Basic Pathways of Autoimmune Dysfunction
Autoimmune diseases tend to be viewed as separate entities. A broader perspective, however, may reveal that shared mechanisms are the cause of disease, rather than just its byproduct. If this perspective were applied, patients would benefit (before the development of irreversible tissue damage) from improved therapies and early intervention. Dr. Majid Ali has long considered that there must be a single initial common pathway to all disease, including immune dysfunction.
One consideration is the continued exposure to heavy metals and environmental pollution that overload the immune system. On a daily basis, we battle with pesticides, herbicides, chemical fertilizers, industrial wastes, cigarette smoke, and automobile exhaust. Our air, water, and food (in particular) are full of toxic substances. There is no doubt that these toxins play a role in immune dysfunction. Even substances considered by most people as safe impair immune function. Sugar consumption in all forms (glucose, fructose, and sucrose) will impair the ability of white cells to destroy biological agents. This effect begins within a half hour of consumption and lasts for 5 hours. After 2 hours, immune function is reduced by 50% (Sanchez 1973; Bernstein 1977).
Oxidative stress plays a role in autoimmune diseases. It can be compared to a piece of metal rusting and results from the action of damaging molecules (ie, free radicals), which are a natural byproduct of the body's metabolism. The electrically charged free radicals attack healthy cells, causing them to lose their structure and function and eventually destroying them. Free radicals are not only produced by our bodies, but are also ingested from toxins and pollution in the air we breathe.
Chronic systemic inflammation is related to several autoimmune disorders, such as lupus, rheumatoid arthritis, Sjogren's syndrome, and fibromyalgia (see separate protocols on these topics). Inflammation can be traced to destructive cell-signaling chemicals known as cytokines, which contribute to many degenerative diseases (Brod 2000). In rheumatoid arthritis, excess levels of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin 1(b) (IL-1b), and/or leukotriene B4 (LTB4), are known to cause or contribute to the inflammatory syndrome that ultimately destroys joint cartilage and synovial fluid. Certain nutritional supplements and low-cost prescription medications will often lower cytokine levels and control the inflammatory state.