The Curse of Fibrin


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).”

“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.” –

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:


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]


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.


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.


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.

13 Responses

  1. 9/2012 while under treatment for RA on Enbrel, pred had spontaneous ankle fracture. REPEATED odd issues FINALLY dx as FORMALDEHYDE poisoning but we igg DEFICIENCY not SURE of RA status as testing LOW based on ANTIBODY tests! SKIN ULCERATED ARMS AND FACE and FIBRIN DRIPPING FROM WOUNDS. OSU DERM Inpatient thought SELF MUTILATOR w WBC over 30k, pro and metamyelocytes w NO ANTIBODIES OR RESPONSE 12/14.


  2. Beautiful,, soothing flowers! I hope to receive fun money for Christmas….gotta catch Santa! Your New Fan, Mair

  3. Ad,

    so sorry for the late reply! Just know that it may take some time to notice a difference. Give it at least 3-4 months. Fibrin is very stubborn, but I’m sure you’ll be feeling better soon! Yes, please do tell me all about your progress!
    thanks and hugs,

  4. I have vitiligo and uterine fibroids. I have always believed that having vitiligo is only a symptom and by reading this article and looking at Chediak-Higashi syndrome, I am almost certain that there is a malfunction in my blood b/c of the fibrin that causes the fibroids and the vitiligo and many of the other symptoms I am enduring b/c of it. I want to try this Serracor-NK and keep up with you to tell you my results. If you have anything to add that I should know, please contact me…blessings!

  5. Hi Sarah,
    Thnk you very much for yor reply.
    I tried to get off my meds but my BP shot up.I have been taking these for 7 years. My doctor is not too cooperative on this issue. I woul rather take Serracornk bundle along with Vit.D 10000 Iu as recomeded by folks at Biomed labs.
    Looking for away out?

  6. Hi Mohan,
    I originally responded thinking this could be a healing crises, but upon looking into your medications, I’m wondering if you should be taking all of this. You’re on two blood pressure lowering medications, one that is technically a diuretic and both are very toxic. They can lead to kidney failure, among many other possibilities. Serracor-NK and Serra-RX will both lower your blood pressure naturally. Did you know that if you take extra blood pressure medication, that your body will sometimes go into over-drive and raise the blood pressure to compensate?

    I think you may want to back off on your supplement treatments and re-think your current regiment of drugs and supplements. It is just my opinion that you need to decide if you want to do things naturally or take medications. Serra-RX and Serracor-NK do an excellent job at lowering blood pressure, among other things. But you simply can’t take everything, in my opinion.

  7. Hi Sarah,
    I have just statred taking SerraRx and SerracorNK along with D3-10000 abot 5 days ago for my PF. I was diagnosed with PF a few weeks ago. I do not know the extent of it but I am still functional and my O2 is at 98%.
    I am on Avapro and thaizide for my high BP. I have noticed that my Bp is on the rise since staring with Serracor. Do you think there could be a connection.
    I would appreciate your help.

  8. Deb,
    Thanks for your nice comments! :) It should be fine to take with your enbrel. Learn about your Enbrel and how it works, and learn about Serracor and how it works. I already know how these things work, but it’s important for YOU to understand what’s going on in your body. You’re the one in charge.

  9. Sara, I just now have started reading your website. I have R.A. and am taking enbrel and predisone for about 2 years. I do take alot glyco nutrients and know about neprinol from my brother who is a vet and told me to try it. However you are now saying to try serracor-NK which is fine. I just need to know if its alright to take in conjunction with my enbrel. I am learning alot here on your site.

  10. Debora,
    It sounds like you need a doctor’s expertise on this one. Are you on any drugs and/or supplements? Keep us posted!
    Best of luck,

  11. Hoping I don’t appear clueless and this article is ind ed about humans, not dogs, I have a question: I’ve recently been experiencing odd clotting from cuts. When removing callouses from my feet (gross, sorry) I nicked myself. The next thing i know I’m standing in a very thick pool of blood and still hanging from the small, surface skin cut was a fibrous (I’m guessing) clot of blood about an inch long and 1/4 in. wide. How it even fit through that nick I don’t know. Several more similar were in tub. Is this fibrinogen? I’m pretty worried

  12. Hi Robin,

    I’ll look into it, thanks. There’s actually a lot of good chewable medications/supplements for dogs and arthritis. Pretty amazing!

  13. Look at Dr. Clemmons research into degenerative myelopathy in German Shepherd Dogs. I have my dog on medication that is supposed to slow down the progression of the disease by decreasing the fibrin.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this: