The path that Autoimmune Disease has taken in the past century impels us to pose some questions as to how and why we continue to treat autoimmunity and immune compromised dysfunction on a disease-specific basis. The key to unlocking the health in people who suffer from Autoimmune Disease is asking the simple yet rarely broached question: Why is this happening?
Autoimmune Disease essentially occurs when an individual’s immune system attacks normal tissue like it would a foreign body or pathogen. The clinical symptoms depend on which tissue is under attack and as such, autoimmunity presents in an array of manifestations.
Since the end of the Second World War, Autoimmune Disease has skyrocketed in prevalence (Campbell, 2014). The trend towards autoimmunity grows even steeper as the true nature of its origin becomes clearer. Type I Diabetes has increased in the last decade, with a growing number of cases occurring earlier, as illustrated by a study in Finland (Harjutsalo V, 2008). Digestive immune dysfunction such as Crohn’s Disease, Ulcerative Colitis and Coeliac disease have taken a similar turn in the last few decades (H Okada, 2010), (Natalia E. Castillo, 2014). Multiple Sclerosis has seen an increase in Europe and the Mediterranean Basin, however data is lacking for incidence in other parts of the world. A well-presented Iranian study showed an increase from 0.68/100,000 to 5.68/100,000 between 1989 and 2006 (Benito-León, 2011). This is coupled with a surge in other immune-related disorders such as asthma and severe allergic sensitivities in Australia’s young population.
There are now around 80 different types of autoimmune disorders, which are categorised into 2 broad types: systemic and localised.
Systemic autoimmune disorders affect many organs or tissues simultaneously, and include diseases such as Rheumatoid Arthritis, Lupus, Scleroderma, Vasculitis and Dermatomyositis.
Localised autoimmune disorders only affect a singular organ or tissue, and include diseases such as Type 1 Diabetes, Celiac Disease, Hashimoto’s Thyroiditis, Multiple Sclerosis, Ulcerative Colitis and Guillain-Barre Syndrome. These diseases have a wide variation in severity, clinical presentation and effected tissue, however the underlying disease process is consistent.
Mainstream treatment options to address autoimmune disease include:
- Supplementation of dysfunctional organ products (e.g. insulin in diabetes T1)
- Corticosteroid anti-inflammatory medications
- Non-steroidal anti-inflammatory medications
- Immunosuppressive medications
- Surgical intervention
These treatment methods look to reduce the severity of symptoms, and to dull the overactive immunological response. Where these interventions fall down is they do not attempt to get to the heart of Autoimmune Disease, and address why it occurs.
A new paradigm
This brings us to ask ourselves the question: What has changed over the past 60 years to trigger these abnormal immune responses? The rapid incline of these disorders over a relatively short period of time is unlikely to be due to purely genetic factors, so then, what are we missing here?
The answer was elucidated by Alessio Fasano and was as many had previously proposed: The gut. In 2000, Fasano discovered a digestive modulator named Zonulin, which appears on the intestinal walls to essentially decide which particles to pass into the blood stream, and which to keep out (Fasano, 2011). It therefore regulates our tolerance to certain macromolecules, and our immune response. Fasano looked at a number of Autoimmune disorders such as Coeliac Disease, Type 1 Diabetes, Asthma, AS, IBS and MS, and found irregularities in the regulation of macromolecules in the gut. In other words, people who suffered from autoimmunity also let through a large number of molecules that would normally be excluded from the blood stream. From here it is postulated that the host immune system is over stimulated with a barrage of abnormal molecules let through by the dysfunctional digestive system, and in genetically susceptible individuals, the host immune system begins to attack normal tissue amidst this chaotic immunological environment.
The demise of the average digestive system, and the correlative rise in “gut dysbiosis” or “leaky gut”, is rooted in a shift in what we put into our bodies, as well as what we are deficient in giving our bodies. Since World War II, we have moved from a largely agricultural diet with little sugar, and largely organic, locally grown produce, to a diet comprised highly of sugar and foods lacking in nutritional integrity. Bad bacteria or flora in our gut feed off many of these refined sugars and carbohydrates, meanwhile we have been starving our digestive systems of the core building blocks they need in order to flourish. The rise in use and exposure to antibiotics, environmental toxins and prolonged low-grade stress further exacerbate the demand on our digestive system, and lead them to an impending fate of dysfunction. It is not within the scope of this article to cover in great detail the issue of the unhealthy gut in modern society, however this will be addressed in future blogs.
This correlates to the previously unexplained link between certain autoimmune disorders and digestive symptoms. This new paradigm of treating autoimmunity gives hope to sufferers; as if we can treat the dysfunctional digestive system or “leaky gut”, then we can stop the attacking of normal tissues.
It is high time we stopped dealing with autoimmunity as a list of singular disorders, and started treating them as a consistent underlying pathology, which affects different areas of the body depending on genetic predispositions. That way, rather than wasting our time trying to Band-Aid symptoms, we can get to the root cause of what feeds this dysfunction and begin the long path in treating and preventing it.
If you would like to speak to Dr David Sokoloff or one of our other practitioners about Autoimmune Disease, gut health or any other issue , please feel free to ask a question, contact us or email us at:
Bach, J. (2002, Sept). The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med , 911-920.
Benito-León, J. (2011, June ). Are the Prevalence and Incidence of Multiple Sclerosis Changing? . Neuroepidemiology , 148-149.
Campbell, A. W. (2014). Autoimmunity and the Gut. Autoimmune Disease .
Fasano, A. (2011). Leaky Gut and Autoimmune Diseases . Clinical Reviews in Allergy & Immunity , 71-8.
H Okada, C. K.-F. (2010). The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update . Clinical & Experimental Immunology , 1-9.
Harjutsalo V, S. L. (2008). Time trends in the incidence of type 1 diabetes in Finnish children: a cohort study. Lancet , 1777-82.
Natalia E. Castillo, T. G. (2014). The present and the future in the diagnosis and management of celiac disease. Gastroenterology Report , 1-9.