Rheumatoid arthritis! – these are not the words anyone wants to hear when they start to experience joint discomfort. It quite naturally engenders fear and worry as the tretaments offered are in themselves a challenge in most cases and avoiding effective treatment can predispose an individual to a shortened and miserable life.
According to the venerable Wikipedia – Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks flexible (synovial) joints. The process involves an inflammatory response of the capsule around the joints (synovium) secondary to swelling (hyperplasia) of synovial cells, excess synovial fluid, and the development of fibrous tissue (pannus) in the synovium.
The pathology of the disease process often leads to the destruction of articular cartilage and ankylosis (fusion) of the joints. Rheumatoid arthritis can also produce diffuse inflammation in the lungs, membrane around the heart (pericardium), the membranes of the lung (pleura), and white of the eye (sclera), and also nodular lesions, most common in subcutaneous tissue.
Although the cause of rheumatoid arthritis is unknown, autoimmunity plays a pivotal role in both its chronicity and progression, and RA is considered a systemic autoimmune disease. (My emphasis)
Whilst there is not a single causative agent agreed upon there are stirring in the scientific literature that support the concept that RA is, in some people caused by bacteria, and that alterations in the ecological mileau may be a contributing factor.
It is not the purpose of this short piece to exhaustively explore all of the proposed aetoliologies or the treatments and management available, rather I want to highlight a convergence of thinking and indicate where this may lead.
Bacteria
Prof Alan Ebringer and colleagues have been diligently recording the relationship of microbial trigger, genetic association and autoimmunity as the likely cause of RA.[1],[2],[3] He and others state that the rapid rise in the number of autoimmune diseases cannot be explained solely on the basis of genetic association, but also through the involvement of exogenous (environmental) factors predominantly in the form of microbial infections.[4]
Whilst we may also say that the epidemiological effects of altered food production and availability would also be a strong contender, a paper out in the April 2012 issue of PloS ONE suggests the billions of bugs in our guts have a newfound role: regulating the immune system and related autoimmune diseases such as rheumatoid arthritis.[5]
Nearly 1 percent of the world’s population has rheumatoid arthritis, a disease in which the immune system attacks tissues, inflaming joints and sometimes leading to deadly complications such as heart disease. Other diseases with suspected gut bacterial ties include type I diabetes and multiple sclerosis. Larger-than-normal populations of specific gut bacteria may trigger the development of diseases like rheumatoid arthritis and possibly fuel disease progression in people genetically predisposed to this crippling and confounding condition, say the researchers, who are participating in the Mayo Illinois Alliance for Technology Based Healthcare.
Diet
Whilst this paper looks at hormones and aging in their mice subjects as a primary mechanism, I would suggest that dietary selection has a greater impact on the microbial milieu than either age or hormones, but that combined the effects will be more dramatic. Just maybe the alteration of food selection that sometimes helps reduce inflammation in RA patients is related to the impact it has on barrier function and bacterial mix rather than a purely anti-inflammatory impact.[6]
Alcohol
Drinking 3 glasses of alcohol weekly (mean average was 4.5) is associated with a decreased risk of developing rheumatoid arthritis (RA), perhaps owing to the downregulation of proinflammatory mediators. [7]
The researchers identified 197 new cases of RA during 7 years of follow-up of 34,141 Swedish women born between 1914 and 1948. Detailed information about alcohol consumption, diet, smoking history, physical activity, and education level was collected in 1987, and again in 1997. Participants were followed up from January 2003 to December 2009, when they were 54 to 89 years of age.
After adjusting for factors such as age, smoking, and dietary habits, researchers found that women who reported drinking more than 3 glasses of alcohol per week in both 1987 and 1997 had a 52% reduced risk of RA compared with never-drinkers at both assessments. One standard glass of alcohol was defined as approximately 500 mL of beer, 150 mL of wine, or 50 mL of liquor. The reduced risk was similar for all 3 types of alcoholic drink.
The author’s state
“A measure of caution here is probably warranted since higher levels of intake have been reported to have a paradoxical or proinflammatory effect in RA. In other words, more excessive levels of intake may have adverse effects in terms of disease risk and progression. The ‘take-home’ here is therefore quite tricky. Obviously, any potential benefit of moderate alcohol intake must be weighed very carefully against the risks [both health-related and societal] of regular alcohol intake. Alcohol intake may be very problematic for patients with established disease as well, particularly given the fact that alcohol use may enhance toxicity to commonly used disease-modifying agents in RA, namely, methotrexate.”
The take home message from all of the links is that lifestyle choices impact on risk, resolution and severity of RA.
References
[1] Ebringer A, Rashid T, Wilson C. Rheumatoid arthritis, Proteus, anti-CCP antibodies and Karl Popper. Autoimmun Rev. 2010 Feb;9(4):216-23. Epub 2009 Nov 4. View Abstract
[2] Ebringer A, Rashid T. Rheumatoid arthritis is caused by Proteus: the molecular mimicry theory and Karl Popper. Front Biosci (Elite Ed). 2009 Jun 1;1:577-86. View Abstract
[3] Rashid T, Ebringer A. Autoimmunity in Rheumatic Diseases Is Induced by Microbial Infections via Crossreactivity or Molecular Mimicry. Autoimmune Dis. 2012;2012:539282. Epub 2012 Feb 20. View Full Paper
[4] Smyk D, Rigopoulou EI, Baum H, Burroughs AK, Vergani D, Bogdanos DP. Autoimmunity and environment: am I at risk? Clinical Reviews in Allergy and Immunology. View Abstract
[5] Andres Gomez, David Luckey, Carl J. Yeoman, Eric V. Marietta, Margret E. Berg Miller, Joseph A. Murray, Bryan A. White, Veena Taneja. Loss of Sex and Age Driven Differences in the Gut Microbiome Characterize Arthritis-Susceptible *0401 Mice but Not Arthritis-Resistant *0402 Mice. PLoS ONE, 2012; 7 (4): e36095 DOI: View Full Paper
[6] Li S, Micheletti R. Role of diet in rheumatic disease. Rheum Dis Clin North Am. 2011 Feb;37(1):119-33. Epub 2010 Dec 4. Review View Abstract
[7] Di Giuseppe D, Alfredsson L, Bottai M, Askling J, Wolk A. Long term alcohol intake and risk of rheumatoid arthritis in women: a population based cohort study. BMJ. 2012 Jul 10;345:e4230. doi: 10.1136/bmj.e4230. View Abstract
