The Curse of Fibrin

clotting

If Fibrin didn’t exist, we would bleed to death, literally. But when Fibrin goes awry, it can lead to a host of diseases including Rheumatoid Arthritis, Cystic Fibrosis, Pulmonary Fibrosis, Fibrocystic Breasts, Endometriosis, Fibroids, Thrombosis, Cardiovascular Disease, Liver Cirrhosis, Heart Disease and a host of many other diseases involving inflammation.

When Fibrin works as it should:

“Fibrin (also called Factor Ia) is a fibrous protein involved in the clotting of blood, and is non globular. It is a fibrillar protein that is polymerised to form a “mesh” that forms a hemostatic plug or clot (in conjunction with platelets) over a wound site.”-Wikipedia

When Fibrin is the bad guy:

Rheumatoid Arthritis:

“Recent research has shown that fibrin plays a key role in the inflammatory response and development of rheumatoid arthritis.”-Wikipedia

Scar Tissue:

Not all scar tissue is considered bad necessarily, but when it’s in your organs, it can lead to terrible problems.  And when it’s in your brain, it can lead to Multiple Sclerosis.

The below paragraph says that there are “no direct treatments for elevated levels”, meaning fibrin levels, yet anyone taking serrapeptase or studying alternative medications and diseases and knows about enzymatic therapy knows that you can reduce fibrin levels with certain supplements and can effectively reduce your CRP.  So why are so many doctors in the dark about this?

“Sometimes fibrinogen (the test) is ordered, along with other cardiac risk markers such as C-reactive protein (CRP), to help determine a patient’s overall risk of developing cardiovascular disease. This use of fibrinogen has not gained widespread acceptance though, because there are no direct treatments for elevated levels. However, many doctors feel that fibrinogen measurements give them additional information that may lead them to be more aggressive in treating those risk factors that they can influence (such as cholesterol and HDL).”-www.labtestsonline.org

“Fibrinogen is an acute phase reactant, meaning that fibrinogen concentrations may rise sharply in any condition that causes inflammation or tissue damage. Elevated concentrations of fibrinogen are not specific — they do not tell the doctor the cause or location of the disturbance. Usually these elevations in the fibrinogen blood level are temporary, returning to normal after the underlying condition has been resolved. Elevated levels may be seen with:

While fibrinogen levels are elevated, a person’s risk of developing a blood clot may be increased and, over time, they could contribute to an increased risk for developing cardiovascular disease.” –www.labtestsonline.org

If elevated fibrinogen levels are involved in inflammatory disorders, then here is a longer list of inflammatory disorders that would greatly improve with the direct decrease of fibrinogen:

“Abnormalities associated with inflammation comprise a large, officially unrelated group of disorders which underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with etiological origins in inflammatory processes are thought to include cancer, atherosclerosis, and ischaemic heart disease.[4]

A large variety of proteins are involved in inflammation, and any one of them is open to a genetic mutation which impairs or otherwise dysregulates the normal function and expression of that protein.

Examples of disorders associated with inflammation include:

Allergies

An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation. A common example is hay fever, which is caused by a hypersensitive response by skin mast cells to allergens. Pre-sensitised mast cells respond by degranulating, releasing vasoactive chemicals such as histamine. These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes.[4] Severe inflammatory response may mature into a systemic response known as anaphylaxis.

Other hypersensitivity reactions (type 2 and type 3) are mediated by antibody reactions and induce inflammation by attracting leukocytes which damage surrounding tissue.[4]

Myopathies

Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. They may occur in conjunction with other immune disorders, such as systemic sclerosis, and include dermatomyositis, polymyositis, and inclusion body myositis.[4]

Leukocyte defects

Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte function often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection.[4] Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chediak-Higashi syndrome), or produce microbicides (chronic granulomatous disease). Additionally, diseases affecting the bone marrow may result in abnormal or few leukocytes.

Pharmacological

Certain drugs or exogenic chemical compounds are known to affect inflammation. Vitamin A deficiency causes an increase in inflammatory responses,[8] and anti-inflammatory drugs work specifically by inhibiting normal inflammatory components.

Cancer

Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration. Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis.[9] On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.”-wikipedia

If you’re not convinced by wikipedia that too much fibrin is bad news, plenty of other good sources for information are out there, including pubmed.  Just do a quick google search on fibrin.

Hodgkin’s Disease: “Fibrin deposits were observed in the involved lymph nodes and/or spleens of 15 patients with Hodgkin’s disease by specific immunofluorescence and by electron microscopy. Two basic patterns of fibrin deposition were observed: 1) intercellular deposits, chiefly associated with nonneoplastic-appearing lymphoid cells and 2) deposits associated with the collagen fibers of young connective tissue. In addition, coarse fibrin deposits were observed in areas of necrosis, presumably a non-specific finding. Fibronectin was also observed in intercellular areas, but staining was less intense than for fibrin. Fibrin deposits were also observed in 3 of 6 cases of non-Hodgkin’s lymphoma, indicating that the finding is not an exclusive feature of Hodgkin’s disease. The pathogenesis and possible significance of fibrin deposition in Hodgkin’s disease are related to earlier observations of activation of the coagulation system on neoplasia and cell-mediated immunity and to the possible role of fibrin, fibronectin, and their breakdown products in angiogenesis and fibroplasia.”-pubmed

Multiple Sclerosis: “Tissue plasminogen activator (tPA), a neuronal as well as the key fibrinolytic enzyme, is found concentrated on demyelinated axons in multiple sclerosis lesions together with fibrin(ogen) deposits. The decreased tPA activity in normal-appearing white and grey matter and lesions of multiple sclerosis is reflected in diminished fibrinolysis as measured by a clot lysis assay. Nonetheless, peptide products of fibrin, including D-dimer, accumulate on demyelinated axons-the result of fibrinogen entry through a compromised blood-brain barrier (BBB). Analysis of tissue samples on reducing and non-reducing polyacrylamide gels demonstrates complexes of tPA with plasminogen activator inhibitor-1 (PAI-1) but not with neuroserpin, a tPA-specific inhibitor concentrated in grey matter. As total tPA protein remains unchanged in acute lesions and the concentration of PAI-1 rises several fold, complex formation is a probable cause of the impaired fibrinolysis. Although the tPA-plasmin cascade promotes neurodegeneration in excitotoxin-induced neuronal death, in inflammatory conditions with BBB disruption it has been demonstrated to have a protective role in removing fibrin, which exacerbates axonal injury. The impaired fibrinolytic capacity resulting from increased PAI-1 synthesis and complex formation with tPA, which is detectable prior to lesion formation, therefore has the potential to contribute to axonal damage in multiple sclerosis.”-pubmed

Since most of us are never ordered a fibrinogen test from the doctor, then my best assumption is that any tests that show an elevation of inflammation, would therefore mean that there is too much fibrin in the blood.  As you can see, too much fibrin results in inflammation and can lead to disease.  The only therapies that I know of that reduce fibrin are enzymatic therapies, which is why I take serrapeptase.   I prefer brands that are enterically coated.  Feel free to share your fibrin story.

Pulmonary Fibrosis

Scarring of the Lungs

Scarring of the Lungs

First, what is Pulmonary Fibrosis?   Pulmonary Fibrosis literally means lung (pulmonary) scarring (fibrosis). The lung scarring occurs in the tissue of the lung called the interstitium, which supports the structures of the lung (air sacs/alveoli). There are an estimated 130-200 related diseases called Interstitial Lung Disease that are similar in characteristics and can result in scarring. Pulmonary Fibrosis causes the lung tissue to thicken and become stiff. Scarring inhibits oxygen from entering the blood stream.”

Symptoms include “shortness of breath (dyspnea), especially during or after physical activity, and a dry cough.” -Mayo Clinic

What damages your lungs?  There are quite a few possible causes, including environmental factors, gerd, radiation, and various medical conditions, but don’t be surprised that it could be your medication. Many drugs can damage your lungs, especially chemotherapy drugs (methotrexate, cyclophosphamide); medications used to treat heart arrhythmias and other cardiovascular problems (amiodarone, propranolol); certain psychiatric medications; and some antibiotics (nitrofurantoin, sulfasalazine).”-Mayo Clinic

If you are in the advanced stages of Pulmonary Fibrosis, your doctor may give you little hope.  “No cure exists for pulmonary fibrosis, and current treatments often fail to slow the progress of the disease or relieve symptoms.”-Mayo Clinic

Before you give up, alternative medications may be your best option.  Why Enzymes work:  “Enzymes eat scar tissue and fibrosis. Fibrosis is scar tissue and most doctors learn in anatomy that it is fibrosis that eventually kills us all. Let me explain. As we age, which starts at 27, we have a diminishing of the body’s output of enzymes. This is because we make a finite amount of enzymes in a lifetime and we use up a good deal of them by the time we reach our 40’s (Cystic Fibrosis patients who have virtually no enzyme production to speak of, even as children usually don’t make it past their 20’s before they die of the restriction and shrinkage in the lungs from the formation of fibrosis or scar tissue).

So our body begins to dole out our enzymes with an eyedropper instead of with a tablespoon. Result: the repair mechanism of the body goes off balance and has nothing to reduce the over abundance of fibrin it deposits in nearly everything from simple cuts, to the inside of our internal organs and blood vessels. It is then when most women begin to develop things like fibrocystic breast disease, uterine fibroids, and endometriosis. We all grow arterial sclerotic (meaning scar tissue) plaque, and have fibrin begin to spider web its way inside of our internal organs, reducing their size and function over time. This is why as we age our wounds heal with thicker, less pliable, weaker and very visible scars.

If we replace the lost enzymes, we can control and reduce the amount of scar tissue and fibrosis our bodies have. As physicians in the US are now discovering, even old scar tissue can be “eaten away” from surgical wounds, pulmonary fibrosis, and kidney fibrosis even colloid years after their formation. Medical doctors in Europe and Asia have known this and used orally administered enzymes for such for over 40 years!

Sounds too good to be true?  If you have no options, why wouldn’t you try alternative medications.  According to Biomediclabs, Within 4 weeks, patients should notice improvement of their symptoms including shortness of breath and coughing with phlegm.  After a 3-6 month treatment, patients should have significant improvement in their lung structure.  We recommend that patients take a chest x-ray before and after the treatment and compare the diagnostic results to monitor their progress.”

Before I tried alternative medications, I didn’t truly believe in miracles.  Serracor-NK was created for Pulmonary Fibrosis.  I know it has changed my life, and I have Rheumatoid Arthritis.  I believe in this product because of what it has done for me.



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