Serrapeptase + 2 Audios and Pdf files

[Guest guest]

I have no financial connections with this product and these website.Shan

Serrapeptaseâ„¢

Insect-Derived Enzyme Fights Inflammation

_http://www.enerex.ca/articles/serrapeptase.htm_

(http://www.enerex.ca/articles/serrapeptase.htm)

Our bodies have a love-hate relationship with inflammation. On the one hand,

inflammation is a natural response, necessary to protect the body from

invading organisms. On the other hand, inflammation can limit joint function,

and

destroy bone, cartilage and other articular structures.

An elusive goal of scientists and physicians has been to find a

side-effect-free substance to reduce the pain and inflammation associated with

fibrocystic breast disease, rheumatoid arthritis, idiopathic edema, carpal

tunnel

syndrome and post-operative swelling. It appears that the search may be nearing

an

end, thanks to an enzyme Serrapeptaseâ„¢ produced by the larval form of the

silk moth.

Serrapeptaseâ„¢ is an enzyme that is produced in the intestines of silk worms

to break down cocoon walls. This enzyme is proving to be a superior

alternative to the non-steroidal anti-inflammatory agents (NSAIDs)

traditionally used

to treat rheumatoid arthritis and osteoarthritis. Its uses have also been

extended to the treatment of chronic sinusitis and postoperative inflammation,

and some researchers believe the substance can play an important role in

arterial plaque prevention and removal.

Harmful Effects of NSAIDs

NSAIDs, which include aspirin, ibuprofen, salicylates, and naproxen, are

among the most commonly prescribed medications for inflammation resulting from

rheumatoid arthritis, joint conditions, osteoarthritis, gouty arthritis, joint

and muscle discomfort associated with systemic lupus erythematosus, and

other musculoskeletal disorders.(1) In some cases, this overeliance on NSAIDs

has

proved deadly. Annually, 76,000 people are hospitalized from NSAID-induced

gastrointestinal complications. The American Medical Association estimates

that from 50-80 percent of those hospitalized for gastrointestinal bleeding are

taking some form of NSAIDs. At this stage in the medication-induced

bleeding, there is a ten percent chance of fatality.(2)

NSAIDs lethal effects result from the inhibition of the biosynthesis of

prostaglandins. NSAIDs block cyclo-oxygenase, the enzyme responsible for

catalyzing the reactions of arachidonic acid to endoperoxide compounds. This

process

results in the inhibition of gastric prostaglandin E, a hormone which

protects the lining of the stomach from acid. After prolonged and frequent

ingestion

of NSAIDs, the stomach remains defenseless and at increased susceptibility

to ulcers.(3-4) If an ulcer erodes into a blood vessel, bleeding results. An

ulcer can destroy part of the stomach and duodenal walls, leaving a gap that

requires immediate surgery.

In one study, 1,826 osteoarthritis or rheumatoid arthritis patients who had

been taking NSAIDs for six months or more and who had been unable to tolerate

continuous NSAID use because of adverse gastrointestinal symptoms were

examined endoscopically for gastroduodenal lesions and ulcers. Clinically

significant gastroduodenal lesions were found in 37.1 percent of the patients.

Of

those, 24 percent had ulcers. The prevalence of gastroduodenal ulcers increased

with age, duration of osteoarthritis, and duration of current NSAID use. The

authors of the study wrote: " These results provide further endoscopic

confirmation of the association between NSAID use and gastroduodenal lesions

and

ulcers and support the contention that safer treatment alternatives to

conventional NSAIDs are required. " (5)

That advice is particularly wise in light of the other effects NSAIDs have

on the gastrointestinal tract. In one group of 312 NSAID takers, 20 percent

had levels of inflammation comparable to that previously reported in patients

with inflammatory bowel disease.(6) Besides damaging the gastrointestinal

tract, NSAIDs also interfere with and suppress bone repair and remodeling. One

paper presented data obtained over a 12-year period, and outlined the effects

of NSAIDs on the matrix synthesis and turnover in 650 arthritic and 180

non-arthritic human cartilages. The study showed that one category of NSAIDs

that

includes Naproxen, ibuprofen, indomethacin, and nimezulide significantly

inhibited matrix synthesis and had toxic effects on cartilage metabolism.(7)

Thus, it appears that the drugs many patients take to relieve their arthritic

pains actually contributes to further destruction of their joints!

Additionally, NSAIDs have been shown to interfere with patients' sleep

patterns. One study of 37 male and female subjects at the sleep laboratory at

Bowling Green State University in Ohio demonstrated that aspirin and ibuprofen,

in comparison to a placebo, increased the number of awakenings and the

percentage of time spent awake. The drugs also decreased sleep efficiency, and

delayed the onset of the deeper stages of sleep.(8)

Even insulin secretion is affected by NSAIDs. Neonatal rat pancreatic cells

were examined partly to determine the effects of insulin secretion caused by

prostaglandin E (PGE) and drugs that inhibit its synthesis—i.e. NSAIDs. Two

NSAIDs, sodium salicylate (aspirin) and ibuprofen, at drug concentrations

similar to those achieved therapeutically in humans, inhibited PGE synthesis up

to 70-80 percent. Augmented insulin secretion accompanied the PGE inhibition.

Both drugs shifted the glucose-insulin response curves to the left at low

glucose concentrations and augmented maximal insulin release at high glucose

concentrations.(9)

Other NSAID-induced side effects include kidney damage, blood dyscrasias and

cardiovascular effects, complication of antihypertensive therapies involving

diuretics or beta-adrenoceptor blockade, and adverse effects in patients

with heart failure and cirrhosis.(10) In one instance, a woman treated for

rheumatoid arthritis with the NSAID sulindac developed gallstones composed of

sulindac metabolites.(11)

Interestingly, NSAIDs have also induced adverse psychiatric reactions. Five

psychiatric outpatients—two with major depressive disorders, one with a

bipolar disorder, one with a schizophrenic disorder and one with an anxiety

disorder—were treated with NSAIDs due to rheumatoid arthritis,

osteoarthritis, or

other painful neuromuscular conditions. All five patients developed moderate

to severe depression. Three patients became paranoid, and four either

attempted or considered suicide. These psychiatric symptoms disappeared once

the

patients stopped taking NSAIDs. When the patients re-started the drugs, the

symptoms returned.(12)

NSAID s Roulette

Due to the detrimental effects of NSAIDs on the body, most physicians resort

to a game of " NSAID musical-chairs, " taking a patient off one NSAID as soon

as side effects become evident or the drug stops working, then treating the

patient with another of the 10 most widely prescribed propionic acid-derived

NSAIDs.

To provide a more consistent form of treatment, researchers have long

searched for a side-effect free anti-inflammatory agent. Researchers have

recently

focused on selective cyclo-oxygenase (COX-2) inhibitors, more precise

versions of NSAIDs. Whereas previous NSAIDs reduced inflammation by inhibiting

all

cyclo-oxygenase activity, these new selective COX-2 inhibitors differentiate

between the two forms of COX: COX-1 appears to regulate many normal physiolog

ic functions and COX-2 mediates the inflammatory response. These selective

inhibitors are believed to reduce inflammation without influencing normal

physiologic functions by inhibiting only COX-2. By leaving COX-1 alone, the

selective inhibitors result in fewer gastrointestinal side effects.

At first glance, these COX-2 inhibitors look like the solution to NSAID

complications. Upon further inspection, however, celecoxib, a highly selective

COX-2 inhibitor, can cause headaches, change in bowel habits, abdominal

discomfort and dizziness in osteoarthritis patients. Fewer adverse effects are

reported in rheumatoid arthritis patients, but because the drug is metabolized

in

the liver by cytochrome P-450 isozyme CYP2C9, serious drug interactions are

possible. Fung and colleagues pointed out that more clinical studies are

needed before the selective COX-2 inhibitors are put into widespread use.(13)

Another new drug, Enbrel, initially showed promise of treating the pain

associated with rheumatoid arthritis. Currently, however, the FDA is advising

physicians about safety concerns of the new drug. Thirty of the 25,000 patients

treated with Enbrel since the drug's approval have developed serious

infections, including sepsis. Several of those patients died as a result of the

infections. Those at greatest risk when taking Enbrel appear to be patients

with a

history of chronic or recurrent infections, pre-existing infections,

diabetes, or other conditions making them more susceptible to infection.(14)

The potentially lethal side effects associated with NSAIDs and other drugs

indicate that a superior anti-inflammatory substance is needed.

A Natural Anti-Inflammatory

Serrapeptaseâ„¢, also known as Serratia peptidase, is a proteolytic enzyme

isolated from the non-pathogenic enterobacteria Serratia E15. When consumed in

unprotected tablets or capsules, the enzyme is destroyed by acid in the

stomach. However, enterically-coated tablets enable the enzyme to pass through

the

stomach unchanged, and be absorbed in the intestine. Serrapeptaseâ„¢ is found

in negligible amounts in the urine, suggesting that it is transported

directly from the intestine into the bloodstream.(15,16)

Clinical studies show that Serrapeptaseâ„¢ induces fibrinolytic,

anti-inflammatory and anti-edemic (prevents swelling and fluid retention)

activity in a

number of tissues, and that its anti-inflammatory effects are superior to other

proteolytic enzymes.(17)

Besides reducing inflammation, one of Serrapeptaseâ„¢'s most profound benefits

is reduction of pain, due to its ability to block the release of

pain-inducing amines from inflamed tissues.(18) Physicians throughout Europe

and Asia

have recognized the anti-inflammatory and pain-blocking benefits of this

naturally occurring substance and are using it in treatment as an alternative

to

salicylates, ibuprofen and other NSAIDs.(19)

In Germany and other European countries, Serrapeptaseâ„¢ is a common treatment

for inflammatory and traumatic swellings, and much of the research that

exists on this substance is of European origin. One double-blind study was

conducted by German researchers to determine the effect of Serrapeptaseâ„¢ on

post-operative swelling and pain. This study involved sixty-six patients who

were

treated surgically for fresh rupture of the lateral collateral ligament of the

knee. On the third post-operative day, the group receiving Serrapeptaseâ„¢

exhibited a 50 percent reduction of swelling, compared to the controls. The

patients receiving Serrapeptaseâ„¢ also became more rapidly pain-free than the

controls, and by the tenth day, the pain had disappeared completely.(20)

Cystic Breast Disease

Serrapeptaseâ„¢ has also been used in the successful treatment of fibrocystic

breast disease. In a double-blind study, 70 patients complaining of breast

engorgement randomly were divided into a treatment group and a placebo group.

Serrapeptaseâ„¢ was superior to the placebo for improvement of breast pain,

breast swelling and induration (firmness). 85.7 percent of the patients

receiving

Serrapeptaseâ„¢ reported moderate to marked improvement. No adverse reactions

to Serrapeptaseâ„¢ were reported and the researchers concluded that

" Serrapeptaseâ„¢ is a safe and effective method for the treatment of breast

engorgement. " (21,22)

Serrapeptaseâ„¢ and Sinusitis

Due to its inflammatory properties, Serrapeptaseâ„¢ has been shown in clinical

studies to benefit chronic sinusitis sufferers. In this condition, the mucus

in patients’ nasal cavities is thickened and hypersecreted. This thickening

causes mucus to be expelled less frequently. Japanese researchers evaluated

the effects of serratiopeptidase (30 mg/day orally for four weeks) on the

elasticity and viscosity of the nasal mucus in adult patients with chronic

sinusitis. Serratiopeptidase reduced the viscosity of the mucus, improving the

elimination of bronchopulmonary secretions.(23)

Other clinical trials support Serrapeptaseâ„¢'s ability to relieve the

problems associated with chronic sinusitis. In one study, 140 patients with

acute or

chronic ear, nose and throat pathologies were evaluated with either a

placebo or the active serratia peptidase. Patients taking the Serrapeptaseâ„¢

experienced a significant reduction in severity of pain, amount of secretion,

purulence of secretions, difficulty in swallowing, nasal dysphonia, nasal

obstruction, anosmia, and body temperature after three to four days and at the

end of

treatment. Patients suffering from laryngitis, catarrhal rhinopharyngitis and

sinusitis who were treated with Serrapeptaseâ„¢ experienced a significant and

rapid improvement of symptoms after 3-4 days. Physicians assessed efficacy of

treatment as excellent or good for 97.3 percent of patients treated with

Serrapeptaseâ„¢ compared with only 21.9 percent of those treated with a

placebo.(24)

Respiratory diseases are characterized by increased production of a more

dense mucus modified in viscosity and elasticity. Traditionally, in respiratory

diseases, muco-active drugs are prescribed to reestablish the physicochemical

characteristics of the mucus in order to restore respiratory function. Some

of these drugs, however, cause a functional depletion of mucus, whereas

Serrapeptaseâ„¢ alters the elasticity of mucus without depleting it.(25,27)

A powerful agent by itself, Serrapeptaseâ„¢ teamed with antibiotics delivers

increased concentrations of the antimicrobial agent to the site of the

infection. Bacteria often endure a process called biofilm formation, which

results

in resistance to antimicrobial agents. In an attempt to prevent this bacterial

immunity, researchers have experimented with various means of inhibiting

biofilm-embedded bacteria. Their search may have ended with Serrapeptaseâ„¢.

One

study conducted by Italian researchers suggests that proteolytic enzymes

could significantly enhance the activities of antibiotics against biofilms.

Antibiotic susceptibility tests showed that serratiopeptidase greatly enhances

the

activity of the antibiotic, ofloxacin, and that it can inhibit biofilm

formation.(28)

Another double-blind randomized study evaluated the effects of administering

the antibiotic cephalexin in conjunction with Serrapeptaseâ„¢ or a placebo to

93 patients suffering from either perennial rhinitis, chronic rhinitis with

sinusitis or chronic relapsing bronchitis. The serratia peptidase treated

group experienced significant improvement in rhinorrhea, nasal stuffiness,

coryza

and improvement of the para-nasal sinus shadows.(29)

Researchers witnessed equally impressive results in the treatment of

infections in lung cancer patients undergoing thoracotomy. Serrapeptaseâ„¢ and

cefotiam, an antibiotic with a broad spectrum of activity against both

Gram-positive

and Gram-negative microorganisms, were administered to 35 thoracotomy

patients with lung cancer. The patients were divided into two groups. A single

dose

of cefotiam was administered to the 17 subjects in Group I. The 18 subjects

in Group II received a combination of Cefotiam and Serrapeptaseâ„¢. The level

of the antibiotic in the tissues versus the blood was significantly higher in

the Serrapeptaseâ„¢ group than the single dose group.(30)

Cardiovascular Implications

Hans A. Nieper, M.D., an internist from Hannover, Germany, studied the

effects of Serrapeptaseâ„¢ on plaque accumulations in the arteries. The

formation of

plaque involves deposits of fatty substances, cholesterol, cellular waste

products, calcium and fibrin (a clotting material in the blood) on the inner

lining of the arteries. Excessive plaque results in partial or complete

blockage of the blood's flow through an artery, resulting in arteriosclerosis,

or

hardening of the arteries, and an ensuing stroke or heart attack. The evidence

to support Serrapeptaseâ„¢'s role in preventing plaque build-up is anecdotal.

Still, further studies are called for in this area as Nieper's research

indicated that the protein-dissolving action of Serrapeptaseâ„¢ will gradually

break

down atherosclerotic plaques.(31)

Conclusion

Regardless of whether Serrapeptaseâ„¢ is used for inflammatory diseases or to

prevent plaque build up on the arteries, it is well-tolerated. Due to its

lack of side effects and anti-inflammatory capabilities, Serrapeptaseâ„¢ is a

logical choice to replace harmful NSAIDs. Thanks to the tiny larvae of the silk

moth, researchers have taken a large step toward finding relief for

inflammatory disease sufferers.

References

1. Raskin JB. Gastrointestinal effects of nonsteroidal

anti-inflammatory therapy. Am J Med. 1999; 106 (5B):3S-12S.

2. No author listed. Regular Use of Pain Relievers Can Have Dangerous

Results. Kaleidoscope Interactive News, American Medical Association media

briefing. July 24, 1997.

3. Fung HB, Kirschenbaum, HL. Selective cyclooxygenase-2 inhibitors for

the treatment of arthritis. Clin Ther. 1999; 21(7):1131-57.

4. Geis GS. Update on clinical developments with celecoxib, a new

specific COX-2 inhibitor: what can we expect? Scand J Rheumatol Suppl. 1999;

109:31-7.

5. Cheatum DE, Arvanitakis C, Gumpel M, Stead H, Geis GS. An endoscopic

study of gastroduodenal lesions induced by nonsteroidal anti-inflammatory

drugs. Clin Ther. 1999; 21(6):992-1003.

6. Tibble JA, Sigthorsson G, Foster R, Scott D, Fagerhol MK, Roseth A,

Bjarnason I. High prevalence of NSAID enteropathy as shown by a simple faecal

test. Gut. 1999; 45(3):362-6.

7. Dingle JT. The effects of NSAID on the matrix of human articular

cartilages. Z Rheumatol. 1999; 58(3):125-9.

8. Murphy PJ, Badia P, Myers BL, Boecker MR, Wright KP Jr. Nonsteroidal

anti-inflammatory drugs affect normal sleep patterns in humans. Physiol

Behav. 1994; 55(6):1063-6.

9. Metz SA, Robertson RP, Fujimoto WY. Inhibition of prostaglandin E

synthesis augments glucose-induced insulin secretion in cultured pancreas.

Diabetes. 1981; 30(7):551-7.

10. Raskin JB. Gastrointestinal effects of nonsteroidal

anti-inflammatory therapy. Am J Med. 1999; 106 (5B):3S-12S.

11. Tokumine F, Sunagawa T, Shiohira Y, Nakamoto T, Miyazato F, Muto Y.

Drug-associated cholelithiasis: a case of sulindac stone formation and the

incorporation of sulindac metabolites into the gallstones. Am J Gastroenterol.

1999;94(8):2285-8.

12. Jiang HK, Chang DM. Non-steroidal anti-inflammatory drugs with

adverse psychiatric reactions: five case reports. Clin Rheumatol.

1999;18(4):339-45.

13. Fung HB, Kirschenbaum, HL. Selective cyclooxygenase-2 inhibitors for

the treatment of arthritis. Clin Ther. 1999; 21(7):1131-57.

14. FDA MedWatch: The FDA Medical Products Reporting Program. May 12,

1999. FDA Talk Paper.

15. Moriya N, Nakata M, Nakamura M, Takaoka M, Iwasa S, Kato K, Kakinuma

A. Intestinal absorption of Serrapeptaseâ„¢ (TSP) in rats. Biotechnol Appl

Biochem. 1994; 20(Pt1):101-8.

16. Miyata, K. Intestinal absorption of Serratia Peptidase. J Appl

Biochem. 1980;2:111-16.

17. 17. Mazzone A, Catalani M, Costanzo M, Drusian A, Mandoli A, Russo

S, Guarini E, Vesperini G. 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(5):379-88.

18. 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(5):379-88.

19. Aso T et al. Breast engorgement and its treatment: Clinical effects

of Danzen an anti-inflammatory enzyme preparation. The world of Obstetrics

and Gynecology (Japanese). 1981; 33:371-9.

20. Esch PM, Gerngross H, Fabian A. Reduction of postoperative swelling.

Objective measurement of swelling of the upper ankle joint in treatment with

Serrapeptaseâ„¢-a prospective study (German). Fortschr Med. 1989;107(4):67-8,

71-2.

21. Kee WH, Tan SL, Lee V, Salmon YM. The treatment of breast

engorgement with Serrapeptaseâ„¢ (Danzen): a randomized double-blind controlled

trial.

Singapore Med J. 1989;30(1):48-54.

22. Aso T et al. Breast engorgement and its treatment: Clinical effects

of Danzen an anti-inflammatory enzyme preparation. The world of Obstetrics

and Gynecology (Japanese). 1981; 33:371-9.

23. Majima Y, Inagaki M, Hirata K, Takeuchi K, Morishita A, Sakakura Y.

The effect of an orally administered proteolytic enzyme on the elasticity and

viscosity of nasal mucus. Arch Otorhinolaryngol. 1988;244(6):355-9.

24. 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(5):379-88.

25. Tomoda K, and Miyatam K. Some information on the composition of

trachael secretions before and after the administration of Danzen. Exper Ther.

1972; 477:9-16.

26. Kase Y, et al. A new method for evaluating mucolytic expectorant

activity and its application to two proteolytic enzymes, serratiopeptidase and

seaprose. Arznelrnitteltorachung. 1982; 32:374-378.

27. Marriott C. Modification in the rheological properties of mucus by

drugs. Adv Exp Med Biol. 1982; 144:75-84.

28. Selan L, Berlutti F, Passariello C, Comodi-Ballanti MR, Thaller MC.

Proteolytic enzymes: a new treatment strategy for prosthetic infections?

Antimicrob Agents Chemother. 1993; 37(12):2618-21.

29. Perna L. Osservazionl Clniche sui traitamento in osppio cleco con

Serratio peptidasl nella neifre perenna naila ninite cronica nacutizzata con

sinusopattia, nella bronchia cronica nacutizzata. Rlv Pat Clin Tuberc Penumol.

1985; 56:509-516.

30. Koyama A, Mori J, Tokuda H, Waku M, Anno H, Katayama T, Murakami K,

Komatsu H, Hirata M, Arai T, et al. Augmentation by Serrapeptaseâ„¢ of tissue

permeation by cefotiam (Japanese). Jpn J Antibiot. 1986; 39(3):761-71.

31. Brewer Science Library website. 1999.

 

RELATED INFO

_http://www.enerex.ca/products/serrapeptase_rx.htm_

(http://www.enerex.ca/products/serrapeptase_rx.htm)

 

_Download Media Player_

(http://www.microsoft.com/windows/windowsmedia/default.aspx) and Listen to the

Radio Show Interview _

Part I_ (http://www.enerex.ca/audio/01%20Track%201.wma) , _Part II_

(http://www.enerex.ca/audio/02%20Track%202.wma) on Serrapeptase Rxâ„¢

Read Serrapeptase News Letter

_Issue I_ (http://www.enerex.ca/bulletin/serrapeptase_newsletter_2003.pdf) ,

_Issue II_ (http://www.enerex.ca/bulletin/serrapeptase_newsletter_2004.pdf) ,

_Issue III_ (http://www.enerex.ca/bulletin/Serrapeptase_newsletter_2005.pdf)

_See research articles_

(http://www.enerex.ca/bulletin/research_articles_serrapeptase_rx.htm)

_View Testimonials_ (http://www.enerex.ca/testimonials.htm#view_testimonials)

Serrapeptase digests non-living tissue, blood clots, cysts, arterial plaque

and inflammation in all forms. The late German physician, Dr. Hans Nieper,

used Serrapeptase to treat arterial blockage in his coronary patients.

Serrapeptase protects against stroke and is reportedly more effective and

quicker

than EDTA chelation treatments in removing arterial plaque. He also reports

that

Serrapeptase dissolves blood clots and causes varicose veins to shrink or

diminish.

Dosage:

Treatment of Inflammation/Pain:

30,000 I.U. - 1 capsule three times per day on an empty stomach or as

directed by a health professional.

60,000 I.U. - 1 capsule, twice per day on an empty stomach or as directed by

a health professional.

90,000 I.U. - 1 caplet, once per day on an empty stomach or as directed by a

health professional.

Treatment for arterial blockage:

30,000 I.U. - 1 capsule three times per day on an empty stomach. Up to 12

capsules per day in divided dosages in acute need. Take the highest dose for 7

days until the symptoms decrease substantially and then reduce to 1-2 per

day.

60,000 I.U. - 1 capsule twice per day on an empty stomach. Up to 6 capsules

per day in divided dosages in acute need. Take the highest dose for 7 days

until the symptoms decrease substantially and then reduce to 1 per day.

90,000 I.U. - 1 caplet twice per day on an empty stomach. Up to 4 caplets

per day in divided dosages in acute need. Take the highest dose for 7 days

until the symptoms decrease substantially and then reduce to 1 per day.

Description

Serrapeptase: A Natural Anti-Inflammatory

Serrapeptase, also known as Serratia Peptidase, is a proteolytic enzyme

isolated from the non-pathogenic enterobacteria Serratia E15. When consumed in

unprotected tablets or capsules, the enzyme is destroyed by acid in the

stomach. However, our special enteric-coated NPcapsTM or Caplets enable the

enzyme

to pass through the stomach unchanged, and be absorbed in the intestine.

Serrapeptase is found in negligible amounts in the urine, suggesting that it is

transported directly from the intestine into the bloodstream.

Clinical studies show that Serrapeptase induces fibrinolytic,

anti-inflammatory and anti-edemic (prevents swelling and fluid retention)

activity in a

number of tissues, and that its anti-inflammatory effects are superior to other

proteolytic enzymes.

Besides reducing inflammation, one of Serrapeptase's most profound benefits

is reduction of pain, due to its ability to block the release of

pain-inducing amines from inflamed tissues. Physicians throughout Asia and

Europe have

recognized the anti-inflammatory and pain-blocking benefits of this naturally

occurring substance and are using it in treatment as an alternative to

salicylates, ibuprofen and other NSAIDs.

In Germany and other European countries, Serrapeptase is a common treatment

for inflammatory and traumatic swellings, and much of the research that

exists on this substance is of European origin. One double-blind study was

conducted by German researchers to determine the effect of Serrapeptase on

post-operative swelling and pain. This study involved sixty-six patients who

were

treated surgically for fresh rupture of the lateral collateral ligament of the

knee. On the third post-operative day, the group receiving Serrapeptase

exhibited a 50 percent reduction of swelling, compared to the controls. The

patients

receiving Serrapeptase also became more rapidly pain-free than the controls,

and by the tenth day, the pain had disappeared completely.

Serrapeptase is thought to work in three ways:

 

* It may reduce inflammation by thinning the fluids formed from

injury, and facilitating the fluid's drainage. This in turn, also speeds tissue

repair.

* It may help alleviate pain by inhibiting the release of

pain-inducing amines called bradykinin.

* It may enhance cardiovascular health by breaking down the protein

by-products of blood coagulation called fibrin. Conveniently, Serrapeptase is

able to dissolve the fibrin and other dead or damaged tissue without harming

living tissue. This could enable the dissolution of atherosclerotic plaques

without causing any harm to the inside of the arteries.

 

 

Serrapeptase is being used as a highly effective support to anti-biotics in

many countries. It treats inflammatory disorders by not only fighting

inflammation, but also by relieving pain and swelling, improving recovery time

and

stimulating the immune system. Serrapeptase has a " scavenging " effect. It

helps remove the heavy metals through which the body releases toxins and hence

modulates the immune system, addresses hormonal imbalances and speeds wound and

tissue repair time.

Serrapeptase Rx is provided in enteric coated vegetable based

microcrystalline cellulose capsules or caplets. Derived from a controlled

fermentation of

the bacterial strain, Serratia sp. T-1 secretes this enzyme in medium.

Successive purification steps, for example micro-filtration, ammonium

sulphyhate,

fractionation, DEAE-Cellulase column chromatography, gel filtration followed by

repeat aseptic filtration and freeze drying yields this product in a highly

purified form, enabling it to be used for medicinal purpose. The

enteric-coated microcrystalline capsules protect the enzyme from inactivation

in the

acidic medium of the stomach. Serapeptase is a stronger saseinolytic

(fibrinolytic) agent than any other known alkaline or neutral protease such as

bromelain

or pronase.

Note: Some manufacturers use 'enteric coated' enzyme in a non-enteric coated

capsule. This is not as effective as using an enteric coated capsule or

caplet as some of the enzyme will be denatured by stomach acid. Enerex's

enteric

coated capsules and caplets ensure that the entire enzyme is delivered to the

small intestine for maximum absorption.

Conclusion

Regardless of whether Serrapeptase is used for inflammatory diseases or to

prevent plaque build up on the arteries, it is well-tolerated. Due to its lack

of side effects and anti-inflammatory capabilities, Serrapeptase is a

logical choice to replace harmful NSAIDs. Thanks to the tiny larvae of the silk

moth, researchers have taken a large step toward finding relief for

inflammatory

disease sufferers.