Autoimmune Disease: A Modern Epidemic?
By David M. Brady, ND T
here is simply no doubt that the incidence of autoimmune disorders has been rising sharply over the past several de- cades in the Western industrialized countries, particularly the United States (See Figure 1). The question is why has there been such a sharp rise in the incidence of these disorders? The an- swers may very well be found in the current medical research, but you would probably never know it by visiting a doctor. This may be because this situation serves as an example of the giant chasm that often exists between Western medical research, which is often outstanding, and the practice of clinical medicine, which often leaves quite a bit to be desired when it comes to the management of chronic complex disorders with high morbidity (disability) but low mortality (death) rates.
The typical conventional medical approach to autoimmune dis- orders focuses on the management of symptoms with various anti- infl ammatory medications and often ultimately the use of chemo- therapeutic drugs and very potent immunosuppressive agents with nasty potential side-effects like leukemia and lymphoma. While these approaches admittedly can provide substantial symptomatic relief to the patient, they do not really get to the cause of these conditions and some research suggests that these approaches may result in a furthering of the underlying disease process. However, modern research into autoimmune diseases suggest radically differ- ent approaches may be required to reverse the above cited trends, including a strong emphasis on very early detection with predictive auto-antibody testing, a focus on optimizing the gastrointestinal health/environment (i.e., the microbiome), including the eradication of infectious immune triggers with antimicrobial therapy, and even the seemingly bizarre use of helminth parasites (worms) as therapy. Some of these concepts have a long history in naturopathic, integra- tive and functional models of medicine, but now are emerging as hot areas of interest in mainstream medical research journals and investigative communities in immunology.
Molecular Mimicry The concept of molecular mimicry is really a simple one, and it is an area attracting considerable research related to why autoim- mune disorders occur. Simply stated, environmental exposure to specifi c antigens (immune system-triggering proteins in food and on microbes like viruses and gut bacteria) can, in genetically suscep- tible individuals, induce a cross-reaction with structurally similar proteins associated with specifi c body tissues. In other words, some- thing from the outside, such as a food or bacteria, that you may be genetically susceptible to over-reacting to, may trigger an immune reaction to also occur against part of your own body.
There are now multitudes of associations that have been fi rmly established between immune incompatibility with specifi c food-
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derived proteins, as well as the overgrowth of certain gastrointestinal bacteria, and the presence of specifi c autoimmune disorders (See Table 1 on page 32). While some of these associations have been known for quite some time, mechanisms of causality (pathways in which an associated triggering antigen can cause autoimmune activity against a specifi c body tissue or structure) are rapidly being established in the research. However, patients suffering from disor- ders like rheumatoid arthritis (RA), ankylosing spondylitis (AS), and autoimmune thyroiditis (i.e., Hashimoto’s or Graves’ disease), mul- tiple sclerosis (MS), lupus (SLE), etc., who visit a rheumatologist or endocrinologist do not routinely have stool analysis to assess their GI microbiota or food sensitivity testing to detect these potential triggers. This is ironic, particularly in the case of bacterial over- growth in the gut, as the conventional medical paradigm typically assumes an infectious cause until proven otherwise. Perhaps this is just another example of resistance to signifi cant change in clinical approach within medicine, even in the face of compelling evidence to do so, as it would then require a least a passive admission that something so seemingly simple was missed for so long.
For example, oral bacterial infection with Porphyromonas
gingivalis, the primary bacterial cause of periodontal (gum) disease, may also play a role in the direct development of some cases of rheumatoid arthritis (RA). Many other researchers have now also gone beyond establishing mere associations between the presence of various microbes and autoimmune disorders. Some have actually experimentally induced autoimmune disease in animals by intro- ducing specifi c bacteria into their gut, and have then resolved it by introducing another, making a compelling argument for a causal relationship between the imbalances in the GI microbiota and auto- immune activity.
Food proteins have also been linked to autoimmune diseases like Hashimoto’s and Graves’ diseases of the thyroid. Celiac pa- tients (those with a severe intolerance to gluten-containing grains) have approximately 10 times the rate of auto-immune thyroid diseases as non-celiac individuals. It may be no coincidence that the emergence of an apparent epidemic of autoimmune diseases has corresponded with the ever-increasing consumption of poor- quality modern processed foods known to both negatively alter the GI microbiome and to contain a constant (often hidden) stream of offending dietary antigens, including gluten-containing grains and genetically modifi ed proteins (GMO foods).
While all of these associations may be interesting to research-
ers, what does this really mean to doctors and their patients? Some critics would argue that there is a lack of interventional data to sug- gest that eradication of these associated organisms and/or avoidance of these dietary antigens positively affects patient outcomes. This
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