with knee OA either 500 mg of turmeric extract (95% curcuminoids, containing 50 mg of actual curcumin per cap) three times daily, or a NSAID (diclofenac) twice daily for one month.
“Curcumin has similar efficacy to diclofenac but demonstrated better tolerance among patients with knee OA. Curcumin can be an alternative treatment option in the patients with knee OA who are intolerant to the side effects of non-steroidal anti-inflammatory drugs.” (Source)
Here I will mention our Liposomal Curcumin/Resveratrol product as, given the liposomal form of delivery, it should be superior to most other turmeric/curcumin products. And, just to put a cherry on top, I looked for any value the Resveratrol component might have for OA. Sure enough, “numerous clinical studies have demonstrated resveratrol’s efficacy as an osteoarthritis management agent”. (Source)
In Part 3, I will conclude with an examination of minerals that have a relationship to OA, both the good and the bad.