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L-Lysine for Herpes

Herpes/L-Lysine by David W. Gregg, Ph.D.

Lysine is the widely recognized treatment for herpes. Experience has shown it is effective for arresting a range of herpes viruses, possibly all of them. Various mechanisms have been postulated/studied, all of which conclude that it works by inhibiting the production of the virus in contrast to enhancing the immune system. One mechanism concludes that lysine disrupts arginine’s contribution to the production of a protein that is essential for the virus to form its capsid. The capsid is the protective protein coat that surrounds the viral genetic material, which could be DNA or RNA. It is DNA for the herpes virus. The genetic material surrounded by the capsid constitutes an intact virus. The prevention of the formation of the capsid prevents the formation an intact virus that can propagate. Thus, arginine and lysine perform opposing functions concerning he herpes virus. Arginine stimulates the production of the virus and lysine inhibits it by blocking the role of arginine.

I believe the mechanism is somewhat different and can best be put in the context of the latest understanding of the relationship between DNA, messenger RNA and micromessenger RNA. It was formerly believed that DNA was a template for making RNA which was a template for making proteins. More recently it has been discovered that the vast area of what thought to be “junk” DNA with no function actually served as templates for the production of RNA’s that didn’t transcribe to proteins, but rather directly controlled the transcription activity of the DNA. Thus, it instructs a DNA virus to make the new DNA needed for a new virus. These RNA’s were named messenger RNA’s. Even more recently was the discovery of a large group of much smaller RNA molecules. They had a very different function. They could bond to the larger messenger RNA molecules and control their activity, such as turning them off. These molecules have been named micromessenger RNA molecules. If we move to the relationship between herpes, arginine and lysine. I believe that arginine promotes the production of the messenger RNA that causes the production of new viruses. Lysine promotes the production of the micromessenger RNA’s that attach to the messenger RNA’s and deactivates them.

Both the proposed capsid and RNA mechanisms indicate a successful lysine treatment would be concentration dependent. Low doses have little effect. You have to reach a treatment dose that is sufficiently high to block the arginine-based reactions that promote the production of more viruses. Experience indicates that of 1-2g/day of lysine seems to have little benefit. Treatment levels seem to be reached at about 6-8g/day. However, each person has to discover the right dose for himself. It is safe to explore because there is little possibility of a significant negative reaction due to an overdose. However, everyone is different so one should always start low and build up carefully watching for the unexpected negative reaction. I have taken 8g/day for over a month without noticing any negative reaction. Long term, continuous use, several months at a time, may not be a good idea because it introduces an imbalance in amino acids in the diet. An unexpected negative reaction may occur.

Both lysine and arginine are amino acids present to different extent in most proteins. Thus, when you eat almost anything they are in your diet, which can be an important factor. When treating with lysine you want to eat foods low in arginine and high in lysine. The included table gives a list of foods and the ratio of lysine to arginine in them. This table can help to guide you in selecting your diet.

4. Both individuals stopped taking the lysine shortly after recovering from their RA and were symptom free for many months.

5. When the symptoms returned they would take the lysine again the symptoms would quickly go away again as totally as they did initially. There was no reduction in the potency of the treatment and no need to increase the dose. If anything, the require dose would be less because they would catch it right away.

6. The first person to try it has kept herself free of her rheumatoid arthritis for at least five years with the periods of remission, needing no lysine, lasting up to a year.

Does this treatment approach apply more broadly to additional autoimmune diseases?

These results don’t just validate the theory and identify a profound treatment for rheumatoid arthritis, they also indicate a direction that could lead to treatment of many additional autoimmune diseases. In order to explore this possibility we have to thoroughly understand the path taken. Lets start at the beginning.

Many years ago I happened to read an article that stated that Rheumatoid Arthritis is characterized by a degeneration of the surface of the bone. It is also characterized as an autoimmune disease where, for unknown reasons, the immune system attacks normal cells. For the case of Rheumatoid Arthritis the immune system was selectively attacking the surface of the bone. Why?

I have always believed that the immune system doesn’t just attack normal cells without a clear reason, which should be understandable once it has been identified. What could it be for Rheumatoid Arthritis? I wondered if I could identify it. It almost immediately came to me that the herpes simplex virus causes lesions in the mouth. Such lesions are the degeneration of tissue. I had heard a theory that the viruses are formed in infected nerve cells. They are then transported along the axons, and exit at the synaptic contacts. The immune system attacks the virus exiting the nerve cells at the synaptic contacts with a standard inflammation attack. This damages normal cells while it is attacking the virus. The lesion thus formed is at the synaptic contact, which can be quite removed from the infected nerve body. Thus, the synaptic contact and cells (tissue) around it are destroyed, but the infected nerve body survives unharmed by the immune attack.

For herpes simplex the synaptic contacts are at the points where the lesions occur. It has been noticed that when the lesions reoccur with another outbreak, they always occur at the same place. That is because the source of the virus, the nerve body, was not damaged by the immune attack.

Could it be that in the case of rheumatoid arthritis the set of nerve cells infected had their synaptic contacts at the surface of the bone? If so, the inflammation attack on the virus would take place there, degenerating the bone surface. Since the infected nerve body would survive unharmed the process could repeat itself indefinitely. It wouldn’t necessarily be continuous. It could be, but it could also turn on and off like herpes simplex. In the case of shingles, it could turn off for years and suddenly cycle on and off again. I also knew that lysine was effective for treating herpes simplex and possibly other versions of herpes.

If my model was correct, one should be able to treat rheumatoid arthritis by arresting the herpes virus with lysine. I was confident my model was correct but didn’t know anyone with rheumatoid arthritis. A year later I was having a discussion with a person interested in my cancer web page when he mentioned that his wife had a severe case of rheumatoid arthritis. I told him that I was confident that lysine would arrest it and why.

They chose to try it and the rest is history with the testimonials presented above.

Now the question is: Does this approach lead to successful treatment for other diseases characterized as autoimmune? The investigation has to start with taking a close look at the very unique mechanism involved for rheumatoid arthritis.

The herpes virus has a number of very special characteristics, all of which have to be present or the virus would not be able to repeatedly trigger the immune attack at a specific location and thus the ongoing inflammation damage. Could the difference between many of the autoimmune diseases be just different discrete sets of nerve systems being infected, with synaptic contacts at different organs? Nerve systems are connected to every organ in the body making every organ vulnerable to such an attack. The strange selectivity of the herpes virus, infecting one set of nerve cells and not others would cause the attack to be organ specific. Each organ attacked could earn a different autoimmune disease name even though they all would have a common cause. Could there be another virus that could also satisfy these conditions. I don’t know of any. Thus this could be the common cause of a large number of diseases classified as autoimmune and the same treatment could be effective for all of them.

Special, required conditions met by the herpes virus:

1. The virus selectively infects highly specialized sets of nerve cells and installs a viral template, a provirus, that cycles between active and inactive. When it is active it produces more viruses.

2. The virus programs the nerve cell so that the immune system does not see the provirus or newly produced viruses while they are still in the nerve cell. This protects the nerve cell from an immune attack.

3. When the provirus is active, producing viruses, the viruses are transported along the axon(s) of the nerve cell exiting the synaptic contacts, which are connected to tissue or other nerve cells.

4. The viruses escape at the synaptic contacts and at this point the immune system sees the virus for the first time and attacks with a standard inflammation attack.

5. Inflammation attacks are relatively indiscriminant and have the characteristic of damaging (attacking) normal cells while attempting to eliminate the invading pathogen (herpes virus). The collateral damage to the normal cells can be quite severe caused by the immune system attacking normal cells. However, it is collateral damage due to the intensity of the attack on the pathogen. It is not an attack purposely directed at the normal cells. Is this the root cause of most autoimmune diseases?

6. In order to sustain the immune attack and thus qualify as an autoimmune disease, it is essential that there be a mechanism that specially separates the immune attack from the primary source of the virus. Otherwise the attack will destroy the source of the virus and arrest the disease itself.

 

That is the only way for repeated attacks to occur. For nerve cells, the axons can be long enough so that the inflammation attack at the synaptic contacts is sufficiently removed from the nerve body so the infected nerve body survives the attack with only a damaged synaptic contact. The infected nerve cell thus survives with the capability to repair itself and initiate another cycle of producing active viruses. This separation of the point of immune attack from the source of the viruses is an essential feature for the survival of virus infection. That is why you never get rid of the infection. It just cycles on and off.

 

7. Only nerve cells have axons that could transport the newly produced viruses away from the cell body source, out of reach from the inflammation attack on the virus.

 

8. The herpes virus must be highly selective as to which set of nerve cells get infected. There may have been versions of the herpes virus that were not so selective. In such cases the infection would spread to all nerve systems and would be rapidly fatal to the host, eliminating the virus with the host. Thus, natural selection has given us the more selective surviving versions of the virus.

 

9. Every organ in the body has nerve connections. Thus the selective nature of the herpes virus could selectively infect any of individual nerve system reaching any organ inducing what appears to be an autoimmune attack on that organ. The attack on each organ would receive a different name as if it was a different autoimmune disease. This mechanism would explain the 80+ identified autoimmune diseases.

 

Is there any other virus that can meet all these essential properties? If there is, I don’t know what it is. If not, it seriously strengthens the case that treatment of the herpes virus with lysine should be the first treatment tested for every autoimmune disease. It has no risk associated with it. It is widely available, has high promise, low cost and no known negative side effects. And, the quickest, least expensive and safest way to test its applicability is to use it and observe the results.

 

Lysine also has the special feature of being an essential amino acid. This means it is not manufactured by our body. If it was, herpes infections would not present a problem to us. It has to be obtained from food. All foods have lysine as a component amino acid in their proteins. For many people this relatively small amount of lysine may be sufficient to inhibit a herpes infection and may explain long periods of remission. Changing diets may be the reason for the start and stop of the attacks. However, for those suffering from an active herpes attack, it is not sufficient. Thus the treatment will always require an aggressive use of lysine during the treatment phase. The 1-2g/day commonly on the label of the bottle is unlikely to be sufficient. The 6-8g/day found to be essential by one person with rheumatoid arthritis might be used as a guide, but each person has to discover the dose and time of use that is right for him/her.

 

Comments on Some Specific Autoimmune diseases:

 

I would like to suggest how the herpes infection might be connected to some specific diseases, some identified as autoimmune and some not:

 

Osteoarthritis also has an inflammation cause and thus is as suspect as rheumatoid arthritis of being triggered by the herpes virus.

 

Heart Failure: Linus Pauling claimed that the combination of lysine and vitamin C would protect against heart attack but he did not explain why. The combination makes sense because the lysine protects against the herpes virus and vitamin C protects against a broad range of others, such as cold viruses. Thus, the combination would protect against a broader range than either alone.

 

When considering the heart specifically and the theory presented above, it is entirely possible for the herpes virus to infect the nerve cells connected to the heart muscle triggering inflammatory lesions there with serious results. This has not been specifically identified as an autoimmune disease, but it would fit the package.

 

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