Rheumatoid arthritis or RA is not only a form of inflammatory arthritis but also an autoimmune disease that primarily attacks the body's own tissues specifically the synovium a thin membrane that lines the joints. As a result of the attack fluid builds up in the joints causing pain and inflammation that can occur throughout the entire body. And because the disease can also cause inflammation and injury in other organs in the body rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.
Rheumatoid arthritis is characterized by periods of disease flares and remissions and can cause permanent joint destruction and deformity. In addition to causing joint problems rheumatoid arthritis can also affect your whole body with fevers and fatigue.
The etiology of the disease is complex and probably multifactorial. Current research supports the notion that RA is caused by a combination of genetic and environmental factors as specific genetic markers have been identified with the condition. While not all individuals who have the genetic predisposition for the disease actually gets the disease it is reasonable to believe that environmental factors will act on an epigenetic level activating these associated genes. There is also evidence that chronic viral infections may play a role in the disease's pathogenesis.
Additionally it also appears that gut microflora balance may have a crucial role in the instigation of the condition. Disturbances in the microflora environment causing disruptions in the delicate microflora balance has been shown to increase populations of pathological bacteria. These bacteria go on to produce inflammatory cytokines such as interleukin 17 and proinflammatory Th17 cells both of which have been associated with the pathophysiology of rheumatoid arthritis and autoimmunity in general.
While nonsteroidal anti-inflammatory drugs (NSAIDs) immune-suppressive agents and corticosteroid medications are the standard of care this approach is fraught with a number of disconcerting side effects. Ironically for instance use of immune-suppressive drugs can increase the risk of infections in a population where as mentioned previously chronic viral infections may contribute to the condition.
As RA is an inflammatory disease it only makes sense that inflammatory pathways including COX and LOX TNF-alpha and various inflammatory interleukins would be a therapeutic target. Boswellia is a known immune and inflammatory modulator and has been shown to be a promising herbal therapeutic agent in a variety of inflammatory and autoimmune conditions including RA.
EGCg the polyphenolic extract from green tea was shown to induce apoptosis of synovial RA fibroblasts by sensitizing the cells to TNF-alpha induced apoptosis while also suppressing TNF-alpha -induced production of MMP-1. In RA matrix metalloproteinase-1 (MMP-1) breaks down interstitial collagen types I II and III.
Curcumin the primary active polyphenol in turmeric has been shown to significantly decrease and inhibit IL-6 and many other associated inflammatory compounds thus becoming another likely candidate as a joint-protective and inflammatory-modulating agent.
Finally vitamin K2 especially in the MK-4 form has been shown to inhibit the proliferation of fibroblast-like synoviocytes and the development of collagen-induced arthritis.
As in most cases of autoimmunity it is perhaps wise to investigate and address both frank and clandestine pathogens gut related issues and food allergies and sensitivities as well as directly addressing the pain and inflammation of this condition. Perhaps in this way we may make a greater therapeutic impact on the disease for our patients.
by Michael Fuhrman D.C.