Nature's Clot-Busters: Nattokinase and Serrapeptase
by James South, M.A.
Blood clotting is not something most people worry about. You get a cut,
a clot forms, the bleeding stops, end of story. Yet excessive clotting
can be deadly. As J. Heinrich and colleagues note: "Coronary thrombosis
is regarded as the final occlusive event in the progress of coronary heart
disease (CHD). Disturbances of the hemostatic system may favor this process
and thus may indicate increased risk of myocardial infarction [or cerebrovascular
event]."1
Translation: inappropriate, unnecessary blood clots may form in your
blood vessels and trigger a heart attack or stroke. This happens to millions
of Americans every year, often leading to permanent disability or death.
The question is: Why? And what can be done about it?
Clot Formation
A clot (technically known as a "thrombus") forms when platelets
and red blood cells clump together. It is the blood protein fibrin that
"glues" them together. Fibrin is formed at the site of a clot
from the soluble circulating protein fibrinogen. If the clot forms at
the site of a broken or cut blood vessel, it is appropriate, even lifesaving.
If the clot forms inside a blood vessel in the absence of a wound or
trauma, it is unnecessary, even life-threatening, since it may plug up
a crucial heart or brain artery. There are more than 20 enzymes involved
in the coagulation cascade that creates clots, but only one enzyme-plasmin-that
can dissolve fibrin and thus break up small clots.
Plasmin, a thrombolytic (clot-dissolving) enzyme, is made from plasminogen
through the action of an enzyme, tissue plasminogen activator (TPA). Thromobolytic
enzymes are produced in blood vessel linings, and their production drops
with age. To make matters worse, even in healthy people fibrinogen levels
rise by 25 mg/dl per decade.2 "There are several pathways
by which acute or chronic increase in fibrinogen levels can lead to a
cardiovascular [or cerebrovascular] event..., including...increased platelet
aggregation and thrombus formation, and increased fibrin formation."3
In other words, high fibrinogen levels tend to promote the spontaneous
formation of unnecessary fibrin-clots. High fibrinogen (and thus implicitly,
high fibrin) levels are such a serious risk factor for heart attacks and
strokes that one major study of 2,116 men found that those who had high
LDL ("bad") cholesterol-but low fibrinogen levels-had only one-sixth
the heart attack risk of men with high LDL and high fibrinogen levels.1
Nattokinase
Fortunately, nature has provided us with a way to augment our gradually
diminishing clot-busting activity. In 1980, while studying physiological
chemistry at the University of Chicago Medical School, Japanese researcher
Hiroyuki Sumi accidentally discovered that a traditional Japanese food-natto-had
the ability to dissolve thrombi.4 He and his research group
published a brief paper on the discovery in 1987, describing the "strong
fibrinolytic [clot-dissolving] activity" of the fermented soy cheese,
natto.5
The Sumi research group was able to purify and identify a specific enzyme
from the soy cheese that he called "nattokinase."5
Because natto has been widely consumed in Japan for over a thousand years,
Dr. Sumi felt safe in performing human and animal experiments with nattokinase.
In 1990 the Sumi research group published the results of a series of experiments
demonstrating nattokinase's potent fibrinolytic activity.6
In the first study, 12 volunteers (six men and six women) were fed 200
grams (seven ounces) of natto, and two methods of measuring their blood's
fibrinolytic activity were used. In the euglobulin clot lysis test, a
blood sample was taken and the formation of a thrombus (clot) was then
artificially stimulated. The time required for the blood to completely
dissolve the clot was then measured. The time needed to completely dissolve
the clot was cut in half compared to those in the control group. The fibrin
plate method was then used on other blood samples. In this test, blood
was added to a plate with a special polymerized fibrinogen to see how
much it would dissolve in four hours. The control group's blood had
no effect in this test, but the natto group's blood dissolved 15 mm²
of fibrinogen in this test.
Next, the research team had volunteers take crude nattokinase tablets
for eight days, using the same two tests plus the fibrin degradation product
test. They also measured tissue plasminogen activator (TPA) blood levels.
These tests further confirmed nattokinase's clot-busting power, with
the men showing an increase in TPA activity as well. While Dr. Sumi had
previously shown that nattokinase had direct fibrinolytic activity,5
the finding of increased TPA activity (which increases plasmin) showed
nattokinase to augment the body's own fibrinolytic activity.
Finally, the Sumi team gave one group of dogs nattokinase tablets and
another group a placebo. The team then created a thrombus in a major leg
vein in each dog which completely blocked the vein, as shown in angiograms.
Within five hours the nattokinase-fed dogs had a complete reopening of
their leg vein circulation, while the dogs fed the placebo still had complete
vein occlusion (blockage) 18 hours later.6
More Nattokinase Research
In 1995 M. Fujita and colleagues reported their results with rats and
nattokinase.7 The carotid artery (which feeds the brain) was
injured to induce thrombus formation, which completely blocked the artery.
Three enzymes-elastase, plasmin, and nattokinase-were then tested on different
rats.
After one hour, elastase (a close "chemical cousin" of plasmin
and nattokinase) had produced no reopening of the blocked carotid artery
whatsoever. Plasmin restored about 16 percent of normal circulation in
one hour. But the nattokinase succeeded in restoring carotid brain circulation
62 percent. As the researchers modestly concluded: "The results indicate
that the thrombolytic [clot-dissolving] activity of nattokinase is stronger
than that of plasmin or elastase in vivo."7
In 1994, an amazing case was reported demonstrating nattokinase's
ability to restore blood circulation. A 58-year-old man suffering from
central retinal vein occlusion in his right eye came to a university hospital.
The clot had caused fluid accumulation and bleeding in the eye, leading
to loss of vision. The researchers prescribed a 100-gram (three-ounce)
dose of natto, to be eaten before bed every night as a way to get nattokinase
to his eye. He was also prescribed a drug to reduce the blockage-induced
bleeding.
By the tenth day eye bleeding was halted. By the twentieth day his eye
circulation was so improved his vision returned and he was released from
the hospital. He continued to eat natto two days weekly, and two months
later a retinal angiogram showed a complete clearing of the retinal blockage.8
Serrapeptase
Serrapeptase, also called serratia peptidase, is an enzyme derived from
the Serratia bacteria, which lives in the intestinal tract of silkworms.
It has been used for over 30 years in Europe and Asia (where it is called
Danzen®) to reduce pain, inflammation and excessive mucous secretion.9,10,11
Serrapeptase has been shown to be well-absorbed from the intestinal tract,
although it must be enterically coated to protect it from degradation
in the stomach.12,13
Hans Nieper, a pioneering medical doctor in Germany, has recommended
serrapeptase for decades to gradually reduce atherosclerotic plaque buildup.
Mazzone and coworkers note that "serritia peptidase (Danzen)...,
which is available in tablet form to enable it to be absorbed from the
intestinal lumen, has been shown to induce intense fibrinolytic, anti-inflammatory,
and anti-edemic activity..."11 Since inflammation increases
fibrinogen levels,2 and increased fibrinogen increases pathological
clotting risk,1,2,3 the powerful anti-inflammatory activity
of serrapeptase10,14 complements its fibrinolytic activity.
An ideal natural clot-busting supplement should therefore combine nattokinase
and enterically coated serrapeptase granules.
Clot-Busting Cautions
Nattokinase , naturally present in and absorbed from natto, has been
consumed safely in Japan for a thousand years. Serrapeptase has been safely
and widely used in Europe and Asia for more than 30 years. They are helpful
in preventing or reversing the pathological hypercoagulation tendencies
common among modern Americans.
Yet not everyone should take nattokinase/serrapeptase (NKSP). People
with bleeding disorders, such as hemophilia or a group of diseases called
"hemorrhagic diathesias," should not take NKSP. People with
ongoing bleeding problems, including ulcers, recent surgery, recent major
trauma, or hemorrhoids, should not take NKSP. Anyone who has ever suffered
intracranial bleeding, or who has had neurosurgery or ischemic stroke
in the previous six months, should also avoid NKSP. Severe uncontrolled
high blood pressure is also a contraindication for NKSP. Last, those taking
blood-thinning drugs such as heparin, Coumadin® or aspirin should
use NKSP only if advised and carefully monitored by their prescribing
physician.
Dosage
In Dr. Sumi's original nattokinase paper, it was reported that natto
had an average of 40 fibrinolytic units (FUs) per gram.5 In
human research, 50 to 200 grams is the typical daily food dose used to
supply nattokinase. This would be equivalent to a dose of 2,000 to 8,000
FUs.
The nattokinase currently available for supplements supplies 20,000
FU/gram, while serrapeptase supplies 60,000 FU/gram. A combination of
36 mg nattokinase and 5 mg serrapeptase would yield 1,020 FUs. Taking
one such capsule two or three times daily on an empty stomach with water
would be a reasonable preventive or maintenance dose. Anyone suffering
any medical condition that might involve bleeding or coagulation issues
should check with a health care professional before using nattokinase/serrapeptase.
References:
1. Heinrich, J. et al. "Fibrinogen and factor VII in the prediction
of coronary risk." Arterioscler Thromb 1994, 14:54-59.
2. Hager, K. et al. "Fibrinogen and Aging." Aging (Milano) 1994,
6:133-38.
3. Montalescot, G. et al. "Fibrinogen as a risk factor for coronary
heart disease." Eur Heart J 1998, 19 Suppl H:H11-17.
4. Interview with Doctor of Medicine Hiroyuki Sumi, Japan Bio Science
Laboratory Co., Ltd., 1998.
5. Sumi, H. et al. "A novel fibrinolytic enzyme (nattokinase) in
the vegetable cheese natto...." Experientia 1987, 43:1110-11.
6. Sumi, H. et al. "Enhancement of the fibrinolytic activity in plasma
by oral administration of nattokinase." Acta Haematol 1990, 84: 139-43.
7. Fujita, M. et al. "Thrombolytic effect of nattokinase on a chemically
induced thrombosis model in rat." Bio Pharm Bull 1995, 18:1387-91.
8. Nishimura, K. et al. "Natto diet was apparently effective in a
case of incipient central retinal vein occlusion." Jpn Rev Clin Ophthalmol
1994, 88:1381-85.
9. Kee, W. et al. "The treatment of breast engorgement with serrapeptase
(Danzen&Mac226;): a randomized double-blind controlled trial."
Singapore Med J 1989, 30:48-54.
10. Tomoda, K. and Miyatam, K. "Some information on the composition
of tracheal secretions before and after the administration of Danzen&Mac226;"
Exper Ther 1972, 477:9-16.
11. Mazzone, A. et al. "Evaluation of serratia peptidase in acute
or chronic inflammation of otorhinolaryngology pathology: a multicentre,
double-blind, randomized trial versus placebo." J Int Med Res 1990,
18:379-88.
12. Miyata, K. "Intestinal absorption of serratia peptidase."
J Appl Biochem 1980, 2:111-16.
13. Moriya, N. et al. "Intestinal absorption of serrapeptase (TSP)
in rats." Biotechnol Appl Biochem 1994, 20 (pt.1):101-08.
14. Esch, P. et al. "A reduction of postoperative swelling. Objective
measurement of swelling of the upper ankle joint in treatment with serrapeptase-a
prospective study" (in German). Fortschr Med 1989,107:67-68,71-72.
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