Systemic Enzymes and Inflammation

Systemic Enzymes Therapy is a cleansing approach that utilizes the catabolic power of enzymes to break up fibrin in the body. Fibrin is associated with blood clotting and is also prevalent in inflammatory states. Many diseases like arthritis, cardiovascular disease, and bowel problems are the result of long term inflammation. Diabetes and “metabolic disorder” (obesity) are now viewed as inflammatory diseases. Other conditions like fibromyalgia are directly related to inflammation which has many complications, including increased oxidative stress leading to dehydration and degeneration of tissue. Systemic enzymes “chew up” many inflammatory by-products and protect cells from damage. They also help mobilize thickened tissue like scar tissue, which forms when the body is damaged (bruised, strained, or cut).

Many enzyme formulas for systemic use are similar to digestive enzymes except the focus is not to help you digest your food, but rather to digest the gristle around your joints, in your tissues, or in your blood. We call it systemic therapy because we are cleansing the entire system. We achieve this by taking the enzymes on an empty stomach which allows the enzymes to enter the bloodstream in sufficient quantity to catabolize and break up fibrin. If you were to take the enzymes with food, they would break down your food and not enter the bloodstream. Taking the enzymes with food reduces the cleansing effect on the blood and tissues.

Fibrin is an insoluble protein involved in blood clotting. When an injury occurs fibrin is deposited around the wound in the form of a mesh, which dries and hardens, so that bleeding stops. We all know that if we get cut the body forms a scab which then becomes a scar. If the cut is not severe, this scar is temporary

It is important to note that with trauma (falling down, getting bruised, or a getting rattled in a car accident) often causes bleeding from the capillaries. Capillaries are the tiniest blood vessels that infiltrate vital tissues. When the body is hit hard, these vessels rupture and blood leaks out into the tissue forming a bruise. The blood then essentially clots in the tissue and as it hardens, it blocks the circulation through that tissue. The result is that the tissue can’t really heal since its blood supply is impeded. Without fresh blood, the tissue is starved of oxygen, nutrients, and hydration. The stagnant tissue builds up residues from blood clots and from inflammation.

It is also very interesting that chronic tension has a very similar effect as trauma. For example if a muscle is always tight, the fresh blood can’t get in to the muscle. At first the blood can’t get in because when the muscle is contracted, the fibers shorten and compress the capillaries, restricting blood flow. Over time, the muscle becomes low in oxygen, nourishment, and hydration. The muscle then begins to fibrose as fibrin accumulates between the muscle fibers. The net result is that the muscle becomes denser, tighter, and less elastic. This thickened and fibrous muscle has less blood supply which further induces more fibrin to be deposited, perpetuating this cycle. Enzymes help shift this pattern of fibrosis and help restore the tissue.

I have found that when the body senses a weakness in a tissue, whether it is due to trauma (injury), overuse (fatigue) or an internal cause (problems with cellular metabolism), the body has predictable responses. Often the body will tighten up around the wounded area in efforts to protect it. This “tightening up” happens on many levels and usually effects all of the nearby tissues. Over time this tightness causes the tissues to get denser and thicker due to deposition of fibrin. After a while, the tissues are unable to return to a neutral state. This process resembles that of a very gnarly tree that has many knots. The wooden fibers of the tree become denser and very tight and they often have a strong rotation (forming the bulbous knot). In some cases the body deposits calcium and other minerals which continue to harden the region. All this is the body’s attempt to stabilize and support the area. While thickening the area does work to temporarily stabilize the area, it creates a reduced circulation which restricts healing. This dense tissue then becomes brittle and weak since it is less elastic and incapable of lengthening. The strain from even ordinary movements can cause small tears in this tightened tissue. As you can imagine, this aggravates the problem.

Systemic Enzymes are helpful with:

  • Reducing inflammation
  • Speed healing
  • Strengthen connective tissues including tendons
  • Pain Syndromes
    • Arthritis
    • Back and neck pain
    • Ganglion cysts
  • Circulation problems (including cold hands and feet)
  • Cardiovascular diseases
  • Cleansing the blood
  • After surgeries (excess scar tissue)
  • Improves digestion
  • Supports immune function

Fibrin is developed in the blood from a soluble protein, fibrinogen. The conversion of fibrinogen to fibrin is the final stage in blood clotting. Platelets, a type of cell found in blood, release the enzyme thrombin when they come into contact with damaged tissue, and the formation of fibrin then occurs. Calcium, vitamin K, and a variety of enzymes are also necessary for blood clotting.
High levels of PAI and alpha 2-antiplasmin have been implicated in metabolic syndrome and various other disease states.
The fibrinolytic system is closely linked to control of inflammation, and plays a role in disease states associated with inflammation.
Dysfunction or disease of the liver can lead to a decrease in fibrinogen production or the production of abnormal fibrinogen molecules with reduced activity

Metabolic syndrome is a combination of medical disorders that affect a large number of people in a clustered fashion. In some studies, the prevalence in the USA is calculated as being up to 25% of the population, the end result of which is to increase one’s risk for cardiovascular disease and diabetes.
High levels of PAI and alpha 2-antiplasmin have been implicated in metabolic syndrome and various other disease states.

Tissue damage due to Multiple Sclerosis (MS) is reduced and lifespan lengthened in mouse models of the disease when a naturally occurring fibrous protein called fibrin is depleted from the body, according to researchers at the University of California, San Diego (UCSD) School of Medicine.

The study, reported online the week of April 19, 2004 in the Proceedings of the National Academy of Sciences, identifies fibrin as a potential target for therapeutic intervention in the disease, which affects an estimated one million people worldwide.

However, the research team cautions that fibrin plays an important role in blood clotting and systemic fibrin depletion could have adverse effects in a chronic disease such as MS. Therefore, additional research is needed to specifically target fibrin in the nervous system, without affecting its ability as a blood clotting protein.

“Multiple sclerosis is a nervous system disease with vascular damage, resulting from the leakage of blood proteins, including fibrin, into the brain,” said the study’s first author, Katerina Akassoglous, Ph.D., a UCSD School of Medicine assistant professor of pharmacology. “Our study shows that fibrin facilitates the initiation of the inflammatory response in the nervous system and contributes to nerve tissue damage in an animal model of the disease.”

MS is an autoimmune disease that affects the central nervous system (CNS), causing a variety of symptoms including loss of balance and muscle coordination, changes in cognitive function, slurred speech, bladder and bowel dysfunction, pain, and diminished vision. While the exact cause of MS is unknown, a hallmark of the disease is the loss of a material called myelin that coats nerve fibers, and the inability of the body’s natural processes to repair the damage.

Although fibrin is best known for its important role in blood clotting, recent studies have shown that fibrin accumulates in the damaged nerves of MS patients, followed by a break down of myelin. However, the cellular mechanisms of fibrin action in the central nervous system have not been known, nor have scientists determined if fibrin depletion could alleviate or lessen the symptoms of MS.

In work performed at The Rockefeller University, New York and the UCSD School of Medicine, in collaboration with colleagues at the University of Vienna, Austria and Hellenic Pasteur Institute, Greece, researchers studied normal mice and transgenic mice with an MS-like condition. The normal mice had normal spinal cords and with no fibrin deposits in the central nervous system. In contrast, the transgenic mice showed fibrin accumulation, inflammation and a degradation of the myelin in their spinal cord. When transgenic mice were bred without fibrin, they developed a later onset of the MS-like paralysis as compared to their transgenic brothers that had fibrin. In addition, the fibrin-depleted mice lived for one additional week longer than the normal, disease-impacted mice. This difference is significant in animal models such as mice that have very short lifespans.

Fibrin’s role in excessive inflammation was shown in a follow-up experiment where transgenic mice were shown to experience high expression of pro-inflammatory molecules, followed by myelin loss, as compared to the fibrin-negative transgenic mice with no signs of inflammation or myelin destruction.

In addition to the genetic deletion of fibrin, the researchers tested drug-induced fibrin depletion, which was accomplished by administering ancrod, a snake venom protein, to the transgenic mice. Consistent with the genetics-based experiments, the pharmacological depletion also delayed the onset of inflammatory myelin destruction and down-regulated the immune response. Previous studies by other investigators who used ancrod in experimental autoimmune encephalomyelitis (EAE), another animal model of MS, also showed amelioration of neurologic symptoms.

In the current study, the investigators also used cell culture studies to determine that fibrin activates macrophages, the major cell type that contributes to inflammatory myelin destruction.

Akassoglou said that “further research to identify the cellular and molecular mechanisms that fibrin utilizes in the nervous system will provide pharmacologic targets that will specifically block the actions of fibrin in nervous system disease.”

The study was funded by grants from the National Institutes of Health, the Wadsworth Foundation Award, and the National Multiple Sclerosis Society.

Sidney Strickland, Ph.D., Laboratory of Neurobiology and Genetics, The Rockefeller University, New York, in whose lab Akassoglou first began her studies, was the senior author of the paper. Additional authors were Ryan Adams, Ph.D., UCSD Department of Pharmacology; Jan Bauer, Ph.D. and Hans Lassmann, M.D., Laboratory of Experimental Neuropathology, University of Vienna, Austria; Lesley Probert, Ph.D., and Vivi Tseveleki, B.Sc., Laboratory of Molecular Genetics, Hellenic Pasteur Institute, Athens, Greece; and Peter Mercado, B.Sc., The Rockefeller University

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