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.

Alternative Options for Multiple Sclerosis

Having an autoimmune disease, or in my case, a few, has increased my interest in learning about other diseases, as well as other treatments.  Of course, I think I have always had an interest in medical literature.
And since I’m on an alternative path of treatments, my interest definitely sways into the natural and homeopathic, even though I am certainly not against conventional medications.   I have no idea where this interest came from, but it has always been there, along with many other interests in my life.  And Mom, please stop telling me I should have been a doctor…I’m an artist, first and foremost!  I didn’t become interested in learning about multiple sclerosis until I had Rheumatoid Arthritis.  Before this, my uncle developed Lou Gehrig’s Disease (ALS), and later, after I developed RA, my father developed Parkinson’s.  Though my uncle is not related by blood, this still added to my growing interest of wanting to put a halt to all the disease in my life.  Perhaps if I could learn about these diseases, I could also come up with theories on how to improve the lives of those that had them?  And why did it seem like diseases were on an upswing?  My quest for answers continues, so I hope you can share in my journey to help the lives of others.

I was on Daily Strength one day when someone with both Rheumatoid Arthritis and Multiple Sclerosis wrote in on one of the posts.  They mentioned how Low Dose Naltrexone had changed their life.  At the time, I didn’t pay much attention to it and later couldn’t find the member.  But months later I had remembered Low Dose Naltrexone and started researching.

Upon research I found communities who knew a lot about Low Dose Naltrexone, and also people who knew how to be terrific supporters.  I gained friends, many who had MS and as a result became more interested in learning about Multiple Sclerosis.  I also hoped to simply learn more about neurological diseases.  My dad, new to Parkinson’s wasn’t as keen as I was in alternative medications at first, but soon I coaxed him into trying LDN.  I don’t think he thought it was doing much until months later when he ran out and realized he noticed a substantial difference.  I also have him taking higher doses of Coenzyme Q10 which has been shown to slow down the progression of both PD and ALS.

Multiple Sclerosis has been particularly interesting to me because the treatments for MS are currently inadequate.  Ask anyone with MS and you’ll hear the same thing.  That’s part of the reason why so many people with MS discovered Low Dose Naltrexone.  You can say the same for Pulmonary Fibrosis and many other diseases where people are given steroids, antibiotics, and other medications hoping to change the course of the disease and yet the disease for the most part, continues to progress without much change.  Pulmonary Fibrosis is a disease that can also be treated with Serracor-NK and Serra-RX because it reduces scar tissue.  Scar tissue can cause many health problems and diseases which is why reducing this scar tissue and fibrin which causes it, using Serrapeptase can be so helpful.

  What is MS?  Watch this video to learn more.

Recently, I’ve been thrilled to see that Serracor-NK is a recommended alternative treatment for Multiple Sclerosis.  It’s also compatible with most drugs, so another great solution if you have MS and are on CRAB drugs, antibiotics, or steroids.  Because I take Serracor-NK and know how well it works for me, I imagine that it would also work well for MS.  There are lots of theories out there that MS and RA are actualy closely related.  Whatever the case, any treatment that works for MS is a miracle.

   Watch an MS relapse to better understand this disease.

In MS, the myelin protective sheath that covers the nerve cells is broken down by immune complexes that are embedded in it. Serracor-NK,Serrra RX80 and other proteolytic enzymes break down the destructive immune complexes and can dramatically reduce MS symptoms. While regeneration of damaged tissue is not possible, regular supplementation with enzymes has been documented to halt the progress of degeneration associated with most stages of MS.”-biomediclabs.

  Reversing MS, is it possible?  Research shows new hope!

Hopefully soon we will find real solutions for our medical issues.  Until that day comes, I hope that you will join in the research, theories and recommendations that myself and many other people provide.  I will always mention, I am no doctor and this is all solely my opinion, but I do hope that this site helps you!  Hugs and thanks, -Sarah

Saying Goodbye to Acupuncture for Now

I don’t want t o give it up acupuncture. I do notice a slight difference and enjoy the attention. But since every Saturday I was having to get up a little earlier than I would naturally and since every week it was costing me $20 and I am currently more broke than ever, I simply can’t afford to keep going. I was noticing the biggest difference in my left wrist. And although I think it’s probably worth the money and time, I’m just so concerned with money right now that I can’t rationalize doing something that’s only making a slight difference. Maybe I’ll go back in the future but so far, unless money is no object, the benefits are not extraordinary enough. Supplements are so costly and I spend a TON on them. So that’s where I’m at. I do feel sad about it because I know it was helping a little. It was definitely improving my life, but I would only recommend acupuncture to people with RA who are near remission. Otherwise, it will probably just make your symptoms worse. I always flared during the visit. But the after effect of less inflammation was worth the flare. In the past however, when I wasn’t on alternative meds and tried acupuncture, I had a terrible flare that lasted weeks. It was awful! So again, I would only recommend acupuncture to those who are doing well with their disease and trying to ease smaller symptoms but not to people who are in the middle of a healing crisis, or worse, still looking for the right cocktail altogether.

Accupuncture Visits for Rheumatoid Arthritis

I admit it, I’ve done a terrible job keeping up with posts on how acupuncture is going for me.  So rather than waiting to write a post where I tell you exactly how many visits I’ve had and what’s happened at each one, etc., I’m just going to take the easy road and make it simple.  I’ve gone to every Saturday appointment except for two and last Saturday I got a parking ticket….so much for letting that relaxed feeling linger……

I can tell you that whenever I do go in for acupuncture, I get a flare during the visit.  You might think that sounds terrible, but to me I think of it as progress.  Anything natural will make you flare up, it’s just part of the process.  And that’s the hardest part really, is how to tell the difference between something that is making you worse or something that is making you better when they both have the same reactions.  This excludes immune suppressive drugs because they work entirely differently.

Within an hour usually, my flare subsides and lately I feel fairly great for a few days before the inflammation comes back to its normal state.  I would definitely say the acupuncture is making a positive difference, however it’s very slight.  I’ve decided to keep going however, based on theory.  So here are my theories on why I should keep going to acupuncture:

1.  Acupuncture increases endorphins.  Endorphins help heal the body.  Therefore, I must be doing some, even if it’s small, amount of healing during the visit.

2.  Acupuncture increases circulation.  Over time, perhaps increasing the circulation will make a bigger decrease in the amount of inflammation in my body.

3.  Even if the decrease in inflammation is very slight, it is still something.  And perhaps that small amount will slow down the erosion and disability.

4.  The Placebo effect.  As long as I don’t get any more parking tickets, perhaps the placebo effect of thinking the acupuncture is helping somewhat, will help decrease the inflammation.

Michael has been using a Chinese technique that would make some people cringe where you prick near the fingernail with a needle in certain spots (on a few of the fingers on each hand) and cause your hands to bleed for a moment.  Maybe that doesn’t sound fun to you, and it isn’t really.  It’s nothing compared to RA pain.  I do, in all honesty feel like it is decreasing the inflammation more so than it was before he had tried this technique.  I was glad that he was open to asking me if I’d like to try it because most people would probably be against the idea.  To me it makes logical sense as well, that it would increase circulation.

So there you have it in a nutshell.  I’m going in tomorrow and this time I’ll circle around for 10 minutes if I have to so I can find a parking spot that doesn’t allow for any more cruel tickets.  I hope you all have a great weekend and thanks as always for visiting!

Gene Varient in Parkinsons Affects B6 Metabolism

I found this article interesting and thought all of you might appreciate it as well.  Here is the link.  (click here)

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