From The Desk of Josh Gitalis

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There are 23.5 million Americans who have been diagnosed with an autoimmune disease. This makes it the third most common category of disease after cancer and heart disease, and the numbers have clearly been increasing over the past 6o years (figure 1). 1

Figure 1
Figure 1

Over 80 different autoimmune diseases have been identified. What you might find surprising, however, is that they all share three common factors. These three factors give us valuable insight into how we might address the treatment of these debilitating diseases.

1. Genetic Susceptibility

Genetics play an important role in our biological fate. They store the information the body needs in order to keep all of the systems running smoothly. This genetic coding comes half from our mother and half from our father. Genes also have their strengths and weaknesses.

When healthy choices are made, the weak genes are not expressed and the stronger genes dominate.  When poor dietary and lifestyle choices are made, the weak genes get expressed. Depending on the genetic susceptibility, different autoimmune conditions are expressed. For example, white people are 2-5 times more likely to get inflammatory bowel disease (IBD) than African or Oriental Americans. Jews are 3-6 times more likely to get IBD than non-Jews.

So, genes are part of the disease process, and genetic susceptibility for a particular disease must be present, but it is not the whole story.

2. Environmental Trigger

Imagine it was a hot summer day and you planned on getting your friend soaked. First, you would have to conjure up a plan – the plan is very much like genetic susceptibility. The information and intention is present, but the insult still must be executed. Next, you acquire some balloons and fill them with water. Now you’ve got an environmental trigger that could possibly get your friend wet.

When it comes to the body, there are many environmental triggers that could execute an insult on the gut (more on gut involvement in a moment). These can be one or many of the following:

  • Infections: bacteria, virus, parasites, mold, fungus
  • Heavy metal
  • Alcohol
  • Gluten or any food protein
  • Stress
  • Drugs
  • Caffeine
  • Chemical food additives
  • “Junk” foods
  • Environmental toxins

3. Intestinal Permeability (Leaky Gut)

So you have the plan to soak your friend (genetic susceptibility), and you have the water balloons all ready to go (the environmental trigger), now your friend must be caught off guard without a rain jacket (intestinal permeability).
Leaky GutThe layer of cells that separate the inside of your small intestine from your blood are one cell thick. This allows for only the  smallest molecules to enter the bloodstream. Another result of the thickness of this layer is that it is highly susceptible to damage from an environmental trigger. If there is damage (see above), then large molecules can enter the blood stream setting off an immune reaction. The immune system attacks these molecules and, if they look like certain tissues in the body, then the immune system attacks those tissues too, resulting in an autoimmune disease. Depending on which tissue is attacked, this is what determines the disease. For example, an attack on the joints results in rheumatoid arthritis, on the nerves multiple sclerosis, and on the gut Crohn’s or colitis.

In Summary

As you can understand now, the many autoimmune diseases that have been identified and given a name all have three similar traits; a genetic component, an environmental trigger, and the presence of intestinal permeability. It has been shown that we can stop the autoimmune process and even reverse it by re-establishing the barrier of the small intestine. 2


  1. Bach JF. The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med. Sep 2002;347(12):911–920.
  2. Nut Clin Prac Gastro & Hep. Sept 2005 Vol. 2 No.9
  1. Bach JF. The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med. Sep 2002;347(12):911–920.
  2. Nut Clin Prac Gastro & Hep. Sept 2005 Vol. 2 No.9