LONGECITY

When I first read a thread that mentioned one of these enzymes as "systemic" that is absorbed into the blood stream and distributed throughout the body not localized in the digestive tract I immediately thought ok enzymes, mostly protein, will be broken down and not absorbed... Apparently this is not the case as was pointed out. Here are a couple of studies showing measured blood levels of nattokinase and serrapeptase after oral administration. Though I haven't found evidence that pancreatic enzymes are also absorbed and found in systemic circulation (mainly because it is harder to search for) I am optimistic they they also are absorbed.

oral serrapeptase
http://sciencelinks....903A0653432.php

oral nattokinase
http://www.jstage.js.../71/9/2184/_pdf

So that being said, what are people's thoughts on the use of "systemic enzymes" for inflammation, cardiovascular support etc etc. Does anyone take them? Has anyone had any positive results? Which enzymes would be the best to take nattokinase, serrapeptase, pancretin, plant based enzymes etc. for general health and anti-aging?

So that being said, what are people's thoughts on the use of "systemic enzymes" for inflammation, cardiovascular support etc etc. Does anyone take them? Has anyone had any positive results? Which enzymes would be the best to take nattokinase, serrapeptase, pancretin, plant based enzymes etc. for general health and anti-aging?

I've been taking serrapeptase for a few years to try to eliminate my remaining hamstring pull adhesions. No noticeable effect. Nattokinase costs a lot more per FU (I love those units. They remind me of the frequent user points from the show "The Loop".), so I don't know if it's worthwhile.

So that being said, what are people's thoughts on the use of "systemic enzymes" for inflammation, cardiovascular support etc etc. Does anyone take them? Has anyone had any positive results? Which enzymes would be the best to take nattokinase, serrapeptase, pancretin, plant based enzymes etc. for general health and anti-aging?

I've been taking serrapeptase for a few years to try to eliminate my remaining hamstring pull adhesions. No noticeable effect. Nattokinase costs a lot more per FU (I love those units. They remind me of the frequent user points from the show "The Loop".), so I don't know if it's worthwhile.

Serrapeptidase is a staple in my arsenel as far as recovery from workouts. Soreness is dramatically impact, short term, and even long-term lingering issues have been significantly improved. This and cissus have really helped my turnaround time to get back to heavy lifts or even endurance exercise.

So that being said, what are people's thoughts on the use of "systemic enzymes" for inflammation, cardiovascular support etc etc. Does anyone take them? Has anyone had any positive results? Which enzymes would be the best to take nattokinase, serrapeptase, pancretin, plant based enzymes etc. for general health and anti-aging?

I've been taking serrapeptase for a few years to try to eliminate my remaining hamstring pull adhesions. No noticeable effect. Nattokinase costs a lot more per FU (I love those units. They remind me of the frequent user points from the show "The Loop".), so I don't know if it's worthwhile.

Serrapeptidase is a staple in my arsenel as far as recovery from workouts. Soreness is dramatically impact, short term, and even long-term lingering issues have been significantly improved. This and cissus have really helped my turnaround time to get back to heavy lifts or even endurance exercise.

what is your dosage neogenic, how many times a day, on an empty stomach?

So that being said, what are people's thoughts on the use of "systemic enzymes" for inflammation, cardiovascular support etc etc. Does anyone take them? Has anyone had any positive results? Which enzymes would be the best to take nattokinase, serrapeptase, pancretin, plant based enzymes etc. for general health and anti-aging?

I've been taking serrapeptase for a few years to try to eliminate my remaining hamstring pull adhesions. No noticeable effect. Nattokinase costs a lot more per FU (I love those units. They remind me of the frequent user points from the show "The Loop".), so I don't know if it's worthwhile.

Serrapeptidase is a staple in my arsenel as far as recovery from workouts. Soreness is dramatically impact, short term, and even long-term lingering issues have been significantly improved. This and cissus have really helped my turnaround time to get back to heavy lifts or even endurance exercise.

krillin no effect, neogenic great effect ? brand issues ? doseage ?

I have been using dr. best. 40,000 ius, but I think I need to bump it up to 80-120k as
I havent noticed an antiflammatory effect

Though I haven't found evidence that pancreatic enzymes are also absorbed and found in systemic circulation (mainly because it is harder to search for) I am optimistic they they also are absorbed.

oral nattokinase
http://www.jstage.js.../71/9/2184/_pdf

The article you quoted indicates that at least the pancreatic lipase is absorbed (ref. 23). Any particular reason you hope these enzymes make it into the blood?

Wobenzym might be highly controversial. I saw a study a while back that debunked it's effects quite a bit. I don't have a link to this study right now. Furthermore, it induced some form of histamine level increase or increase of sensivity in my case, so I decided to stop.
I second the serrapeptase effects. I take 20mg a day, on empty stomach, each morning. 4 tablets of the serraflazyme product, enterically coated ofcoarse.

I've also been looking for the original natto stuff the Japanese use, but was not able to find it. I'm told it tastes quite bad, so maybe me not finding it is not entirely a bad thing...

When I had inflammation in my achilles tendon I tried serrapeptase (Doctor's Best) on an empty stomach but found no effect. I later tried high doses of Bromelain (Now) on an empty stomach and experienced a dramatic reduction in the inflammation. Based on my personal experience I am now a big advocate of Bromelain on an empty stomach for chronic inflammation problems.

i use a combo product that has a few different proteases, bromelain, papain, a serrapeptase analoug, rutin & tumeric...i first used it when i yanked my back doing heavy T-bar rows, and it was quite effective.


the question which no one seems to be able to answer, is would using systemic enzymes to reduce inflammation post workout or on a regular basis have the same negative effects on muscle synthesis as nsaids/other anti-inflamitories
Edited by ajnast4r, 29 February 2008 - 12:53 PM.

krillin no effect, neogenic great effect ? brand issues ? doseage ?

I have been using dr. best. 40,000 ius, but I think I need to bump it up to 80-120k as
I havent noticed an antiflammatory effect

I started out with 40K (Dr's Best) for a while, then cut back to 20K (Now) when I saw it wasn't doing anything. CoQ10 takes care of muscle soreness prevention, so I haven't tested it for that.

My dad suffered from thrombosis shortly before his death from brain cancer. I sit at the computer way too much and suffered the same for quite a while up until about a year ago when I started taking Doctor's Best's nattokinase, two 2,000 FU caps a day.

I just started a bottle of nattokinase, also Dr. Best 2 caps a day. I already notice an improvement in my circulation in my feet and legs. So far, I think this stuff is excellent.

This is the study review I was referring to earlier. The studies were executed in a disease context, not on healthy subjects, but nevertheless the remarks regarding the quality of the studies is applicable to all of us I guess. So, on the positive side of interpretation, proteolytic enzymes might work, but we just don't know.

But maybe I'm generalizing to much...?

[Proteolytic enzymes as an alternative in comparison with nonsteroidal anti-inflammatory drugs (NSAID) in the treatment of degenerative and inflammatory rheumatic disease: systematic review][Article in German]


Heyll U, Münnich U, Senger V.
Abteilung Medizinische Beratung, Deutsche Krankenversicherung AG, Köln. dr.uwe.heyll@dkv.com

BACKGROUND AND PURPOSE: The comparably high number of severe side effects due to treatment with nonsteroidal anti-inflammatory drugs (NSAID) calls for better tolerated substances. One possible alternative is seen in the systemic treatment with proteolytic enzyme preparations for oral administration. The aim of this study was to determine whether the results from controlled randomized trials on enzyme therapy prove equal anti-inflammatory effectiveness compared to NSAID in the treatment of degenerative or inflammatory rheumatic disease. METHODS: All drug preparations registered in Germany as having anti-inflammatory properties were listed. Among these preparations, a systematic search was carried out for randomized clinical therapeutic trials giving evidence for the anti-inflammatory effectiveness of enzyme preparations or their components. RESULTS: The anti-inflammatory effectiveness of three out of eight registered enzyme preparations was investigated in randomized trials. In total, seven trials were judged to be sufficiently documented and to allow valuation. All studies show severe methodical deficits, and the standard trial design (clinical trials during inpatient rehabilitation in combination with extensive accompanying treatment) does not allow clear-cut conclusions. CONCLUSION: According to the present state of knowledge, oral proteolytic enzyme treatment does not offer a justified alternative in comparison with NSAID in the anti-inflammatory treatment of rheumatic disease.

PMID: 14631536

But on the other side, to add to the state of confusion we are in:

[Experimental evaluation of the wound healing dynamics][Article in Russian]


Minaev SV.
The experimental clinical investigation of the influence of systemic enzymotherapy on the course of the wound process was carried out in rats and in clinic. The rats of the experimental group have demonstrated more rapid debridement of the wound from blood clots and tissue detritus, intensive formation of granular tissue and its ripening. The experimental investigation has shown that using the preparation of systemic enzymotherapy (Vobenzyme) stimulates processes of healing at the expense of quicker changing the inflammation phases as well as prevents the development of early and late complications on the side of postoperative wounds. It was confirmed by clinical observations in 36 patients from 4 to 14 years of age.

PMID: 14569780 [PubMed - indexed for MEDLINE]

[The use of vobenzym in the comprehensive treatment of patients with digital flexor tendon injury][Article in Russian]


Strafun SS, Tovmasian VV.
The results of treatment of 56 patients with tendons of digital flexors were analyzed. In 28 of them in complex of treatment vobenzim was included, and an early active mobilization as well. Considerable antiinflammatory, antioedematous, secondarily analgetic effect of preparation, its application in early period permitted to realize active movements, to reach high functional result of treatment of patients' were noted.

PMID: 10857342 [PubMed - indexed for MEDLINE]

[The pathogenetic basis for and clinical use of systemic enzyme therapy in traumatology and orthopedics][Article in Russian]


Neverov VA, Klimov AV.
The authors have generalized their experiences with using "Wobenzym" in 140 patients. Schemes of the effective systemic enzyme therapy are proposed for patients of the orthopedic-traumatological profile.

PMID: 10491833 [PubMed - indexed for MEDLINE]

And this. With my limited level of knowledge I would evaluate this as being negative. What confuses me is this bit "These findings point to an immunomodulatory capacity of WE in adjuvant tumor therapy". What's your opinion?

Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation.Zavadova E, Desser L, Mohr T.
Institute of Applied and Experimental Oncology, University of Vienna, Austria.

Polymorphonuclear neutrophils (PMN) can be primed for enhanced release of reactive oxygen species (ROS) by exposure to cytokines and biological response modifiers. ROS are considered to possess tumoricidal activity. The polyenzyme preparation Wobenzym (WE) contains pancreatin, papain, bromelain trypsin and chymotrypsin and is used in adjuvant tumor therapy. We investigated killing of WE-exposed PMN against tumor cells and analyzed WE influence on ROS production in a chemiluminescence assay in PMN in vitro and in vivo. Depending on dose WE stimulates the cytotoxic capacity of PMN in vitro against tumor cells (50 micrograms/ml:p < 0.01). Exposure of PMN to Wobenzym caused a time-dependent significant (p < 0.02) increase in release of ROS. Similarly, oral administration of Wobenzym to healthy volunteers (n = 28) resulted in significant increases (p < 0.01) in ROS production, depending on dose (peak with 20 tablets) and time (peak 4 hours after Wobenzym administration). In contrast, ROS production was not elevated in the PMN of healthy volunteers receiving placebo (n = 8) or no treatment (n = 16). These findings point to an immunomodulatory capacity of WE in adjuvant tumor therapy.

PMID: 7663574 [PubMed - indexed for MEDLINE]

Edited by brainbox, 01 March 2008 - 12:44 PM.

And this. With my limited level of knowledge I would evaluate this as being negative. What confuses me is this bit "These findings point to an immunomodulatory capacity of WE in adjuvant tumor therapy". What's your opinion?

Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation.Zavadova E, Desser L, Mohr T.
Institute of Applied and Experimental Oncology, University of Vienna, Austria.

Polymorphonuclear neutrophils (PMN) can be primed for enhanced release of reactive oxygen species (ROS) by exposure to cytokines and biological response modifiers. ROS are considered to possess tumoricidal activity. The polyenzyme preparation Wobenzym (WE) contains pancreatin, papain, bromelain trypsin and chymotrypsin and is used in adjuvant tumor therapy. We investigated killing of WE-exposed PMN against tumor cells and analyzed WE influence on ROS production in a chemiluminescence assay in PMN in vitro and in vivo. Depending on dose WE stimulates the cytotoxic capacity of PMN in vitro against tumor cells (50 micrograms/ml:p < 0.01). Exposure of PMN to Wobenzym caused a time-dependent significant (p < 0.02) increase in release of ROS. Similarly, oral administration of Wobenzym to healthy volunteers (n = 28) resulted in significant increases (p < 0.01) in ROS production, depending on dose (peak with 20 tablets) and time (peak 4 hours after Wobenzym administration). In contrast, ROS production was not elevated in the PMN of healthy volunteers receiving placebo (n = 8) or no treatment (n = 16). These findings point to an immunomodulatory capacity of WE in adjuvant tumor therapy.

PMID: 7663574 [PubMed - indexed for MEDLINE]

This one is positive too, ROS (oxygen ions, peroxides, free radicals etc.) are a way neutrophils and other immune cells take care of things like cancer and pathogens and we want them to do this, we also want to be able to clean up this mess after the neutrophils etc. get done. Basically these cells seek out foreign invaders or trouble making or damaged cells, attach to them and release ROS to destroy them. So this in moderation and when it is not aimed at healthy cells (ala autoimmune) is a good thing.
Edited by edward, 01 March 2008 - 05:47 PM.

Ok, I was under the impression that elevation of ROS would occur while the immune system was actively pursuing it's duty, e.g. while dealing with disease or trauma. Platelets producing ROS to signalise the release of more platelets. A similar mechanism involving the recruitment of leukocytes. In this context I assume(d) that elevated ROS would not be good in the sense that it signalises some form of pathology. On the other hand, the immune systems is never inactive and the transition from healthy state to disease is a very gradual one indeed.

But I'm still sceptic about the increase of ROS in healthy individuals only as a reaction on the intake of a few enzymes......
Edited by brainbox, 01 March 2008 - 09:44 PM.

Are there any advantages or disadvantages of nattokinase over serrapeptase? They are measured with the same fibrinolytic units (FU), so are they basically equivalent? Everything I've read seems to indicate they have similar effects, but I have not seen any conclusive explanation of the similarities or differences between these two enzymes.

I do understand that nattokinase has a lower molecular weight than serrapeptase (27kDa vs. 60kDa). Wouldn't this result in easier transport across the gut, into tissues, etc?

It sounds like some have taken nattopeptase and serapeptase for inflammation. I always thought those two were for reducing fibrin and not inflammation.

The proteolytic are for inflammation.

William Donald Kelley used enzymes to treat his pancreatic cancer. Nicholas Gonzalez studied Kelley's work as a summer intern project in med school but I believe he still uses enzymes in his practice today.

I know there is a blood test for fibrin. It seems like some concerned with blood clots, stroke, thrombosis might want to get the blood test and THEN try some fribinolytic enzymes to see how the follow up test looks. Studies are fine but seeing the results on your own lab reports seems better to me.

From what I have read Nattokinase is more effective for cleaning up the circulatory system and serrapeptase is more effective for tissues. Anecdotally, serrapeptase seems to help with post exercise soreness and my back issues (mild scoliosis causes me back pain and some swelling pretty regularly). I didn't notice that much from natto so I stopped taking it, but then again I dont have any cardio issues.

Serrapeptase helps prevent bacteria from forming biofilms and thus establishing persistent infection.

Nattokinase may induce hemorrhage in succeptible individuals

Listeria monocytogenes is a notably invasive bacterium associated with life-threatening food-borne disease in humans. Several surface proteins have been shown to be essential in the adhesion of L. monocytogenes, and in the subsequent invasion of phagocytes. Because the control of the invasion of host cells by Listeria could potentially hinder its spread in the infected host, we have examined the effects of a protease treatment on the ability of L. monocytogenes to form biofilms and to invade tissues. We have chosen serratiopeptidase (SPEP), an extracellular metalloprotease produced by Serratia marcescens that is already widely used as an anti-inflammatory agent, and has been shown to modulate adhesin expression and to induce antibiotic sensitivity in other bacteria. Treatment of L. monocytogenes with sublethal concentrations of SPEP reduced their ability to form biofilms and to invade host cells.


http://www.ncbi.nlm....Pubmed_RVDocSum

Microbiological testing suggested that infection persisted in only one (5.6%) of eighteen animals in the serratiopeptidase-and-antibiotic group, whereas it was present in six (37.5%) of sixteen animals in the antibiotic-only group (p = 0.001). Histological evaluation showed similar results (kappa = 0.92). CONCLUSIONS: Serratiopeptidase was effective for eradicating infection caused by biofilm-forming bacteria in this experimental animal model. The antibiofilm property of the enzyme may enhance antibiotic efficacy in the treatment of staphylococcal infections.

http://www.ncbi.nlm....Pubmed_RVDocSum

Among the different mechanisms of bacterial resistance to antimicrobial agents that have been studied, biofilm formation is one of the most widespread. This mechanism is frequently the cause of failure in the treatment of prosthetic device infections, and several attempts have been made to develop molecules and protocols that are able to inhibit biofilm-embedded bacteria. We present data suggesting the possibility that proteolytic enzymes could significantly enhance the activities of antibiotics against biofilms. Antibiotic susceptibility tests on both planktonic and sessile cultures, studies on the dynamics of colonization of 10 biofilm-forming isolates, and then bioluminescence and scanning electron microscopy under seven different experimental conditions showed that serratiopeptidase greatly enhances the activity of ofloxacin on sessile cultures and can inhibit biofilm formation.

http://www.ncbi.nlm....Pubmed_RVDocSum

We report a patient, having used aspirin for secondary stroke prevention, who had an acute cerebellar hemorrhage after taking nattokinase 400 mg daily for 7 consecutive days. In addition to the hemorrhagic lesion, multiple microbleeds were demonstrated on brain MR images. We suggest that nattokinase may increase risk of intracerebral hemorrhage in patients who have bleeding-prone cerebral microangiopathy and are receiving other antithrombotic agent at the same time.

http://www.ncbi.nlm....Pubmed_RVDocSum

Edited by wiserd, 04 October 2008 - 07:43 AM.

Nattokinase may induce hemorrhage in succeptible individuals

If this happened to many people, I'm sure we would've heard about it by now. You never hear this happening, and Nattokinase is still sold without problem. Concluding from this, I doubt the percentage of "susceptible individuals" is substantial or even existent at all.

There is one case report of someone who was taking aspirin for stroke prevention and developed cerebral "microbleeds" after taking nattokinase at 400mg daily for a week. That is the only report I have heard of nattokinase doing anything dangerous.

Serrapeptase helps prevent bacteria from forming biofilms and thus establishing persistent infection.

Nattokinase may induce hemorrhage in succeptible individuals

Listeria monocytogenes is a notably invasive bacterium associated with life-threatening food-borne disease in humans. Several surface proteins have been shown to be essential in the adhesion of L. monocytogenes, and in the subsequent invasion of phagocytes. Because the control of the invasion of host cells by Listeria could potentially hinder its spread in the infected host, we have examined the effects of a protease treatment on the ability of L. monocytogenes to form biofilms and to invade tissues. We have chosen serratiopeptidase (SPEP), an extracellular metalloprotease produced by Serratia marcescens that is already widely used as an anti-inflammatory agent, and has been shown to modulate adhesin expression and to induce antibiotic sensitivity in other bacteria. Treatment of L. monocytogenes with sublethal concentrations of SPEP reduced their ability to form biofilms and to invade host cells.


http://www.ncbi.nlm....Pubmed_RVDocSum

Microbiological testing suggested that infection persisted in only one (5.6%) of eighteen animals in the serratiopeptidase-and-antibiotic group, whereas it was present in six (37.5%) of sixteen animals in the antibiotic-only group (p = 0.001). Histological evaluation showed similar results (kappa = 0.92). CONCLUSIONS: Serratiopeptidase was effective for eradicating infection caused by biofilm-forming bacteria in this experimental animal model. The antibiofilm property of the enzyme may enhance antibiotic efficacy in the treatment of staphylococcal infections.

http://www.ncbi.nlm....Pubmed_RVDocSum

Among the different mechanisms of bacterial resistance to antimicrobial agents that have been studied, biofilm formation is one of the most widespread. This mechanism is frequently the cause of failure in the treatment of prosthetic device infections, and several attempts have been made to develop molecules and protocols that are able to inhibit biofilm-embedded bacteria. We present data suggesting the possibility that proteolytic enzymes could significantly enhance the activities of antibiotics against biofilms. Antibiotic susceptibility tests on both planktonic and sessile cultures, studies on the dynamics of colonization of 10 biofilm-forming isolates, and then bioluminescence and scanning electron microscopy under seven different experimental conditions showed that serratiopeptidase greatly enhances the activity of ofloxacin on sessile cultures and can inhibit biofilm formation.

http://www.ncbi.nlm....Pubmed_RVDocSum

We report a patient, having used aspirin for secondary stroke prevention, who had an acute cerebellar hemorrhage after taking nattokinase 400 mg daily for 7 consecutive days. In addition to the hemorrhagic lesion, multiple microbleeds were demonstrated on brain MR images. We suggest that nattokinase may increase risk of intracerebral hemorrhage in patients who have bleeding-prone cerebral microangiopathy and are receiving other antithrombotic agent at the same time.

http://www.ncbi.nlm....Pubmed_RVDocSum

Thanks for compiling this information, it is potentially very important to anyone with Lyme disease because biofilms are thought to be partially responsible for the resistance of Lyme to antibiotic treatment. Is serrapeptase the only enzyme that has any evidence supporting its use for this purpose?

More on oral nattokinase doing something beneficial in humans:

Hypertens Res. 2008 Aug;31(8):1583-8.
Effects of nattokinase on blood pressure: a randomized, controlled trial.
Kim JY, Gum SN, Paik JK, Lim HH, Kim KC, Ogasawara K, Inoue K, Park S, Jang Y, Lee JH.

Yonsei University Research Institute of Science for Aging, Department of Food and Nutrition, College of Human Ecology, Yonsei University, and Department of Family Medicine, Mizmedi Hospital, Seoul, Korea.

The objective of this study was to examine the effects of nattokinase supplementation on blood pressure in subjects with pre-hypertension or stage 1 hypertension. In a randomized, double-blind, placebo-controlled trial, 86 participants ranging from 20 to 80 years of age with an initial untreated systolic blood pressure (SBP) of 130 to 159 mmHg received nattokinase (2,000 FU/capsule) or a placebo capsule for 8 weeks. Seventy-three subjects completed the protocol. Compared with the control group, the net changes in SBP and diastolic blood pressure (DBP) were -5.55 mmHg (95% confidence interval [CI], -10.5 to -0.57 mmHg; p<0.05) and -2.84 mmHg (CI, -5.33 to -0.33 mmHg; p<0.05), respectively, after the 8-week intervention. The corresponding net change in renin activity was -1.17 ng/mL/h for the nattokinase group compared with the control group (p<0.05). In conclusion, nattokinase supplementation resulted in a reduction in SBP and DBP. These findings suggest that increased intake of nattokinase may play an important role in preventing and treating hypertension.

PMID: 18971533

Funk,

Thanks for the study showing serrapeptase can break up biofilm. Although it wasn't directly applied to Lyme, there's no reason to think this wont work. Things seem to be looking up. When will you start using and any idea of those? Higher doses are better?

Does serrapeptase (or nattokinase) dissolve small non-malignant cysts?

(I don't know if "dissolve" is the correct word to use but you get my drift)

Does serrapeptase (or nattokinase) dissolve small non-malignant cysts?

(I don't know if "dissolve" is the correct word to use but you get my drift)

As long as there is sufficient blood flow to said cysts and the natto or serra is at sufficient concentrations they should help break up cysts but I think this application would be overkill. I became convinced that continuous use of these agents is not the best idea in populations that are already taking anticoagulants (that includes us, many if not most herbs and some supplements have anticoagulant or blood thinning properties). Prescription clot busters such as alteplase (very similar to nattokinase and serrapeptase) are used only sparingly and in specific cases. When there is any risk of bleeding, old injuries or use of anticoagulants they are not recommended. Using nato and serra for a few weeks once or twice a year seems to be a better strategy to clear out the junk or perhaps daily at very very low amounts. Then again this is just my opinion.

Thanks edward! I do appreciate the advice.
Edited by pycnogenol, 04 March 2009 - 11:13 PM.

I began taking serrapeptase around three years ago for its purported property of thinning mucous in hopes of clearing my sinuses. I suffered past traumas to the nose and dealt with poor drainage, frequent sinus infections, and chronic restricted air flow especially at night hampering sound sleep.

I originally took one Dr Best 40K unit each day and, surprisingly, within days I noted significant loosening and drainage. today, I take one, sometimes two, per week for maintenance and my ability to breath through my nose at night remains totally unrestricted enabling a sound restful slumber. when I take it, it is nearly always before I begin a 30-50 mile bike ride. Subsequently, I experience light drainage during the ride that clears easily enabling me to breath freely and sustain an optimal pace.

in addition to thinning and clearing mucous, I suppose serrapeptase may have reduced sinus inflammation enabling the freer air flow.

I know that medically you have to go through a very selective protocol to be a candidate for fibrinolysis, and this applies to very specific events: acute myocardial infarction, thrombotic stroke, and pulmonary thrombotic embolism. Outside of that they are considered fairly dangerous; some pretty nasty stuff can happen if your prothrombin time shoots up too high. Even at sub-acute doses I imagine a healthy individual could turn themselves into a bit of a hemophiliac; then you get bruised all the time and might have to go through a leukemia scare. Not fun.
I'm not aware of how fibrionlytics interfere with Vitamin K, and many people here are jumping aboard the K2 train (myself recently included); I have a hard time imagining that there's no interaction, but that is pure speculation. I would think if you start early enough with the K2 + D3 + mixed A combo, you really shouldn't have to go messing with these enzymes to protect your vascular system; and to elaborate on what edward said, Omega 3 is probably the most used supplement here and overall, and it has anticoagulant properties.