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Because many of the symptoms of Lyme disease involve the nervous system, it was speculated that the spirochete produced a toxin that disrupted normal nerve function. Through the use of DNA manipulations and a database of known protein toxin DNA sequences, a match was made with a selected Borrelia burgdorferi (Bb) gene and a specific toxin in the database. Protein generated from this cloned Bb gene was examined biochemically and found to have characteristics similar to that of botulinum, the toxin of Clostridium botulinum, a zinc endoproteinase.

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The action of botulinum (as well as the toxin from the Lyme spirochete) is to prevent, through its action as a proteolytic enzyme, the release of the neurotransmitter acetylcholine.

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[Acetylcholine] is biosynthesized by the body as required in nerve activation and transmission. Supplementation by the precursors of acetylcholine synthesis would be of value to Lyme patients since they have a deficiency of this substance.

* Phosphatidylcholine (Lecithin)
* Acetyl-L-Carnitine
* Vitamin B5 (Pantothenic Acid)
* Vitamin B6 (Pyridoxine)
* Vitamin C (Ascorbic Acid)
* Lysine (Amino Acid)
* S-Adenosylmethionine (SAM) (Sulfur-bound Adenosyl Methionine)

If the inhibition of acetylcholine release were total, Lyme patients and those suffering from food poisoning would not be able to move; they would be completely paralyzed. Since the blockage is only partial, any increase in the amount of available neurotransmitter would benefit anyone experiencing neurotransmitter blockage. For this reason, dietary supplements increasing the amount of available acetylcholine have been shown to benefit Lyme patients.

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Nitrous Oxide (NO), A Potential Lyme Therapeutic Agent
Nitrous oxide (chemical formula NO) is a gas, at one time commonly used as an anesthetic (laughing gas). In more recent times, the biochemical activity of NO has been related to the relaxation of the small muscle fibers in the walls of blood vessels. They serve to either relax or constrict the flow of blood passing through those vessels. The mechanism of NO bioactivity has also been learned; this involves the substance c-GMP (cyclic guanosine monophosphate). The amount of c-GMP at any time is regulated by the enzyme, phosphodiesterase type 5 (PDE-5), having the capacity to destroy it. c- GMP fits into a cavity on the surface of PDE-5, the "active site" of this enzyme. Any other substance capable of being bound by the active site of PDE-5 inhibits the activity of the enzyme by blocking the entry of c-GMP, thus allowing a greater survival of c-GMP. To summarize, any inhibitor of PDE-5 allows an increase in the amount of available c-GMP and consequent relaxation of blood vessels, permitting a greater flow of blood through those vessels.10

It has been demonstrated that NO is toxic to Borrelia burgdorferi, the causative organism of Lyme disease.11 Therefore, any inhibitor of PDE-5 is a potential therapeutic agent for Lyme disease. Inhibitors of PDE-5 in common use today are the drugs sildenafil (more commonly known as Viagra), Levitra, and Cialis. Whether these drugs act therapeutically against the Lyme spirochete has not been demonstrated clinically and remains unknown.

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Inhibitors of the Lyme Spirochete Toxin
A large amount of work is being conducted today in an effort to uncover more inhibitors of the Lyme spirochete toxin. One known inhibitor of toxin activity is the substance glycyrrhizic acid (GA), the active principle of licorice root, used in Oriental medicine for thousands of years.12 GA is also the active principle of the American Biologics product, Biorizin�. The molecular structure of GA includes a steroid with large bulky substituents. Being a large molecule, GA is capable of binding into the active site of the toxin, thereby blocking the normal substrate, two adjacent amino acids in the protein SNAP-25.

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Lyme-Induced Arthritis Linked to Various Strains of Bb
It has been noted clinically that some Lyme-induced arthritis patients are affected by the disease to different degrees. A laboratory study demonstrated that different strains of Bb were capable of activating to various degrees a particular enzyme (matrix metalloproteinase) found in human synoviocytes. These cells are found in the synovial fluid of joints and form some of the substances found in this fluid. Matrix metalloproteinases are proteolytic enzymes capable of degrading most of the proteins in the extracellular matrix. Different strains of Bb activate these proteases to varying degrees, explaining variations seen clinically in the severity of Lyme-induced arthritis. To date, more than 50 strains of Bb have been identified.

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Similarity Between DNA Sequences of Brain Tissue and Bb OspA

DNA sequences of Bb outer surface protein A (OspA) compared with a data bank of DNA sequences of human neural tissue yielded three sequences that were identical. The three corresponding Bb peptides were synthesized, and antibodies were induced against them. The antibodies cross-reacted with human neural tissues.

These findings imply that antibodies developed by Lyme disease patients against OspA will also bind to their own neural tissue, representing a form of autoimmune disease in which a person's immune system attacks his own tissues.

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Carbohydrates Consumed by Lyme Spirochete
An effort to determine which carbohydrates Bb consumes revealed that the organism utilizes the monosaccharides glucose, mannose and N-acetylglucosamine, as well as the disaccharides maltose and chitobiose. A popular treatment for arthritis includes the administration of chondroitin sulfate and N-acetylglucosamine. If the arthritis is Lyme-induced, N-acetylglucosamine is contraindicated.

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Cave,

I am so in agreement with you. You can't be too careful about adding potent herbs and even foods without understanding the known contraindications, etc.

Part of the pain of this battle with the neuro issues is how it is impairing my ability to to something I truly love: detailed research... so that I am well informed before I take a new idea to my health care providers .

So, back to the original article:

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Inhibitors of the Lyme Spirochete Toxin
A large amount of work is being conducted today in an effort to uncover more inhibitors of the Lyme spirochete toxin. One known inhibitor of toxin activity is the substance glycyrrhizic acid (GA), the active principle of licorice root, used in Oriental medicine for thousands of years. GA is also the active principle of the American Biologics product, Biorizin�. The molecular structure of GA includes a steroid with large bulky substituents. Being a large molecule, GA is capable of binding into the active site of the toxin, thereby blocking the normal substrate, two adjacent amino acids in the protein SNAP-25.

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Glycyrrhizic acid in liquorice--evaluation of health hazard.

* Stormer FC,
* Reistad R,
* Alexander J.

National Institute of Public Health, Oslo, Norway.

Literature on case reports, clinical studies and biochemical mechanisms of the sweet-tasting compound glycyrrhizic acid in liquorice was critically reviewed to provide a safety assessment of its presence in liquorice sweets. A high intake of liquorice can cause hypermineralocorticoidism with sodium retention and potassium loss, oedema, increased blood pressure and depression of the renin-angiotensin-aldosterone system. As a consequence, a number of other clinical symptoms have also been observed. Glycyrrhizic acid is hydrolysed in the intestine to the pharmacologically active compound glycyrrhetic acid, which inhibits the enzyme 11 beta-hydroxysteroid dehydrogenase (in the direction of cortisol to cortisone) as well as some other enzymes involved in the metabolism of corticosteroids. Inhibition of 11 beta-hydroxysteroid dehydrogenase leads to increased cortisol levels in the kidneys and in other mineralocorticoid-selective tissues. Since cortisol, which occurs in much larger amounts than aldosterone, binds with the same affinity as aldosterone to the mineralocorticoid receptor, the result is a hypermineralocorticoid effect of cortisol. The inhibitory effect on 11 beta-hydroxysteroid dehydrogenase is reversible; however, the compensatory physiological mechanisms following hypermineralocorticoidism (e.g. depression of the renin-angiotensin system) may last several months. It is not possible, on the basis of existing data, to determine precisely the minimum level of glycyrrhizic acid required to produce the described symptoms. There is apparently a great individual variation in the susceptibility to glycyrrhizic acid. In the most sensitive individuals a regular daily intake of no more than about 100 mg glycyrrhizic acid, which corresponds to 50 g liquorice sweets (assuming a content of 0.2% glycyrrhizic acid), seems to be enough to produce adverse effects. Most individuals who consume 400 mg glycyrrhizic acid daily experience adverse effects. Considering that a regular intake of 100 mg glycyrrhizic acid/day is the lowest-observed-adverse-effect level and using a safety factor of 10, a daily intake of 10 mg glycyrrhizic acid would represent a safe dose for most healthy adults. A daily intake of 1-10 mg glycyrrhizic acid/person has been estimated for several countries. However, an uneven consumption pattern suggests that a considerable number of individuals who consume large amounts of liquorice sweets are exposed to the risk of developing adverse effects.

PMID: 8386690 [PubMed - indexed for MEDLINE]

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