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» LymeNet Flash » Questions and Discussion » Medical Questions » Elastase and sodium

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Author Topic: Elastase and sodium
Marnie
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Elastase and Na (sodium)

What is elastase?

An enzyme, a protein, that breaks down elastin connective tissue. It is the body's normal response to injury and inflammation. It breaks down proteins so that they can be removed and recycled by the body, but if its action is not regulated, it will begin to break down healthy tissue.

Where is it?

In human leukocytes (white blood cells) and in the pancreas.

What causes it to be triggered?

In the lung, air pollutants (ie., toxins) stimulate the production.

What damage does it do?

In CFS patients mycoplasm infections are frequently seen. The phagocytic response mycoplasmas induce in monocytes, neutrophils and T-cells results in increased production of a protease, elastase, which has been implicated in Rnase L fragmentation. Oh, oh...not good!

What is the body's protective means?

Alpha -1 antitrypsin (AAT), a protein that is produced in the liver and released into the blood stream works to protect the lungs from elastase.

What role does salt play?

The activity of elastase is significantly affected by salts...NaCl and KCL cause a 50% INHIBITION at 50-70 mM and copper sulfate 50% INHIBITION at 0.01 mM.

The above research is contrary to what Gi Gi posted:

``The high salt intake PROMOTES the activity of the enzyme elastase, which has a strong anti-spirochetal effect.''

Ahhhhhh. The difficulty with research...one resource says one thing, another says the opposite! This does not help when trying to understand what is happening.

Who else has elastase problems?

Large numbers of neutrophils with UNOPPOSED neutrophil elastase (NE) proteolytic activity are found in the lower respiratory tract secretions from most patients with cystic fibrosis (CF).

What else plays a part (you get an ``A'' if you already figured out I was going to discuss Mg)?

``Magnesium enhances human pancreatic elastase DIGESTION of elastin.'' PMID: 8292494

How does Mg do this?

It is speculated the antagonism of Mg to Ca plays a fundamental role in the maintenance of elasticity. A decrease in Ca = increase in elasticity. If the opposite is happening then it would follow an increase in Ca = LESS elasticity. Not healthy.

Can this knowledge by applied another way?

Yes. High salinity (salt) has been shown to have keratolytic effects, softening the horny layer of the skin to allow penetration of minerals and magnesium. It also elutes (extracts) a high amount of the human leukocyte elastase...at least as a psoriasis (horrible skin disease) treatment. High salt increases the photosensitivity of the skin and thus promotes photo-therapy for skin problems.

The association between high Mg concentration and anit-inflammatory effects has been demonstrated in animal models. It acts as a surface disinfectant and stimulates blood flow within the skin.

(Hence the advantage of adding baking soda - Na bicarb. To Epsom Salt baths to promote the skin to absorb more Mg.)

What else did I find?

A significant increase in urinary and pancreatic TAP (trypsinogen activation peptide) as well as INCREASED TRYPSIN and ELASTASE activities were found in animals fed the Mg depleted diet.

Documentation:
http://www.nutri-notes.com/novdec97_simple.htm
http://www.serva.de/products/sheets/20929.shtml
http://ajrccm.atsjournals.org/cgi/content/full/159/1/258
http://www.mavena.com/english/3clinic1.htm
http://www.kats-korner.com/health/health.html
http://www.phoenix-cfs.org/The%20SITE/IntracellularImmunityCFS04.htm http://www.labtestsonline.org/understanding/analytes/alpha1_antitrypsin/sample.html
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ProduktNr=224334&Ausgabe=229623&ArtikelNr=73947
http://www.labtestsonline.org/understanding/analytes/alpha1_antitrypsin/sample.html
http://www.camlt.org/DL_web/956_patty_panc.html
http://www.fibroandfatigue.com/clinical.htm
http://www.alcor.org/printable.cgi?fname=Library%2Fhtml%2Fstandby7.html
http://64.233.167.104/search?q=cache:Xm1xeU1HHAEJ:www.cmj.org/information/full.asp%3Fid%3D1357++sodium+elastase+inhibitor&hl=en
http://www.fasebj.org/cgi/content/full/14/5/805 (regarding NO - nitric oxide)
http://www.serva.de/products/sheets/20929.shtml

PMID: 10417158



Posts: 9426 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
Marnie
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To the top for the others who are, like me, trying to piece this all together...what is Bb doing to us and how can we naturally combat it (without drug "side effects")? Support our own defenses.

Posts: 9426 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
lymed04
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I'm new Marnie so excuse me if I ask a dumb ?

Do you only advocate the use of antibiotics in early stage LD and IV mag along with nutrition and supplements after?

Im interested.

Teddi


Posts: 16 | From The Land of Pleasant Living | Registered: Jun 2005  |  IP: Logged | Report this post to a Moderator
GiGi
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Marnie, How about this one:
This is my doctor's explanation regarding the ORAL SALT THERAPY that he handed to me after I had been asking too many questions that time allowed to answer. This is from a researcher in the field and I as a lay person understand it.

"Certain while blood cells display several distinct mechanisms that may be employed for the purpose of killing invading microorganisms. One of these deserves particular attention in relation to killing the causative agent of Lyme Disease, namely, the spirochete Borrelia burgdorferi.

Neutrophils (a class of WBC) contain two essentially different types of storage granules, peroxidase-positive granules and peroxidase-negative granules. Peroxidase-positive granules contain myeloperoxidase, an enzyme that uses hypochlorous acid in conjunction with hydrogen peroxide, providing a source of nascent (atomic) oxygen for the purpose of killing invading microorganisms.

Peroxidase-negative granules contain a family of large polypeptides known as cathelicidins or, in humans, hCAP-18. A segment of this larger or precursor protein, also known as Bacteriacidal Permeability-Increasing Protein is proteolytically removed by the enzyme e l a s t a s e found in peroxidase-positive gransules. The more well-known substrate of e l a s t a s e is the elastic protein elastin, found in skin and other tissues requiring elasticity. By incorporating elastase inhibitors into skin creams, attempts are made to inhibit the activity of this enzyme, thereby decreasing the aging of skin. In Lyme therapy there is an advantate to increasing the activity of this enzyme, thereby stimulating the natural antimicrobial system. These short peptides, ranging from 12 to 100 amino acids, have the ability to assemble into larger units that form pores in the membrane surrounding microorganisms, thereby increasing the permeability of those membranes. In humans, one of these antimicrobial peptides has been dubbed LL-37.

Both of these proteins, the cathelicidin and e l a s t a s e, meet in the phagocytic vacuole, the cytoplasmic chamber in which resides the phagocytized microorganism. Within this chamber, e l a s t a s e removes a short peptide capable of forming a molecular pore in the surface membrane of the microorganisms. The pore formed from a group of the cathelicidins allows the efflux of potassium ions from the orgnism, resulting in swelling and eventual lysis.

Research has shown that, of all the proteins in neutrophil granules, the only protein capable of releasing the cathelicidin active peptide is e l a s t a s e . It has been demonstrated that the activity of elastase is enhanced by an increased salt concentreation. Through oral salt (12 g per day) combined with large doses of vitamin C, the indirect killing activity of elastase is dramatically increased.

Increasing the sodium concentration surrounding the spirochete may also facilitate cell killing by allowing sodium ions to enter the spirochete through the pore created by the antimicrobial peptide. An increased intracellular sodium concentration, combined with a decreased potassium concentration, leads to spirochete death. The exact mechanism by which the human cathelicidin LL-37 kills Bb is unknown."

Add to this the KMT22 with its spiked inhibitory frequencies including the most recently discovered ones, at the right
amperage and voltage (biological range)!

Take care.

Snake Oil that works -


Posts: 9834 | From Washington State | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
Marnie
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Na-Vitamin C lots of questions

The Na-Vitamin C treatment as I understand it, ``promotes the actions of elastase'' in neutrophils.

Since many researchers are thinking elastase should be reduced, you should understand my confusion. Why does it need to be promoted?

In cystic fibrosis patients, they have a lot of sodium channels and too much elastase. In fact, they are trying sodium channel blockers with some success to reduce the inflammation.

Is the increase in sodium channels a ``protective'' attempt? Since:

The elastolytic activity of elastase is significantly affected by salts: NaCl and KCl cause 50% inhibition at 50 - 70 mM and copper sulfate 50% inhibition at 0.01 mM, while millimolar concentrations of zinc, manganese, cobalt, magnesium or calcium had no effect (1).
http://www.serva.de/products/sheets/20929.shtml

And Na (sodium)

It also elutes a high amount of the harmful human leukocyte elastase from psoriatic lesions.
http://www.mavena.com/english/3clinic1.htm

So high salinity removes elastase from (skin) cells?

Does it remove elastase from neutrophils, leaving behind the most valuable component - Bacteriacidal Permeability-Increasing Protein?

Elastase triggers TNF alpha.

Let me see if I understand how this treatment is supposed to work:

Neutrophils, the most numerous of our WBCs, contain 2 lethal ``packages''... peroxidase-positive granules and peroxidase-negative granules.

The negative ones contain cathelicidins which contain Bacteriacidal Permeability-Increasing Protein.

Elastase inside peroxidase positive granules helps to remove bacteriacidal permeability increasing protein from the negative granules.

Inside neutrophils, elastase causes the release of the bacteriacidal permeability increasing protein which poke holes in the cell wall of the keet and if increased sodium is present, potassium leaves, the keet swells up and blows up.

Now, the intracellular levels of sodium and vitamin C is elevated in, I assume, all the cells...ones that are not infected also. What is that impact?

Does this combo - Na and vitamin C also cause the release of elastase from pancreatic and other cells also? Mast cells? Macrophages?

What else does increasing elastase release do?

It is concluded that elastase released [EC 3.4.21.37] by neutrophils is the most relevant enzyme for cartilage degradation. Copyright 2002 Elsevier Science (USA).

PMID: 12020136

Does vitamin C prevent the above?

``Activated neutrophils elaborate elastase that, if unchecked by the proteinase inhibitor, can cause destruction of lung tissue.

Furthermore. they release oxygen radicals and chlorinated oxidants that can oxidize the methionine at the active site of alpha-1-antitrypsin. Such oxidation decreases the rate of association of the inhibitor with neutrophil elastase 2000-fold, markedly reducing its ability to inhibit elastase activity. The unopposed elastase activity is thought to cause destruction of the lung.''

I suppose the thought is to use vitamin C to prevent the oxidizing problems and protect the lungs.

Okay, any problems with large doses of vitamin C?

Vitamin C enhances iron absorption and is contraindicated in cases of iron overload.

Sudden discontinuation of high dosages can cause rebound scurvy so that supplementation should be tapered gradually over several days to weeks.

Vitamin C enhances aluminum absorption and should not be taken with aluminum-containing substances especially in the presence of renal insufficiency.
http://www.farmacopia.net/nutrient_danger.html

Many people do not realize that man is one of the few mammals which does not manufacture its own supply of vitamin C, also known as ascorbic acid. The rates of production by a number of different animals like the cat, dog and goat have been measured. The heavier the animal the more vitamin C it produces.

However, a 154-pound man would need to produce between 1.75 and 3.50 grams per day to keep up with the other animals. There are experts who feel that taking more than 140 milligrams per day of this vitamin is wasteful because, for many people, more than this amount results in urine containing the vitamin--``Expensive Urine.''

Loading tests have shown that 20 to 25 percent of a 1 gram per day dose shows up in the urine within 6 hours. When much larger doses are taken, as much as 62 percent can show up within hours.

Generally speaking, the recommended daily allowances have been based on the amounts needed to prevent scurvy in healthy young men. But healthy young men represent only a small part of the total population. To my knowledge, no one has determined how much of any vitamin is required by unhealthy old men--or women.

The results of a test involving 88 patients, half being schizophrenic, are reported in Dr. Linus Pauling's book How to live Longer and Feel Better. Each was given 1.75 grams of vitamin C by mouth. During the following 6 hours each patient's urine was collected and then analyzed.

The amounts excreted varied from 2 percent to 40 percent of the amount ingested. The mental patients excreted about 60 percent less than the others. This clearly indicates that the need for vitamin C is quite variable. Just as one size shoe doesn't fit every foot, the recommended daily allowance is not going to fill everybody's need for this essential vitamin.

If you take a lot of vitamin C and stop taking it suddenly, your liver will take it out of your immune system leaving you vulnerable to infection.
http://www.americanfreepress.net/Alternative_Health/17_02%20HS%20How%20Mu ch%20Vitamin%20C%20Is%20.htm


Other concerns:
http://www.inchem.org/documents/pims/pharm/ascorbic.htm#SectionTitle:7.2%20%20Toxicity[/ URL]

Elastase, once activated, digests the elastin in blood vessel walls causing vascular damage. The actual mechanism by which the enzymes become activated is still a major question.

One theory is that there is hyperstimulation of pancreatic acinar cells similar to the mechanism seen with scorpion stings and insecticide poisoning.

Another theory speculates that obstruction, bile reflux, and/or duodenal reflux disturb pancreatic acinar cell function, causing intracellular activation of the trypsin enzyme.
[URL=http://www.camlt.org/DL_web/956_patty_panc.html]http://www.camlt.org/DL_web/956_patty_panc.html

Recent advances in the study of intracellular communication are providing key insights into the immunological defect that may be underlying Chronic Fatigue Syndrome and Fibromyalgia. A number of research groups have reported

an abnormality of an enzyme called human leukocyte elastase (HLE).
http://www.fibroandfatigue.com/clinical.htm

Hummm. Wonder why the human leukocyte elastase ENZYME is damaged? Wonder what happens when that DAMAGED enzyme is released?

Does this treatment impact the beneficial bacteria in a negative way?

Finally...how do we know for SURE that this treatment is eliminating Bb specifically? This is one of natures toughest pathogens. Have tests been done in vitro or in vivo?

This is not an argument by any means and please do not interpret it as such. I am merely wondering. I would need lots of questions answered before I would feel entirely comfortable with this treatment.

Weigh the potential risks with the potential benefits to make an educated decision.

Some treatments, while they may seem good, may cause unexpected harm. I'm not the "first on my block" to try new drugs. I'd rather stick with the old ones. I'm just more cautious than many others. Could be partly due to my age ;-)

[This message has been edited by Marnie (edited 25 June 2005).]


Posts: 9426 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
   

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