The Key How To Heal And Prevent Autoimmune Disease

In conventional medicine autoimmune disease is a chronic life-long health condition that is considered to be incurable. This is what we are led to believe. However, a new discovery in the field of autoimmunity gives not only hope but opens new treatment opportunities.

During last decades different models such as molecular mimicry, “bystander effect” and viral persistence were proposed as possible mechanisms that initiate the overreaction of the immune system and lead to an autoimmune disease.

Molecular mimicry is the most popular model and is based on the assumption that an environmental trigger or an antigen such as bacteria or virus enters the human body and causes an immune response by producing antibodies. The antibodies attack antigens and also mistakenly cross-react with a healthy tissue that is similar to an antigen causing an autoimmune disease.

Interestingly, some studies have shown that molecular mimicry cannot completely describe the autoimmunity in humans and is rather a one of contributing factors that explains the progression of the existing autoimmune disease than an actual cause of autoimmunity.

According to the “bystander effect”, antigen damages the healthy tissue and the immune system starts to attack the antigen AND the damaged tissue that can result in an autoimmune disease.

In the viral persistence model infections that were not completely cleared by the immune system become persistent. Constant presence of a virus can lead to the damage of healthy tissue during the attacks of the immune system on the virus. Antiviral antibodies can further drive the immune response and initiate an autoimmune disease.

All these models do not explain the pre-existing conditions that lead to the autoimmunity and suggest that once the autoimmunity is “turned on” it cannot be “turned off” or stopped. Even if the initial antigen that caused autoimmunity is removed or gone, the body continues to produce antibodies to attack and destroy the healthy tissue.

A New Discovery

A series of recent studies conducted by a researcher and MD Prof. Alessio Fasano presented a new model that explains the autoimmunity from a new prospective and suggests that autoimmune disease can be not only stopped and reversed but also prevented.

According to the Prof. Fasano, there are 3 components of autoimmunity that have to be present in the person for an autoimmune disease to develop:

  1. A genetic predisposition to autoimmunity.
  2. An exposure to at least one environmental trigger.
  3. Increased intestinal permeability or leaky gut syndrome.

In the Prof. Fasano’s model increased intestinal permeability is the key element in understanding how the environmental triggers or antigens enter the human body and “turn the genes on” causing the autoimmune disease.

Tissue damage and loss of its function occurs in all autoimmune diseases. It can be systemic when many organs are affected as it happens in lupus (SLE) or organ specific when the immune response is directed against certain organs such as the thyroid gland in Hashimoto’s thyroiditis.

All theories on what causes autoimmune diseases agree that a combination of genetic and environmental factors is necessary for autoimmunity to develop.

While we are all exposed to environmental triggers, not everybody who has genetic susceptibility will develop autoimmune disease.

Less than 10% of those with increased genetic predisposition progress to clinical disease manifestation and get diagnosed.

This fact indicates a strong impact of environmental triggers in the pre-disease state but also that the antigens such as viruses, parasites, bad bacteria, fungus and other undesirable organisms and macromolecules have to find their way to enter our body in order to initiate an immune system response.

What Kick-Started Your Autoimmune Disease?

More and more scientific studies suggest that there is a third component to triggering autoimmunity that is directly related to how the antigens enter our body systems. The intestinal epithelium is the largest mucosal surface and a protective barrier that provides an interface between the external environment and our internal systems.

Traditionally the main function of the gastrointestinal tract was seen as digestion and absorption of nutrients and keeping electrolytes and water balance. However, it also has two other very important functions that are often overlooked:

1. Support the immunity

2. Maintain a protective barrier between the environment and our body that prevents antigens and macromolecules from entering the system and causing diseases and imbalances.

When this mechanism becomes deregulated and results in the loss of the protective function of mucosal barriers that interact with the environment, both intestinal and non-intestinal autoimmune disorders can develop in genetically susceptible individuals.

In most cases, increased intestinal permeability or leaky gut syndrome precedes the disease and opens the way for antigens and macromolecules to go through the protective barrier and trigger the multi-organ autoimmune attack that can lead to systemic autoimmunity and multiple autoimmune conditions in the same person.

How Leaky Gut Causes Autoimmune Disease

There is no single trigger of most autoimmune diseases and usually multiple stressors on the digestive system are necessary to increase intestinal permeability. The stressors add up over time and cause inflammation of the intestinal lining that can result in a substantial damage to the mucosal barrier and the microvilli, enough to let antigens and big molecules through.

The intestinal damage is typically five-folds:

  1. It results in up to 70-80% loss of the immune system that resides in the gut leaving the person highly susceptible to infections. The remaining immune defence becomes over-reactive fighting antigens and pathogens and this creates a perfect set up for the autoimmune disease development according to the viral persistence model we discussed earlier.
  2. The antigens are now able to get through the protective intestinal barrier and cause an immune response that can result in the autoimmune disease and many other chronic health conditions that can develop following the molecular mimicry model. It is important to note that because these antigens can move freely to anywhere inside the body, autoimmune disease can develop and affect any part of the human body including the organs, muscles and joints.
  3. Large food antigens are foreign to the body’s defense system, so it attacks them resulting in the production of antibodies against once harmless foods, and consequently food sensitivities develop.
  4. The microvilli become damaged and the person loses the ability to properly digest and absorb foods. The person does not get enough nutrients to support bodily functions and goes into the starvation mode and develops malapsorption, vitamin and mineral deficiencies.
  5. The undigested food particles feed harmful parasites, bacteria, yeast and fungi that promote an imbalance in the gut flora also known as dysbiosis and further increase intestinal permeability. There are many factors that can increase the permeability of the intestinal wall such as alcohol and caffeine, drugs, especially antibiotics, anti-inflammatories and antacids, food additives, diets high in refined carbohydrates and stress.

How to Restore Immune Balance and Stop Autoimmune Confusion

According to this new finding, autoimmune disease can be stopped and even reversed if the interplay between genes and environmental triggers is prevented by re-establishing the integrity of the intestinal barrier function. Both animal models and recent clinical studies support this new view on autoimmunity and provide a foundation for new approaches to prevent and treat autoimmune diseases.

A fast-growing number of diseases are recognized to involve changes in intestinal permeability and include celiac disease, Hashimoto’s thyroiditis, multiple sclerosis, rheumatoid arthritis, type 1 diabetes, inflammatory bowel diseases, ankylosing spondylitis and other autoimmune diseases and conditions such as asthma, glioma (type of tumor that starts in the brain or spine), diseases of the nervous system (schizophrenia, neuromyelitis optica), and neoplastic conditions (abnormal cell proliferation in lung cancers, oral squamous cell carcinoma, pancreatic carcinoma, hepatocellular carcinoma with Hepatitis C virus infection).

Healing leaky gut syndrome and restoring gut micro-flora seem to be key ingredients and can help to treat an underlying cause of autoimmune diseases but also chronic illnesses, inflammation and cancer. Without addressing this issue many people will never be able to feel 100% and restore their health.

Autoimmune disease seldom gets better on its own, but almost always gets worse over time.

The main reason why many treatments and diets fail or give only a temporarily symptoms relief to people with autoimmune diseases is that leaky gut syndrome was never addressed and/or intestinal damage did not heal completely. Most diets focus on removing the foods that are suspected to trigger immune response and leave it at that.

Natural healers of diseaseAccording to Prof. Fasano, the autoimmune disease can be completely reversed only after removing the triggers of the overreaction of the immune system from the diet and healing the intestinal damage. When the functions of the intestinal barrier are restored it is supposed to keep antigens out, antibodies drop and the whole autoimmune process shuts off.

The good news is that this new model is not just a theory without any practical implementation and many patients have already experienced amazing results in reversal of their autoimmune disease first hand.

How did they do it?

Leaky gut cure

Learn about leaky gut and get FREE Gut Healing Techniques used by the leading natural medicine doctors HERE

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References:

1. Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease. Clin Microbiol Rev. 2006 January; 19(1): 80–94. doi:  10.1128/CMR.19.1.80-94.2006

2. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8. doi: 10.1007/s12016-011-8291-x.

 

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