Antibiotics as a Treatment for RA?
In a recent post on the rheumatoidarthritis.net Facebook page, a person mentioned that they had been treated for RA with a long-term antibiotic. This fosters an interesting, oft-neglected, scantily researched, and misunderstood treatment option. It is grounded in the idea that bacteria are a causative agent of rheumatoid arthritis. In an earlier post, I discussed the three currently accepted hypothesized causes of RA - 1. an environmental trigger, 2. a genetic susceptibility, and 3. a so-called "leaky gut”. The environmental trigger could apply to the notion that bacteria actually cause RA.
The germ theory of disease - the idea that diseases are caused by microorganisms such as bacteria and viruses - was hypothesized by Louis Pasteur and further described by Robert Koch via his Postulates. While not applicable to all diseases, the theory has been successfully applied to a myriad of diseases leading to amazing treatments, cures, and vaccines in this modern scientific era.
Microorganisms, primarily bacteria, have been hypothesized as a cause of rheumatoid arthritis for years. In fact, some early treatments of RA included antibiotics and similar drugs. Sulphasalazine is one such drug and is still prescribed for RA today. But most scientists believe that no bacteria can be directly linked to triggering rheumatoid disease. Recently, scientists from Harvard University and New York University reported research on mice that demonstrated a relationship between the presence of a common bacteria found in the gut and an immune response leading to arthritis.  Mice genetically susceptible to autoimmune arthritis were raised in germ-free environments. They demonstrated a lack of arthritic symptoms. The mice were then exposed to a single type of gut bacterium and they immediately began to show symptoms of arthritis. They also found that a certain type of T cell connected to the production of arthritis-causing antibodies was connected to the presence of bacteria. The researchers argued that the mice didn’t “catch” arthritis from bacteria, but that there’s an interaction between the genetic make-up of the mouse and the autoimmune response to bacteria.
One small group of primitive bacteria called mycoplasmas have also been implicated as a causative agent of various diseases generally and RA specifically. These primitive bacteria don’t have cell walls and only live inside the body of another organism as a parasite. They are extremely hard to isolate in people but one set of researchers examining mycoplasmas argued that a large proportion of RA patients have mycoplasma infections. While mycoplasmas may be present in RA patients, this does not prove a direct cause and effect link between these bacteria and RA. Never the less, some researchers argue for further investigation in order to develop possible treatment options.
If bacteria are linked to RA, then antibiotic therapy would logically follow suit. The tetracycline family of antibiotics, which are effective in treating mycoplasmas, is proposed for antibiotic protocol therapy. The most commonly used tetracycline antibiotic proposed for treating RA is minocycline. Some studies show that patients given antibiotic protocol did not show benefit.   Other studies demonstrate a reduction in RA symptoms.  Two fairly recent reviews of controlled experimental studies on the efficacy of the antibiotic tetracycline family revealed mixed results leading to insufficient conclusions.  The exact reason why antibiotics may impact RA is not fully understood but it may include antibiotics killing off bacteria that are causing RA or it may simply be that antibiotics cause a reduction of inflammatory cytokines. The scientific evidence for the use of at least the tetracycline family of antibiotics remains unclear at this time.
Antibiotic protocols (AP) are not widely espoused by official medical rheumatology medical societies and non-profit arthritis organizations. In spite of this, there are several groups devoted to antibiotic treatments for autoimmune diseases and a small number of rheumatologists will prescribe it.
What does this mean for those of us with RA? Probably not much for the immediate future. We can’t live in germ-free environments like the mice in the study. A general wiping out of bacteria in the gut would wreck havoc on the digestive system and current antibiotic treatments don’t work for everyone with RA. But perhaps this research will spark more attention and funding on these issues leading to potential discoveries of causes of autoimmune diseases leading to the development of effective treatments.
The gut bacteria/genetics combination recently discovered shows the most promise. But I suspect that any resultant treatments from this line of research - many years down the line - are not likely to be generic, whole body administration of antibiotics. They are more likely to be genetic-based treatments designed to impact some biochemical process connected with bacteria’s impact on the immune system.
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