Rheumatoid Arthritis (RA) Causes

Inflammation and autoimmune activity

In RA, several cytokines are involved in almost all aspects of joint inflammation and destruction -  e.g. interleukin (IL)-1, IL-6, IL-8, IL-12, IL-17, tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) and granulocyte-macrophage colony-stimulating factor (GM-CSFG), . In particular, TNF-α and IL-6 are considered to be pivotal cytokines in the development of RA.

What is initiating this uncontrolled inflammation?

•    Bacteria or virus.   Research suggests a connection to periodontal disease and smoking

•   Repetitive over-use of a joint;

•   A so-called "leaky gut".    It is an almost universal clinical observation that inflammation of the gut is frequently associated with inflammation of the joints and vice versa, but the nature of this relationship remains elusive.

Factors promoting "Leaky Gut"   i.e. Gut Permeability

•  Poor gut microbiome.   A healthy gut needs a diverse population of good bacteria; lectin-tolerance is very much tied into microbiome health;

•   Use of NSAIDs or other drugs

•  Dietary lectins.    A study of 800 people with autoimmune conditions, most with elevated TNF-α, went on diets that cut out high-lectin-content foods for 6 months, after which those that complied with the diet had normal TNF-α levels. Their diet avoided grains, sprouted grains, pseudo-grains, legumes, soy, peanuts, cashews, nightshade plants, melons, squashes, cow's milk products (from cows producing casein A1 milk), and grain- and/or bean-fed animal meat. (Gundry &Steven, 2014)

 Dietary substances, especially lectins, directly or indirectly (by increasing pathogenic bacteria populations, especially with unhealthy gut flora) inflame /damage villi lining the gut, allowing both lectins and pathogenic bacteria to enter the bloodstream. In circulation, the immune system (IS) recognizes them as antigens (foreign substances to be marked for destruction by antibodies). Evidence suggests that dietary lectins interact with IS white blood cells to facilitate the movement of both dietary and gut-derived pathogenic antigens into peripheral tissues. Immune system complexes formed by antigen and antibodies trigger the IS to release compounds to destroy them, and if deposited in joints of genetically susceptible individuals, will also damage the surrounding joint tissue. These pathogenic antigens may even interact directly with synovial tissues. (Cordain et al, 2000)

Stress

Researchers found a strong connection between stress and the risk of developing RA.   A meta-analysis of 16 small studies published in Arthritis Research & Therapy found that stress tends to make RA symptoms worse, that childhood trauma increases risk of rheumatic diseases (a 2009 study found that people who reported two or more traumatic childhood events - including physical, emotional, or sexual abuse -- had twice the risk of rheumatic disease compared with those who reported no childhood trauma), and that those with PTSD have a higher risk of developing RA and other autoimmune disease.    (Hassett & Clauss, 2010). Another study found that stressful events often precede onset of RA.

Increased collagenase activity

Collagenase is an enzyme that breaks down collagen.   This would further cartilage damage in a joint 

References

Hassett, A. L., & Clauw, D. J. (2010). The role of stress i n rheumatic diseases. Arthritis research & therapy, 12(3), 123. doi:10.1186/ar3024 LInk

Gundry, Steven R, Abstract P354 :Elevated Adiponectin And TNF-a Levels are Markers for Gluten and Lectin Sensitivity, Circulation, 2014; 129:AP354

Loren Cordain, L. Toohey, M. J. Smith and M. S. Hickey, Modulation of immune function by dietary lectins in rheumatoid arthritis, Brit. J of Nutr. (2000), 83, 207-217