Living pain-free on a daily basis is something that is easily taken for granted by those who have not experienced chronic pain. In addition to everyday aches and pains, living with chronic pain can wreak havoc on one’s mental state, as over time, dealing with it can cause exhaustion, hopelessness and frustration.
Approximately one in four Americans are currently living with chronic pain, which is most commonly attributed to lower back pain, fibromyalgia, neuropathy or arthritis. While some of these conditions may be a consequence of wear and tear on the body over the years, others may stem from immune system dysfunction, such as rheumatoid arthritis (RA). Rheumatoid arthritis is an autoimmune condition in which the body’s immune system mistakenly attacks the joints, resulting in pain, swelling and stiffness in these areas.
We do not know what causes the body to suddenly turn against itself in autoimmune conditions such as RA. What we do know is that scientists and researchers are turning over new stones daily, searching for ways to help manage these diseases. In fact, mounting research has begun to support the role of vitamin D in autoimmune conditions, as it has been found to play a part in the regulation of the immune system and inflammation.
In a new study, researchers evaluated the effect of vitamin D status on disease activity and endothelial cell function in individuals with early RA. A total of 70 individuals, 35 patients with RA and 35 matched, healthy controls, were included for analysis.
All individuals were tested for several clinical values including C-reactive protein, a marker of inflammation, blood insulin, blood glucose, HOMA-IR, a marker of insulin resistance, and 25(OH)D levels. Additionally, for the patients, RA severity was determined by the Disease Activity Score 28 (DAS28), which is based off of pain and swelling in 28 major joints. Higher scores of the DAS28 indicated increased disease severity. Last, endothelial cell function was measured, as endothelial cell dysfunction is part of the pathogenesis of acute inflammatory conditions such as RA.
This is what the researchers found:
- Only one patient was considered vitamin D insufficient while the other 34 were all vitamin D deficient.
- Compared to the healthy controls, those with RA had significantly increased inflammation, lower vitamin D levels and worse endothelial cell dysfunction (p < 0.0001).
- Those with increased disease activity had more severe insulin resistance and lower vitamin D levels than those with more moderate disease activity (p < 0.05 and p < 0.0001, respectively).
- There was a positive correlation between vitamin D status and endothelial cell function (p = 0.001).
The researchers concluded,
“In early RA patients with moderate and high disease activity, low serum levels of vitamin D were associated with disease activity, increased insulin resistance, and endothelial dysfunction.”
Of course, any study is only as strong as its weaknesses. Though this study had significant findings and case-control comparisons are quite useful, it was observational, and thus does not prove causality. Additionally, the sample size was very small, and studying a larger group would improve the generalizability of the findings.
Despite the weaknesses of this study, the mounting evidence supporting vitamin D’s relationship with RA is difficult to ignore. To optimize health and possibly manage the severity of RA, the Vitamin D Council recommends supplementing with between 5,000-10,000 IU per day, and maintaining a vitamin D level of between 40-80 ng/ml (100-200 nmol/l).
As mentioned earlier, there is a high prevalence of chronic pain-related conditions, and some of you have already reached out to us to share your experience. If you have a story you have yet to share with us, please do. Sharing your story inspires action from others who have yet to find their answer. You can reach us at [email protected].
Peterson, R. & Cannell, JJ. Severity of rheumatoid arthritis may be mediated by vitamin D status, according to recent study. The Vitamin D Council Blog & Newsletter, 1/18.