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The Hygiene Hypothesis

Allergic disorders, including asthma and anaphylaxis from foods, are widespread problems in modern wealthy countries. Interestingly, these disorders are fairly rare in less developed parts of the world. This fact is very revealing in regard to the nature and causes of allergy. One of the main differences between modern, wealthy countries and less developed countries is the presence of parasites and other microorganisms. Wealthy countries have developed advanced sanitation technology and have become very clean eliminating many parasites and bacteria from the water supply, ensuring clean sources of food, and treating infection. This advance has drastically reduced the number of preventable diseases that people in wealthy countries are exposed to. While this is a great development, it is also a double-edged sword with unforeseen consequences.  Researchers refer to this concept as the Hygiene Hypothesis.

The immune system is a sophisticated collection of defense pathways meant to protect the body from infection. It evolved over many centuries to detect foreign proteins that should not be found in your body and that are likely to be harmful. Over the time that this system evolved, humans have had constant exposure to parasites and bacteria, a situation still found in less developed parts of the world. So when parasitic infections decline due to advances in sterility (or cleanliness), that part of the immune system is no longer occupied with the usual targets, despite maintaining its potential for defense.  Since it does not disappear, it instead finds other targets. So the part of the immune system that used to attack parasitic worms now attacks grass pollen or cat hair. 

The main type of antibody involved in parasitic infections is known as IgE – short for immunoglobulin E – which is also the primary driver of allergy symptoms. IgE is one of the least common antibodies but it causes the largest immune response. Because it targets large organisms, such as worms, it produces a large inflammatory response, which brings a lot of immune firepower to the site of contact. This inflammation can cause different symptoms, depending on where the IgE interaction occurred. For example, if it was in the nose, then you will get a runny nose and start sneezing; if it was in the eye, then you will get itchy, watery eyes; and if it was in the lungs, you will start coughing and wheezing and could develop asthma symptoms (tightening of the lungs, difficulty breathing).

Contrary to the effects of IgE, the most prevalent antibody, IgG, does not produce a broad inflammatory response. IgG is the primary antibody for handling bacterial infections. Since bacteria are much smaller than worms they can simply be swallowed by immune cells and destroyed without having to set off a broad immune response. So, as IgG encounters invasive bacteria, it simply marks them for disposal and the immune cells remove them. 

The bacterial and parasitic immune system pathways are different.  The bacterial pathway is known as the Th1 response, based on the types of immune cell involved (T Helper cells 1); the parasitic pathway is known as Th2. People with allergic disorders have an immune system that is inappropriately biased toward the Th2 response, which is the driver of inflammation.

The causes of this shift toward the inflammatory Th2 response in allergic patients are still being investigated. There is evidence that early life exposure to parasites and bacteria allows the immune system to develop in a balanced way through the development of regulatory mechanisms. However, the lack of exposure to these microorganisms appears to cause the immune system to develop without adequate control, which allows harmless proteins, such as those found in grass pollen, to produce an excessive immune response when encountered in large numbers during pollen season.

Early life interventions to prevent this phenomenon from occurring are still experimental. However, once allergies are developed, immunotherapy (allergy shots) has been shown to push the immune response toward a better controlled Th1 response through gradual, controlled exposure to the allergens.