Autoimmunity – A Nutritional Strategy

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Until recently, the issue of autoimmunity was not even accepted within the scientific community.  Although initially introduced in late 70’s, the mechanism of autoimmunity was considered radical until the late 1980s.  Throughout the ’90s, autoimmune diseases proliferated until it seemed almost common to know a person with an autoimmune disease.

Autoimmunity literally means that the immune system has developed antibodies to attack its own tissues.  There are many theories as to why this may happen.  This document will present three of the main theories behind this event.  Traditional medical approaches seem to concern themselves only with trying to control the secondary symptoms of autoimmunity instead of addressing the underlying causes, which are still enigmatic and mysterious.

One possible mechanism of autoimmunity concerns the integrity of the cellular and nuclear membranes.  When these membranes begin to lose their integrity, leaking minute amounts of nuclear genetic material directly into the bloodstream, these nuclear proteins are perceived by the liver as indication that upstream tissue damage has occurred.  In response, the liver develops what are called natural tissue antibodies (NTA’s) that are put into circulation and are designed to target the upstream tissue, breaking down and degrading the perceived damage before infection by an external agent can occur.  This seems an intelligent response on the part of the body, and may be addressed simply by encouraging healthy membrane physiology through the application of healthy essential fatty acids and phospho-lipids, which are the primary components of the cellular and nuclear membranes.

A second mechanism thought to cause autoimmunity is described as molecular mimicry.  In this model, it is possible for certain inoculants to induce immune responses to protein sequences that are similar to normally occurring tissue.  The best example of this is the relationship between acquired immunity to German measles from vaccination and the autoimmune disease of Ankylosing Spondylitis, in which the nucleotide sequences in the proteins of these two tissues are almost identical with only one nucleotide sequence different.  This causes the acquired immunity of the vaccination to attack the normal occurring tissue in the body thinking that is a foreign protein.  Many such mechanisms are speculated to be involved in multiple sclerosis and other neurological diseases.

A third and final theory, called the dual signal hypothesis, describes the possibility of the immune system being up-regulated and hyper-reactive simultaneous to another injury occurring.  As a result, the overly ambitious immune system identifies this injury as an antigenic marker, and thus begins to attack that tissue is if it were an infection.  It is very common to note that many autoimmune diseases onset following severe physical or emotional trauma within 6 to 12 months.

In any of these cases, the employment of foundational therapies seeking to balance all systems of the body can assist in bringing resolution to the autoimmune diseases.  Down-regulation of immune activity by reducing inflammatory and chronic infection burdens and simultaneously balances bio-terrain issues, and can gradually improve symptoms and result in remission.  While it is difficult to repair tissue that has been attacked and damaged by an autoimmune response, it is reasonable to expect an interruption to the progression of the autoimmune disease.  In this way autoimmunity can be contained without the ongoing use of imbalancing and dangerous drug therapies.

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