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:
“Recent research has shown that fibrin plays a key role in the inflammatory response and development of rheumatoid arthritis.”-Wikipedia
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.
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:
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. 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.
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.
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. 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.
Certain drugs or exogenic chemical compounds are known to affect inflammation. Vitamin A deficiency causes an increase in inflammatory responses, and anti-inflammatory drugs work specifically by inhibiting normal inflammatory components.
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. 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.
Filed under: Alternative Medications and Solutions, Alternative Treatments, Arthritis, Autism, Fibromyalgia, Lupus, Multiple Sclerosis, Osteoarthritis, Parkinson's, Psoriasis and other skin dissorders, Pulmonary Fibrosis, Rheumatoid Arthritis, Sarcoidosis | Tagged: acne, allergic reaction, allergies, anti-inflammatory drugs, asthma, autoimmune diseases, blead to death, cancer, cardiovascular disease, Chediak-higashi syndrome, chemical compaounds, coronary heart disease, CRP, cystitis, disease, diseases, drugs, elukocyte defects, endometriosis, enterically coated, ESR, Fibrin, fibrinogen, fibroids, granulomatous disease, HDL, heart disease, hodgkin's disease, hypersensitivities, IBS, impaired fibrinolytic capacity, infections, inflammation, inflammation that leads to disease, inflammatory response, liver cirrhosis, Multiple Sclerosis, myocardial infarction, myopathies, PID, prostatitis, Pulmonary Fibrosis, reduce fibrin levels, reduce inflammation, reducing scar tissue, Rheumatoid Arthritis, Sarcoidosis, scar tissue, sedementation rate, stroke, thrombosis, tumors, tumours, vasculitis | 13 Comments »