What is autoimmune disease?

Some people are born with a genetic or epigenetic potential for autoimmune disease that can be initiated by a trigger or a group of triggering events. Once triggered, the autoimmune process involves one's immune system damaging one's own body. One theory holds that the immune system becomes confused and can no longer differentiate between self and invading toxins or infections. The approach to treating autoimmune disease with this model is to use medicines that limit the immune system’s ability to attack with immunosuppressive medication. This approach is effective but achieves a true remission for RA patients less than 20% of the time. Another theory for autoimmune disease proposes that the trigger(s) may still be in the system and the immune system is not so confused. This model invites the rheumatologist to look harder for deficiencies, toxins and infections that may still be present and help patients eliminate them from their system. Researchers working with Reactive Arthritis have published studies showing improved outcomes when a rheumatologist combines the standard approach with antibiotic treatment of a triggering infection (PMID: 23440251, PMID: 20155838). We think this broader approach makes sense and prefer it over the strictly immunosuppressive approach.

Notice that Dr. Carter and colleagues targeted Chlamydia infection using combination antibiotic treatment for 6 months and this improved arthritic symptoms in the majority of patients. There is an airborne Chlamydia called Chlamydia pneumoniae (Cpn). Even with an imperfect blood test for Cpn, 80% of people are testing positive. Cpn has been linked to autoimmune disease and other chronic diseases such as atypical pneumonia, asthma, bronchitis, pharyngitis, middle ear infections, atherosclerosis, multiple sclerosis, Alzheimer’s disease, macular degeneration, aortic aneurysms and cancer. Cpn is an airborne parasite that enjoys the rare ability to infect and persist inside of our macrophages (our critically important white blood cells). Once one’s macrophages are filled with parasites (and medical science currently lacks the ability to know when this has happened to a patient), the immune system is compromised in a manner that is invisible to all clinicians. The parasitized macrophages are gradually distributed throughout the body and are unable to properly fight infection. Since Cpn infection can promote every other form of infection, it is a reasonable target to consider when treating illness associated with chronic viral, fungal, yeast and bacterial infections. Visiting PubMed and searching “Chlamydia pneumoniae” yields 5000 articles on a variety of conditions related to this ubiquitous infection.

What does hibernation have to do with human disease?

In September 2016, researchers from UCSD and Stanford published a paper linking chronic fatigue syndrome (CFS) with a dormancy state found in nematodes called dauer (http://www.ncbi.nlm.nih.gov/pubmed/27573827). Dormancy is a metabolically slowed state that bears use to survive the winter. It is sometimes referred to as “walking hibernation”. The chemical changes observed in dormancy are found in patients with CFS, fibromyalgia and inflammatory conditions. Dr. Powell received a patent for the diagnosis and treatment of human dormancy syndrome in 2003 and has been researching methods for the reversal of dormancy since 2001.

Immune function is at its weakest during hibernation and, not surprisingly, most infections are manufacturing molecules that interact with the host’s hibernation (survival) mechanism. Cpn infection within the liver should promote dormancy by increasing heat shock protein 60 (Hsp60) production, known to be elevated during hibernation. Hsp60 is also associated with carcinogenesis and atherosclerosis, two conditions known to be associated with Cpn infection. We are still without a commercially available Hsp60 test for clinicians to order. Fortunately, transforming growth factor beta1 (TGFB1), released from infected macrophages, is a readily available blood test that can be used to monitor therapy.

When did RA begin and what triggered it?

Rheumatoid arthritis (RA) dramatically increased in prevalence in the 1800's. What changed? Please read this brief article from "The Rheumatologist" to better understand triggers you may have some control over: The Rheumatologist

Why Did Rheumatoid Arthritis Begin?

For more detailed information (more technical) information about the relationship between autoimmune disease and organisms that can live in humans, please read this excellent article: Rheumatology Practice News (pdf)

What can be done?

As the above article suggests, when the source of immune system triggering comes from a virus or bacteria, one can use antivirals or antibacterials with success. One should also ask “Why were these organisms able to have their way with this person? Why couldn’t the patient’s immune system handle them?” That brings us to environmental medicine related questions:

  • Are there toxins accumulating from repeated exposure that might be impairing immune function?
  • Are there deficiencies that compromise immune function and/or increase inflammation?
  • Are there factors promoting leaky gut thereby allowing more toxins into the bloodstream?
  • Are there mucosal biofilms in place making it difficult to clear toxins and infections?
  • Does the patient have habits that promote the growth of infections or inflammation?
  • Are there environmental exposures to molds or chemicals that affect immune function?
  • Are there dental infections that are silently activating the immune system?
  • Are there sinus, tonsil, lung, gallbladder, intestinal infections silently activating inflammation?
  • Are there immune system impairments (low IgG subclass, low IgA, complement deficiency)?
  • Are there methylation deficiencies or other genetic issues that facilitate chronic infection?

By employing a broader scope of practice, Integrative Rheumatologists are able to enjoy greater success than they knew when they used immunosuppressive medications alone.