A Fibrin Cyst & Biofilm Dissolver
Fibrin Cysts and Biofilms have recently come to the forefront as one of the key roadblocks to killing many chronic disease bacteria and viruses. This includes:
Lyme disease Herpes
MRSA Staph Hepatitis
Fibromyalgia HIV and Aids
Chronic Fatigue Shingles
It is a remarkable breakthrough and will have a huge effect on Lyme disease sufferers, and others, to make our Monolaurin formula even more effective! Finally, a long term answer!
Our first choice is to always look for a natural remedy for illness and disease. In the case of Lyme disease, we strongly support antibiotic treatment in the early stages!
However, as time drags on, our Protocol becomes better and better as a natural remedy for Lyme disease! Many, many clinical studies show monolaurin will kill the Lyme bacteria (and co-infections). Now, with recent research, we know an additional natural treatment, Biofilm Enzymes, dissolve Cyst & Biofilm. This will work with our Monolaurin to make the healing process more effective. It will help speed the results of both Monolaurin and antibiotics. Let’s see how it works.
Lyme’s Protective Shields
Unfortunately, B. burgdorferi has an ability to form (and re-form) protective cysts and biofilms. After the antibiotic or immune system attack is gone, a cyst can dissolve and the bacteria in it reactivate. Biofilm shields are even worse since Bb can stay active under it. This helps explains why Lyme infection can be so persistent and re-occur after antibiotics.
Obviously, it would be great if we could kill the bacteria protected by the cysts and biofilms as well exposed Bb. The longer Lyme disease persists, the more important our protocol becomes.
We mentioned elsewhere that the Lyme Borrelia burgdorferi bacteria can form cysts or biofilms. When it senses an antibiotic or immune system attack, it can very quickly put up defensive shields. They can be in the form of a cyst (similar to a butterfly’s cocoon), or it can form a ‘biofilm’ coating around a bacteria or a cluster of bacteria for protection.
This is one reason antibiotics can often have a limited or short term effect on Lyme disease. Most antibiotics can’t attach to the bacteria (or are severely limited). Meanwhile, the Lyme can continue to be active – especially in the biofilm type of protective shield. When the antibiotic is stopped, or additional stress happens to the body, the Lyme disease, and its effects can come roaring back.
The good news is that these defensive shields do not seem to totally stop monolaurin except, perhaps, for the cyst form. However, they do appear to slow monolaurin down. Therefore, it makes a lot of sense to dissolve these shields if we are able to.
The Major Players
Fibrin is a protein formed in the human body that plays a major role in the formation of blood clots and scar tissue. But, to understand why the body sometimes needs help defending itself against fibrin, you first need to understand a bit more about the fibrin itself.
During wound and blood clotting, a soluble protein, fibrinogen, converts into an insoluble protein, fibrin. Biofilm formation requires the conversion of fibrinogen to fibrin. Fibrin strands are then laid down inside the damaged area. The fibrin strands assemble into a net-like gel that hardens to patch the damaged wound or vessel. So, fibrin does play a vital role in the healing process. (1)
However, as we age, the concentration of fibrinogen increases in our blood. (2) High levels of fibrinogen increase fibrin production. As fibrin begins to accumulate in the blood vessels it generally leads to the formation of blood clots, scarring, and other problems. (3)
In addition, many bacteria and viruses use fibrin to form protective barriers around themselves. This is especially true when they are under attack from the immune system or antibiotics. They use the fibrin to build up biofilms or cysts around themselves. Then the immune system and most antibiotics can’t penetrate or attach themselves to the bacteria or coating.
When viruses and bacteria (including Lyme Bb), build biofilms, they rapidly weaving this protective fibrin web or matrix around themselves. They’re crafty in creating a way to protect themselves, survive and hide from the immune system. The layer of fibrin covering these microbes makes them undetectable by the immune system.
However, when fibrin is dissolved, our Monolaurin and the immune system can more easily identify and eliminate the bacteria. When it comes to improving your health as you age, one of the most important targets an enzyme can seek and destroy is the fibrin protein protecting bad things.
Enzymes, in general, can be thought of as proteins on a mission (usually helping to dissolve and break down foods to absorb). However, there are a few specialized enzymes that will dissolve the fibrin tissue and scar tissue being used to protect the bad guys. Fortunately, our body actually produces a fibrinolytic enzyme that will dissolve excessive fibrin!
Plasmin is a natural body enzyme that breaks up fibrin in blood clots and other places. Our bodies normally secrete sufficient levels of plasmin – this enzyme that dissolves many fibrin plasma proteins and blood clots. Plasmin (also a natural blood thinner) is responsible for maintaining normal blood solvency by removing unnecessary accumulated fibrin.
Healthy younger individuals usually have sufficient levels of plasmin. Unfortunately, as with many other things, plasmin production slows down as we get older. Then, our normal ability to remove excess fibrin is reduced. The result can be cardiovascular disease, heart attacks, strokes, pulmonary emboli, deep vein thrombosis (DVT) and other related disorders. (4-8)
Another type of protective barriers Bb can build are called “cysts”. They look like small sacs attached by slender threads. Cysts contain immature spirochetes in a metabolically inactive form. The immune system attempts to destroy the invading foreign bodies (cysts) but with little success. (9)
Bb can quickly change surface antigens to protect itself (placing fibrin in 10 to 20 minutes in some studies). Antibodies made against one strain may be effective in killing that strain. However, the new strain now has different surface antigens. It will take up residence in a different tissue where it escapes detection and survives. It is apparent that Bb has evolved disguises and biological techniques to guarantee its survival and avoid attempts to kill it. (10)
Research has shown that protein-dissolving (proteolytic) enzymes can slow the production of fibrin and enhance its removal from the body. (1) However, cysts are tighter woven and can take longer to dissolve. Persistence with both our Monolaurin and Fibrin Dissolver will usually get them.
In some long-standing cases, the cysts can fall into the realm of the Bb spirochetes that penetrate body cells. When they penetrate body cells, monolaurin and antibiotics can’t get to them. Our body cell actually protects them. In these cases, after the active manifestation is gone, people will drop to a teaspoon a day (1 scoop) of Monolaurin. Then, monolaurin is in the blood stream. If any spirochetes come out, looking to reactivate, the monolaurin can come into contact with them and kill them before they can build up.
Biofilms – A Cloaking Disguise
Biofilms are a cloaking device bacteria and some viruses also use to survive in adverse conditions. Lyme bacteria can form a slimy matrix over themselves that shields them from antibodies and white blood cells from the immune system.
Lyme uses your own body’s fibrin, protein, and heavy metals to form the protective cysts. Because it is your own body’s tissues, the immune system doesn’t see these cysts as a threat and does not attack it. Also, antibiotics are unable to penetrate the biofilm. Once pathogens have formed biofilms, colonies can be up to 1,000 times more resistant to antibiotics! This means if something is not taken to dissolve it, a person will never completely get well, and will relapse after stopping the antibiotics. (11)
In biofilms, microbes adhere to each other or to living surfaces. In the biofilm, single or multiple types of organisms can surround themselves with a complex matrix, better known as “slime”. (12) Biofilms start as just a few microorganisms adhering to each other or to a surface. Then, they begin to communicate and initiate a change in gene expression and become a protective matrix. The matrix colonies then can develop into complex three-dimensional structures housing millions of individual microbes. Like cities, they have towers, columns, bridges and channels for the flow of nutrients.
A mature biofilm is usually composed of three layers:
- An inside film layer that binds the biofilm to the surface;
- A film made up of colonies of single or multiple species of bacterial and/or fungal organisms;
- The surface film releasing microorganisms that can colonize other places.
Biofilms are also notorious for their ability to withstand extraordinarily high concentrations of antibiotics that are otherwise lethal in smaller doses to their planktonic counterparts. Biofilms have even been seen in brain tissue. This may be why neuroborreliosis, (“neuro Lyme”) is so hard to cure – and why it causes dementia.
The National Institutes of Health estimate that nearly 80 percent of chronic microbial infections in the human body are due to biofilms. This includes chronic lung infection in cystic fibrosis patients, catheter infections, chronic urinary and middle ear infections, gingivitis, sinusitis and even fatal endocarditis.
Monolaurin is more able to penetrate biofilms than cysts. There are often more gaps and, having the same molecular size as the lipids in biofilms (as in Bb), it is able to absorb and penetrate. The purpose of Biofilm Enzymes is to help speed up the monolaurin penetration and results.
- Meletis CD, Barker JE. Therapeutic enzymes: using the body’s helpers as healers. Alt Comp Ther. 2005;74-77.
- Meade TW. Fibrinogen and cardiovascular disease. J Clin Pathol. 1997;50:13-15.
- Milner M, Makise K. Natto and its Active Ingredient Nattokinase: a potent and safe thrombolytic agent. Alt Comp Therap. 2002;8(3):157-164.
- Koenig W. Fibrin(ogen) in cardiovascular disease: an update. Thromb Haemost. 2003;89:601-609.
- Lefevre M, Kris-Etherton PM, Zhao G, Tracy RP. Dietary fatty acids, hemostasis, and cardiovascular disease risk. J Am Diet Assoc. 2004;104:410-419.
- Kannel WB. Overview of hemostatic factors involved in atherosclerotic cardiovascular disease.Lipids. 2005;40:1215-1220.
- Eidelman RS, Hennekens CH. Fibrinogen: a predictor of stroke and marker of atherosclerosis.Eur Heart J. 2003;24:499-500.
- Nesheim M. Myocardial infarction and the balance between fibrin deposition and removal. Ital Heart J. 2001;2:641-645.
- Fujita M, Hong K, Ito Y, et al. Thrombolytic effect of nattokinase on a chemically induced thrombosis model in rat. Biol Pharm Bull. 1995;18:1387-1391.
- Grier, T. The Complexities of Lyme Disease, from: Lyme Disease Survival Manual, 1997.
- Flemming H-C, Wingender J, Griegbe, Mayer C. Physico-chemical properties of biofilms.In: Evans LV, editor. Biofilms: recent advances in their study and control. Amsterdam: Harwood Academic Publishers; 2000. p. 19-34.
- Eva Sapi Ph.D. University of New Haven, Department of Biology and Environmental Sciences, Dodds Hall 314, 300 Boston Post Road, West Haven CT 06516.