Question for Jackie re fibrinogen levels

Jackie

I have been taking Nattokinase for over a year. I started with a dose of 6,000FU and later reduced it to 4,000, which I have been taking for the last 9 months.

It is difficult to get fibrinogen tests in UK so I had one done in August 2011 while on holiday in the US. The Fibrinogen Activity score was 339. I am in the US again this week and had a repeat test. The score was 297.

I remember you saying that the aim was a score below 300, and I'm pleased that I have achieved that. My question is this: is 297 a satisfactory level or should I aim for lower?

Thank you as always for your good advice.

Gill

Hi Gill - 300 is the upper range. My doctor likes to see lower...to avoid thick, sticky blood. However, there's more than fibrinogen to consider as contributory to viscosity or hypercoagulability. I just read a good commentary on that topic which I'll dig out and post shortly.

The original post titled Red Flags to Beat the Odds listed several important markers including fibrinogen..
[www.afibbers.org]

Jackie

Gill – Here’s more. The focus is on elevated blood viscosity or hypercoagulability. It’s important to realize that fibrinogen is just one of many correlating markers that can and should be monitored. It’s unfortunate that the tests mentioned in both the Red Flags post and the Sticky, Thick Blood post are not considered routine and that we have to request them if they are available at all. [www.afibbers.org].

Additional advice includes hydrating well continually as well as consideration for donating blood or prescribing phlebotomy when marker levels of fibrinogen and ferritin are elevated. Silent, systemic inflammation contributes significantly to elevated blood viscosity so monitoring the markers is very significant.

Garry F. Gordon, MD, who is legendary in the practice of chelation therapy and Orthomolecular Medicine, states repeatedly in his lectures that he doesn’t treat with anticoagulant drugs but rather relies on enzymes such as serrapeptase, nattokinase and preferably, lumbrokinase and has yet to have a patient suffer from stroke or MI in many years of using the enzyme approach and eliminating toxic metals and inflammatory influences. He uses a whole protocol for prevention.

Testing of blood viscosity began with the research results of the late pioneer, Kenneth Kensey, MD, of Rheologics, which is now incorporated into the specialized testing offered by Meridian Valley noted in the following report. Note the mention of three types of tests for viscosity.

The topic of elevated blood viscosity or hypercoagulability is discussed in this very informative report by Drs. Larsen and Holsworth titled Measuring Blood Viscosity to Improve Patient Outcomes… the introduction begins:

(quote)
Despite decades of treatments to lower cholesterol, regulate heart rhythms, and reduce salt and fat, cardiovascular disease is still the number one killer of adults in the industrialized world. It has been associated with nearly 300 independent risk factors, among them high LDL, low HDL, male gender, smoking, obesity, insulin resistance, sedentary lifestyle, age, and hypertension. Blood viscosity is the common factor ties all these factors together.

Blood viscosity – a measurement of the thickness and stickiness of an individual's blood – is associated with each of those risk factors, either as a contributor or an effect. Understanding blood viscosity and how it contributes to the development of atherosclerotic plaques and thrombosis, how to test for it, and how to treat it are essential to our practices as primary care physicians. There are effective natural treatments that can alter blood viscosity safely, preserving health and potentially saving lives.

The Physics of Blood Viscosity
To understand blood viscosity and how it affects the arterial walls, it is useful to understand the physics involved in fluids. Blood is not the same thickness and stickiness – or viscosity – at all times. While water is no thicker in a still pond than in a fast-running stream, blood actually thickens as it slows down. During diastole, slower-moving red blood cells cling together more easily and can even form rouleaux, structures that look like stacks of coins under a microscope. These clinging red blood cells make the blood more viscous. During slow flow, aggregation of platelets and intermolecular reactions between plasma and cellular components further contribute to increasing viscosity. At the other end of the cardiac cycle – systole – blood flows more rapidly, resulting in dispersion of blood components and decreased viscosity. Therefore, blood viscosity fluctuates with every heartbeat, from lesser to greater and back. Blood at diastole can be anywhere from 5 to 20 times as viscous as the same blood at systole. However, even blood at systole can be more viscous than optimal, and this plays an important role in the development of atherosclerotic plaques.
Continue: [www.townsendletter.com]


Jackie



Edited 1 time(s). Last edit at 10/31/2012 10:24AM by Jackie.

Jackie,

I would be a bit leary of putting too much faith in the statements of David Berg. His statement that platelet aggregation is the LAST step in the coagulation cascade is just plain wrong. Thrombus (blood clot) formation involves three steps - in the order listed:

Platelet activation and aggregation (antiplatelet agents like aspirin works here)
Blood coagulation (warfarin works here)
Fibrinolysis (nattokinase works here)

So, platelet activation and aggregation is actually the FIRST step. Also, the INR test essentially measures warfarin concentration. I doubt very much that enzymes would affect it. In any case, an INR of 5.4 would be associated with a huge increase in the risk of hemorrhagic stroke and is certainly not something you want to strive for. Perhaps you could throw some light on the enzyme/INR question? Is your INR elevated?

Hans

I'll repeat what I have noticed with regular fibrinogen testing while I used nattokinase...my fibrinogen range beginning from the mid 300's at the start of 4000 fu's natto to the upper 400's as the months went by. I tried three different brands with the same results. Strangely, while off the natto, my inflammation markers decreased dramatically (likely a coincidence?). I did not notice any difference in my health that would key to the cause of the increase of fibrinogen.

There are too many covert variables affecting the production of fibrinogen to rely on nattokinase as a first-line stroke defense based on my experience.

I do plan to reinstate nattokinase as a circulation enhancer once I'm off warfarin, as the use of nattokinase coincided with improved peripheral circulation.

Tom

Hans... I'm going to delete that additional portion of this thread... The quote was not from David Berg, but rather an observation mentiioned in a blog conversation by a FM MD... I didn't do a good job in presenting for clarity so I'm deleting it.

I will add additional information about the need for knowing blood viscosity and the influencing factors such as elevated fibrinogen.

Sorry about the confusion.

Jackie

Continuing on with comments on fibrinogen testing, it’s should be remembered that fibrinogen is just one key marker among many for determining thick, sticky, toxic blood related to the importance of managing elevated blood viscosity or hypercoagulability which is very for afibbers.

Some markers are called Acute Phase Proteins which typically increase in blood as a result of inflammation, tissue injury and disease. Heavy metals, toxic chemicals, elevated blood glucose levels/Diabetes or anything that contributes to increased blood thickness and inflammation needs to be monitored. Be mindful of sources such as stealth viruses and bacteria, (Chlamydia, CMV, Lyme) and the various forms of nanobacteria that secrete a protective and toxic biofilm now traced to inflammatory responses that cause a variety of disease conditions including coronary artery disease.

Heavy metal toxicities, dioxins, PCBs, BPA are especially prevalent these days and are found in drinking water, the air we breathe (including exhaust fumes), fish, many inorganic foods and packaging materials. The toxic loads everyone carries often result in thick, sticky blood (hypercoagulability) which predisposes us to enormous immune system insults that may culminate in devastating problems like cancer and heart disease. (Sinatra Health Report)

As stated previously, unfortunately, testing for these markers is not yet considered routine by most physicians although those practicing functional medicine typically do test because their focus is to evaluate toxic load interferences on body function so testing and detoxification protocols are important priorities in those practices.
Afibbers especially need to know their markers, but actually, everyone should.

Other tests in addition to fibrinogen include those previously mentioned: Homocysteine, Lipoprotein(a), C-reactive Protein, Serum Ferritin, Hemoglobin A1C at a minimum…there are others as well.

Over a decade ago, Integrative Cardiologist, Stephen Sinatra warned about components of toxic blood:

“Fibrinogen is a coagulation-type protein that determines the stickiness of blood platelets. While you need adequate fibrinogen to stop excessive bleeding from cuts and trauma, higher levels are associated with too much. A high fibrinogen level is an independent factor for increased risk of heart disease independent of or in the absence of other indicators. By itself, elevated fibrinogen can cause the abrupt formation of coronary thrombosis. An association is found between elevated plasma fibrinogen concentration and coronary artery calcification.” (Sinatra’s Health Report)

Relevant to fibrinogen testing.
Dr. Sinatra cautions women who smoke or take oral contraceptives or are menopausal that they absolutely must know their fibrinogen levels.
He says a woman in any of these groups is a walking time bomb.

n. pl. fi•bri•nol•y•ses
The breakdown of fibrin, usually by the enzymatic action of plasmin.


In a report on Fibrinolysis, former director (for 25 years) of Arizona Coagulation Consultants and founder of HEMEX laboratories in Phoenix, AZ, David E. Berg, MS, CLS(NCA) FAHA describes what we need to know about fibrinogen and other markers of elevated blood viscosity. David Berg is a renowned expert in this area, and his lab (now sold) HEMEX, pioneered coagulation testing to assist doctors in more successfully treating patients.

He says, “The fibrinolytic system is responsible for keeping the tubular ducts open and fluids moving properly throughout the human body. It is an active, enzyme-based system that dissolves any debris in the lymphatic, circulatory, renal, urinary, mammary duct and central nervous system. Where there is movement of fluid, a functional fibrinolytic system keeps all the channels open.”

The system is made up of enzymes which act as activators and inhibitors to keep everything in balance. In this system, the major protease zymogen (enzyme inhibitor) is plasminogen activated by tissue Plasminogen Activator (tPA) to the active and very powerful enzyme, Plasmin, which can digest anything, including clots, fibrin and damaged dead or living cells. It is an active component of the apoptosis process or the ongoing replacement of cells and tissues.

Inhibitors of this Plasmin include alpha-2-AntiPlasmin (a2AP), Lipoprotein (a) and Plasminogen Activator Inhibitor (tPAI-1)

Alpha-2-Anti-Plasmin is an acute-phase protein that goes up under stress, infection or damage to the body as the body wants to protect the fibrin formed in the clotting cycle. When low or consumed faster than replaced, the patient is in a special disease state called disseminated intravascular coagulation which occurs in cancer patients at end-stages of life.

There are positive effects as well to elevated a2AP that occur in acute phase reaction such as when the body is faced with trauma, infection or such and prepares itself for fibrin formation in the coagulation or clotting cycle. Quick formation of a blood clot or fibrin deposits can prevent blood loss or wall off invading pathogens such as bacteria or viruses which help prevent a systemic infection throughout the body. This keeps bacteria at bay until the immune system can clear the infection.

Two normal inhibitors of fibrinolysis.(preventing the breakdown of fibrin) are Lipoprotein(a) and PAI-1. [We’ve discussed elevated PAI-1 in the nattokinase posts.] Since Lp(a) cannot be activated to plasmin, no breakdown of fibrin occurs and the higher the Lp(a), the less plasmin is generated. (Meaning, it’s important to test Lp(a) and maintain proper levels.)

Dr. Berg notes there are six genotypes and 23 phenotypes of the Lp(a) molecule. The smaller the Lp(a) molecule, the higher the blood value of Lp(a) and less fibrinolysis.

The other inhibitor, PAI-1, is secreted from endothelial cells lining blood vessels. Three polymorphisms of PAI-1 determine blood values. One results in normal blood values, another has higher values as seen in Type II diabetes and metabolic syndrome and another, has the highest blood values of PAI-1. The higher the value, the lower the amount of fibrinolytic (breakdown) activity. [We have talked about making sure we always have a substantial dose of nattokinase to carry through the sleeping hours and early morning when PAI-1 is elevated which increases risk for stroke and MI.]

Outside factors also can initiate fibrinolysis. Emergency rooms often give rTPA, urokinase and streptokinase which are prescription medications.

Another class of activators are nutraceuticals and include bromelain, Wobenzym, serrapeptase, nattokinase and lumbrokinase (boluoke) which are effective to varying degrees in activating plasminogen to plasmin directly in the plasma and bypassing the endothelial cell process of plasmin generation. (end of The Fibrinolosys notes by David Berg).

Deitrich Klinghardt, MD, PhD who is well known for neural therapy and heavy metal detoxification protocols relates a comment offered by David Berg on nutraceuticals for hypercoagulation…

He estimated effectiveness of various natural agents for hypercoagulation at:
50% - Bromelain
60% - Wobenzym
70% - Serrapeptase
80% - Nattokinase
95% - Lumbrokinase

Japanese nattokinase researchers have determined that not all brands of the same activator have comparable potency. Attempts to standardize the potency and reliability of nattokinase supplements has been unsuccessful thus far and some indications are for many brands, although they carry what was once a labeled assurance (the NSK-SD) designation, the assays show a variety of “less than advertised” potency which can only be determined by looking at each manufacturer for their in-house studies which may not be easily available.

Now there is an improved, patented nattokinase called Cardiokinase..(I believe Shannon has mentioned this in his posts) which is considered to be a more potent, reliable and effective product. This new formulation is based on a new strain that produces higher fibrinolytic activity and is 200% more effectiveness compared to other nattokinase products. The dosing is in I.U.’s rather than the FUs of the old formulations.. It’s pricey but stronger and reliable.

Check the various websites discussing Cardiokinase. This one has a handy comparison chart. [www.forresthealth.com]

Other details:
[www.pureprescriptions.com]

Lumbrokinase (Boluoke) by Canada RNA Biochemical Inc. and as noted is 95% effective, indicates in their product
• Extensively proven by clinical studies
• Suitable for patients with soy allergy
• Optimizes circulation by lowering fibrinogen, lowering endothelin, lowering platelet aggregation, lowers blood viscosity
• Regulates inflammation by lowering CRP, TXa2, PAI-1
• Modifies CA-cell adhesion
• Decreases microbial resistance: breaks down biofilm
• Does not significantly affect INR or PTT

Again, this is a pricey product but highly effective for anyone with elevated markers.
www.CanadaRNA.com


Jackie

Jackie

Many thanks for all the information. I have just had a letter from my EP telling me that i can have fibrinogen tests here in London. How often do you think the test needs to be done?

Gill