Friday, August 5, 2011

Serrapeptase Questions

Dear Doctors,

Please kindly point to an angioCT/Doppler evidence for Serrapeptase efficiency in arterial plaque removal. Or if you have any other evidence that serrapeptase can remove arterial plaque by sending me to a clinical study, I would appreciate it.

Thank you,
Dr. Hughes


Dr. Hughes,

Takeda Pharmaceuticals is the largest producer of serrapeptase in the world.  Their estimated worldwide sales of Dansen (Serrapeptase) exceed 6.7 Billion Yen.  So we are convinced Serrapeptase has safety and efficaciously. Being that serrapeptase is not a patentable ingredient it has received little clinically funded research.  Only about 40 controlled studies worldwide to be exact. As for the cardiovascular benefits of Serrapeptase, the evidence supporting this is mostly anecdotal and based in large part on the research of the late Hans A. Nieper, M.D., an internist from Hannover, Germany, who is widely known and also considered antiestablishment. He studied the effects of Serrapeptase on plaque accumulations in the arteries. A book about Dr. Nieper’s work, entitled, The Curious Man: The Life and Works of Dr. Hans Nieper (Avery Penguin Putnam, December 1998), provides insight into his studies. An Italian study done at the University of Naples in the department of vascular surgery, did show that Serrapeptase was effective and well tolerated in patients with inflammatory venous diseases. But more research is necessary to accurately and specifically determine the effects Serrapeptase can have on cardiovascular health.

Currently approved indications of Dasen (prescription serrapeptase)
Remission of swelling in the following diseases or symptoms:
  • After operation and trauma, chronic sinusitis, galactostasis (in cases where breast massage or pumping is performed)
  • Difficulty of expectoration in the following diseases with hard-to-eliminate sputum and frequent hacking:
  • Bronchitis, pulmonary tuberculosis, bronchial asthma
  • Difficulty of expectoration after anesthesia
We wish that there was more conclusive evidence available for reference.   

Sincerely,

Thank you sincerely,
Support Team
www.serrapeptase.org

Dear Sir,

Grateful thanks for your comprehensive explanation!
I apologize for interfering again with your privacy with a further question:

Do proteolytic enzymes (Serrapeptase or its Neprinol combination) act upon 
arterial plaques by a mechanism that might result in their sudden fragmentation and subsequent life-threatening thrombotic events, or by a very mild decomposition of them? Should it be used in patients at high risk (Lp-PLA2-PLAC 288 ng/ml) to sensitively lowering the cerebrovascular risks, or the other way around (by possibly increasing the risk of sudden plaque "rupture"...) It obviously depends upon the concrete way of the enzymes' action, whether in such cases it should be strongly indicated as prevention therapy, or should be seen as an absolutely contraindicated approach.

Please kindly advise.


Thanks in advance,

Dr. Hughes

Dr. Hughes

We usually like to start by explaining enzyme mechanics, as this makes their safety almost self-explanatory. Since your question is cardiovascular in nature, we will concentrate on Nattokinase, since this enzyme has been studied for its superiority in improving circulatory health.   In general, about 10% of its affect is based on direct fibrinolytic activity whereas 90% is based on its ability to upregulate the plasminogen system.  These percentages are variable depending on the particular enzyme, but consistent enough for general explanation.  Basically, it is an enzyme that digests fibrin both directly and indirectly. Indirectly, it activates pro-urokinase and tissue plasminogen activator (t-PA), supporting the fibrinolytic activity of plasmin. These combined actions promote healthy platelet function, circulation and blood flow.   As mentioned before Nattokinase works to up-regulate the body’s natural plasminogen system, which systematically regulates itself. Because of this, nattokinse does not circumnavigate the body’s own checks and balances. Studies examining the effect of nattokinase administration on tissue plasminogen activator (tPa), euglobulin lysis time, fibrin degradation products, and blood fluidity tests have not revealed contraindications on these parameters, though all individuals are different. Physicians have occasionally measured euglobulin lysis time (ELT) in patients taking Nattokianse. ELT indicates the activity of plasmin. There have not been any observed indications of excessive activity of the plasminogen system in the individuals tested.  Furthermore, an acute toxicity study demonstrated that nattokinase was safe at levels hundreds of times greater than the recommended human dose.

While enzymes do have a direct effect on plaques and fibrin, it is small and mostly attributed to their ability to lyse proteins, by breaking their peptide bonds, releasing amino acids.  This action is identical to the action our pancreatic enzymes digest food.  We can therefore assume that even in patients at high risk ie.  (Lp-PLA2-PLAC 288 ng/ml), these enzymes will only enhance the natural degradation of arterial plaques by complementing the plasminogen system.  We can also say with a great degree of certainty that this would be the most recommended source of treatment for patients with high risk of arterial plaque fragmentation, since it complements our body’s inherent treatment mechanisms.

Since the actions enhance plasminogen I would suggest possibly researching the effects of pro-urokinase and tissue plasminogen activator (t-PA), on vulnerable plaques.  In laymen’s terms the enzymes are only complementing how our bodies naturally eliminate arterial buildup and wouldn’t have a pharmaceutical or artificially induced side effect.

Thank you sincerely,
Support Team
www.serrapeptase.org