The gastrointestinal tract is a large surface area containing trillions of microbes that make up a large percentage of the immune defenses. Dysfunction to the intestinal mucosal barrier leads to a condition commonly referred to as leaky gut syndrome. Closer inspection often reveals a condition called villous atrophy. When this takes place there tends to be a very high level of inflammation that is present.
There is now an increasing body of evidence that shows that gut dysfunction is a primary factor in autoimmune diseases such as RA, lupus, MS and AS.
There are many studies which cite the association between intestinal dysbiosis and the development of autoimmune conditions. Studies such as this one, demonstrates that in the autoimmune condition ankylosing spondylitis, 70% of patients had gut inflammation.
There are a plethora of medical studies which demonstrate that pathogenic infections are present in those with RA, AS, and many other autoimmune diseases. Certain studies postulate that the anaerobic bacterium Proteus Mirabilis causes RA. Proteus is a microbe that resides in the GI tract as well as the urinary tract. It is a primary cause of urinary alkalosis. Certain types of bacterium such as yersinia can induce "molecular mimicry", that is, certain pathogenic bacteria can mimic certain molecular actions in the body, such as mimicking hormone binding sites for TSH (thyroid stimulating hormone).
While the link to infectious pathogens and autoimmune conditions has certainly been well established, the bigger question of how and why these pathogens have set up shop in the body is often not addressed. A very plausible theory is that diminishment of GI immune function causes a terrain in which pathogens thrive.
In a dysbiotic gut terrain, immune function is necessarily compromised and opportunistic bacteria will tend to run rampant. The tight junctions in the gut become less, villi are atrophied, immunoglobulin levels are depressed, many antigens and pathogens can cross through into the bloodstream causing immune-mediated cascades, which can result in high levels of inflammation-inducing cytokines such as interleukins and TNF's.
The gastrointestinal immune system and its loss of function may be the pivotal factor in autoimmune development. Another question begs: how did GI function become compromised, and what other factors are at play?
One very plausible theory is the bombardment of environmental toxicity, combined with inadequate nutrition causes a situation where the body is less capable of functioning. Toxins such as mercury, halides, fluoride, halogens, aluminum, hydrocarbons are toxic, and demand that organs such as the liver and kidneys function in high demand in order to eliminate these toxins from human tissues. Inadequate detoxification of these substances from the body can and will result in a loss of function in various parts of the body.
The function of the liver is critically dependent upon dietary considerations such as sufficient protein, water intake and hydration. Certain nutritional factors such as betaine from beets, Vitamin B-12, sulphur from protein and cruciferous vegetables are capable of facilitating enhanced phase I and phase II liver detoxification pathways. Deficiencies or depletion of certain dietary factors will necessarily compromise the liver's ability to function. Processed foods and synthetic, artificial flavorings such as aspartame have deleterious effects on human cells and tissues.
Refined and processed foods, rampant antibiotic usage, chemical and metal toxicity all derail the health of the intestinal micro-flora. Studies have demonstrated that the gut flora plays a critical role in regulating inflammatory cascades, including the factors which incite tissue inflammation.
I would argue that there is no such thing as a localized autoimmune disease. Certainly various tissues, glands or organs may be affected in one person more than another. However, autoimmune conditions are more systemic than they are localized. Certainly if gut dysbiosis can cause inflammatory cascades in tissues all over the body, the effects of autoimmune signaling are indeed systemic.
This is why someone with Sjogren's for example, can have inflammation ensuing in multiple tissues of the body besides only the tear ducts. It is very common in fact, that autoimmune types of pain can be both localized and systemic. This begs the questions: what metabolic factors are at play in autoimmune activity? Are there any clues as to the nature of metabolic dysfunction?
A couple of important clues are:
Serum albumin, cholesterol, triglycerides, glucose, insulin all play important roles in the body. When liver function is impaired, cholesterol synthesis is aberrant. Often it is common that many autoimmune patients have low cholesterol values. It is well known that cholesterol is an anabolic anti-inflammatory lipid. In fact, cholesterol neutralizes the most virulent pro-inflammatory immune-derived mediators such as leukotriene. Leukotriene is a key pro-inflammatory fatty acids produced via the 5-LOX pathway from arachadonic acid. Activation of leukotriene sets off an inflammatory, tissue-destructive cascade.
Serum albumin is a critical "delivery truck" protein to your cells. It transports nutrients, hormones and electrolytes. Low levels of albumin (<4.1) reflects dysfunction of the liver as well as a decrease in healthy, anabolic activity. Almost all of the albumin in the blood is produced by the liver.
It is often the case that autoimmune patients have lower than optimal levels of albumin, cholesterol and may tend to have electrolyte abnormalities. This may be reflective of dysfunction within a variety of metabolic processes, including the liver.
When there are a high amount of toxins and pathogens in circulation, the liver is working overtime. The importance of improving diet, restoring gut ecology, appropriate probiotic supplementation and anti-oxidant therapy can not be overstated in autoimmune conditions.
The biochemical effects that proteolytic enzymes exert in the body can prevent, and even reverse immune-destructive signalling. Tumor Necrosis Factor alpha (TNF-a) is a cytokine signalling protein. TNF-a is released mostly by macrophage cells. It is the TNF-a which induces cell apoptosis, or cell death. The activation of TNF-a is one of several immune factors, which induces the inflammatory response. Numerous studies cite the increase in TNF-a when autoimmune conditions are present, as well as decreases in symptoms when TNF-a is decreased either through drugs or through antioxidant therapy. TNF-a induces inflammation.
The proteolytic enzyme Bromelain, synthesized from pineapple has been demonstrated in studies to significantly reduce TNF-a, as well as other pro-inflammatory immune cell-released mediators such as Prostaglandin E2 and Thromboxanes. Therefore, systemic, proteolytic enzymes have a lot of implications for a wide variety of health conditions.
The proteolytic enzyme serrapeptase may posses an even greater level of anti-inflammatory effect.
Enzymes when taken orally on an empty stomach can cross into the bloodstream and effect the biochemical processes that are necessary.
Proteolytic enzymes can be used for a wide range of health issues and symptoms with little, if any side effects. Some of the common health issues they are used for include:
Michael McEvoy has a private nutritional consulting practice. He works with clients nationally and internationally. Please contact him to learn more about his nutritional consulting services and programs.