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Leaky Gut as a Cause of Disease

Leaky Gut as a Cause of Disease:

When for some reason the intercellular pores are further apart than normal, larger than normal substances, undigested proteins and germs (or substances produced by them) can penetrate through the cells of the intestine into the intercellular space where they would be recognized as foreign generating:

Toxicity due to the passage of toxic substances into the bloodstream

A state of local inflammation and basal systemic inflammation of greater or lesser intensity due to immune activation against these substances and germs.

The generation of specific antibodies against allergenic food proteins, chemicals or against neoantigens that would cause

 Food allergies and intolerances on the one hand, and Autoantibodies and autoimmune diseases: some of these antibodies would react against proteins in our body due to their similarity, favoring some autoimmune diseases such as celiac disease, type II diabetes, autoimmune hypothyroidism, different types of arthritis, fatty liver or chronic digestive symptoms or fatigue, muscle pain, fibromyalgic symptoms.

Permeability could increase in response to many factors, and it would itself be responsible for generating more immune activation at the intestinal level, which would generate greater permeability, entering a vicious circle where causes and effects overlap.

To better understand the role of tight junction dysfunctions in the development of diseases, especially autoimmune and allergic diseases, trying to confirm these hypotheses, establish causal relationships and search for effective treatments.

Some proponents base their ideas on the autoimmune disease model of celiac disease and wheat gluten. In it, in genetically predisposed subjects and when exposed to gluten, antitransglutaminase antibodies are produced in some cases that are directed against the gliadin of gluten, but which also attack intestinal cells and can also be directed against other organs such as the thyroid, some areas of the brain or pancreas, being related to the development of type 1 diabetes or gluten ataxia. In these patients there is an increase in intestinal permeability that acts as an adjuvant.

The autoimmune hypothesis establishes that the interaction between genetic predisposition, impaired communication between innate and adaptive immunity, and exposure to environmental triggers (infections, foods, chemicals, stress…) are at the core of the origin of diseases autoimmune.

In recent years, a fourth factor is being added, the loss of the intestinal barrier function secondary to intercellular dysfunction of the tight junctions, which would influence intestinal immune communication disorders, key in the development of autoimmune diseases. It would be one more factor that interacts for the development of this type of disease.

Some studies support the model that repeated cycles of increased intestinal permeability would generate a state of subsequent immune activation that would contribute to the progress of some autoimmune diseases or those related to systemic inflammation.

This process could be modulated or reversed by decreasing or avoiding the continuous interaction between genes and environmental (epigenetic) factors. Thus, restoring the barrier and avoiding its dysfunction would be seen as a new approach to these diseases.