Monday, July 18, 2011
Sunday, April 3, 2011
Tuesday, March 29, 2011
I am not a medical doctor and thus do not attempt to treat people; but, in an effort to help a new friend, Barbara, who suffers from Crohn's Disease (CD), I performed a literature search, and thought deeply about the disease. Within this process I identified two new potential approaches that I thought might be helpful. Neither approach had been used for CD before. I provided Barbara with the results of my search along with my first theory about how CD might be remedied. She discussed it with her physician. She told me that he said that he didn't see how trying it would do her any harm. She had abdominal pain, which had lasted for more than three months with varying degrees of severity, even though she was under a doctor's care and her disease was in partial remission. Barbara decided to try the suggested remedy. She was working half days because of the inflammation, went home at noon as usual, purchased the material at a health food store at minimal cost and applied it. Her abdominal pain was reduced to a mild sensitivity within an hour. That was in February 1995. She was able to return to work full time shortly thereafter. Her disease has been under control ever since then without other medications being required. She gradually recovered her full physical strength and general health, and has noticed no ill side effects from the remedy. She said that before this time she rarely had one good day a month. Shortly after starting the "treatment" she said she felt terrific and rarely had one bad day a month. Her disease management cost changed from approximately $5,000 per year (covered by insurance) with conventional medications, which did not work very well and had substantial negative side effects, to approximately $50.00 per year (no insurance coverage needed) with far better control of the disease and absolutely no negative side effects.
Since that time more than twenty other people with Crohn's Disease and several with Ulcerative Colitis (UC) have chosen to try it. It seems to work equally well with both diseases. They purchased and applied their own material. Their reported success rate has been better than 90%. They have been able to discontinue other medications and enjoy freedom from abdominal pain and intestinal inflammation. Once it works for an individual, there are no cases of a person becoming desensitized to its benefits. It continues to work, with additional applications as needed, indefinitely. According to my theory, the remedy does not just block the pain, it stops both diseases by stopping the common process that causes the degeneration of the intestine.
The time span between my first learning about Barbara's disease (I had never heard of Crohn's Disease before) to my identification of the first projected remedy was three days. She tried it the next day and to my amazement she said it took effect within an hour. This relatively brief time to effectiveness has been repeated many times with many people. I have been told of pain relief time ranging from 20 minutes to four hours.
I should make it clear that I am not selling anything and have no financial interest in the remedies. My motivation is strictly humanitarian. I would simply like to contribute what I can to help eliminate the horrible suffering associated with these diseases.
I. Dimethyl Sulfoxide (DMSO) as a Remedy for Crohn's Disease
In order to appreciate the profoundness of the remedy, which is deceptively trivial in appearance, I believe it is important not only to present the results, but also to take the reader through the technical reasoning I employed. I have a formal education in chemistry and chemical engineering and am now retired after spending more than 30 years performing research at a national laboratory. During that time I developed a personal fascination with the potential of nutritional supplements for helping a broad range of physical and mental problems. It started when I was on the board of directors of a youth home with 70 problem children (wards of the court) and wanted to explore possible approaches for helping the children. This gradually led me into making a serious study of nutrition, biochemistry, medical physiology and psychology and the interrelation between them. I was deep into studying textbooks and performing literature searches on Medline (on the Internet) when I first met Barbara. She was the secretary for the new group I had joined at the national laboratory. I found her to be an exceptionally pleasant person with an exceptionally serious, disabling illness. So, I told her that I would use the capabilities I had developed to try to find something that might help her. I was proud and shocked when the first suggestion I made, derived from my first technical analysis of the cause of Crohn's Disease, was totally successful.
Upon starting the literature search I quickly discovered that the conventional treatment for CD used steroids or sulfa drugs with only moderate success. Failure of the steroids frequently resulted in the need for surgeries removing the damaged part of the intestine. Multiple surgeries eventually end with the need for an ileostomy or a colostomy where excretion of the feces is diverted through the abdominal wall and is collected externally in a bag for disposal. Many other treatments had been tried with little success. The attempts at different treatments seemed almost random, possibly because there was no clear understanding of the cause of the disease. Some believed it was an autoimmune disease, but the evidence for that was not conclusive.
I decided to take a more logically tight, systematic approach, as I would do with one of my typical research projects. This involved first postulating a damage mechanism, checking it against the literature to see if it survives, and designing what should be a logically tight treatment based on the assumed mechanism. In order for me to have any chance of success with my extremely limited access to almost anything sophisticated, I knew I had to approach the problem with a very different thought process than the elaborate research facilities had. The first thing I did was to mentally separate the primary, complex cause of the disease from the damage mechanism, which I hoped may not be so complex. I then focused on the damage mechanism, which I hoped would be more amenable to a simple solution. I reasoned that the damage mechanism was very likely hydroxyl radical attack on the intestinal cells. From reading the medical literature, I discovered that there was considerable evidence that this mechanism might be a primary cause of colon cancer. They are well known to have the capability of destroying cells through oxidative attack and I thought Crohn's Disease might be another expression of their damage. A literature search identified more than 15 publications in the last five years in which the authors also felt this might be true.
In a previous Medline literature search I had done on DMSO, focused on evaluating its toxicity, I discovered not only a lack of toxicity but also that it had been measured to be a powerful antioxidant. The search over the previous five years of medical publications yielded 1117 abstracts describing instances where DMSO was used. Many of the abstracts openly stated that DMSO was a well-tolerated material, and there were no publications indicating any level of toxicity. DMSO had been used in a variety of medical applications, but never for Crohn's Disease. One paper presenting results for a number of materials being tested for antioxidant activity, listed the compounds in order of antioxidant effectiveness and then added the statement that none of them were as effective as DMSO.
DMSO has another very important feature that distinguishes it from commonly used vitamin antioxidants. It will rapidly diffuse through the skin into the blood stream. (There is no need or advantage to taking it orally.) According to my initial theory, this is not just an application convenience, but an essential feature that would make it more effective in the treatment of CD than other antioxidants.
I reasoned that if the damaging hydroxyl radicals are generated inside the intestinal cells, the antioxidants will have to penetrate the cell membranes to get at them. Vitamin antioxidants can have a difficult time penetrating the membranes, which may explain why they are ineffective for treating CD. However, DMSO cannot be stopped by any membrane. That is why it can rapidly diffuse directly through the skin. Thus, only DMSO (and now a second material with a slightly different mechanism, Melatonin, which I will discuss below) would be able to penetrate the cell membranes rapidly and quickly enough to deactivate damaging hydroxyl radicals generated inside the cells before they do damage. I postulated that because of this very unique penetrating characteristic, only DMSO, and now Melatonin, might be effective in reducing the intestinal damage associated with Crohn's Disease. If my theory is true, treatment with DMSO would also serve to illuminate the biochemical cause of CD.
With these thoughts in mind, I thought DMSO had a reasonable chance of helping Barbara with her CD. When I talked to her about it, she told me that she had owned horses for many years and was quite familiar with DMSOs frequent use in veterinary medicine. She felt it would be a safe thing to try, in small amounts, even though she was aware that its use for application to humans had been approved by the FDA only for the treatment of interstitial cystitis. She consulted her physician and he thought it could safely be applied topically. When Barbara started using DMSO she was working half days because she was trying to recover from repair surgery and the deterioration caused by a major relapse of her disease. She went home at noon, as usual, and bought some DMSO at a health food store. She applied "about a teaspoon full or less" to her abdomen. (The body location is not important!) She then went to an afternoon movie. An hour into the movie Barbara noticed that something was missing. Most of her abdominal pain was gone!
Shortly thereafter Barbara was able to return to work full time and was feeling "wonderful". After this success, I am amazed at how many people then called me to find out about it. I discovered that this horribly painful, commonly fatal disease is very prevalent. I am thus compelled to write this paper in an attempt to get this information into the Crohn's Disease and Ulcerative Colitis community so it can be further evaluated, and hopefully provide near-term, safe help.
If my theory is correct, DMSO does not stop the primary cause of Crohn's Disease. It only stops the damage mechanism, very rapidly. Thus, DMSO may have to be used on a continuing basis. The people using it so far apply it only when they feel the onset of abdominal pain. The DMSO quickly stops the pain (and the intestinal damage process) commonly in less than one hour but it can take up to a few days of repeated application. One of the benefits of its rapid action is that it does not have to be taken in a preventive mode, and there are no withdrawal problems. This is in contrast to the steroid treatment, which takes several weeks to take effect and thus often has to be taken in a preventive mode, and where withdrawal must be done with great care. The natural course of Crohn's Disease is to cycle between active and remissive states. The DMSO appears to prevent damage during the active state, and may be required sporadically during remission. It appears to be an extremely affordable remedy that a person can live with comfortably. I recently talked to Barbara and she said it continues to control her CD when it becomes active, but she had to use it only twice in the last year
II. Melatonin as a Remedy for Crohn's Disease
Melatonin is well known as an effective, nonprescription sleeping pill. In the book "Melatonin" by Ray Sahelian, M.D., he references research done by Hardeland, et al. that states "Melatonin has been found to be the most potent physiological scavenger of hydroxyl radicals ever detected. Melatonin stops damage immediately and is more effective as an antioxidant than even vitamins C and E." He also states that Melatonin has the advantage of being able to freely enter and permeate all parts of a cell.
Given the experience with DMSO helping Crohn's Disease, upon reading this, it seemed reasonable to me that Melatonin might be another likely remedy for C.D. I brought this to the attention of Barbara and discovered that she had just started taking Melatonin to help her sleeping problems. She decided to stop using DMSO and see if the Melatonin would control her C.D. It seemed to work for approximately two months when she started to get a recurrence of abdominal pain. At this point she returned to using DMSO, which controlled the pain in its characteristic short time.
Since Barbara's experience, many people have tried both DMSO and Melatonin and both have worked quite well. It is difficult to say if they would both work quite well on the same person because different individuals seem to have chosen one or the other approach and remained with it once it worked. There seemed to be one significant difference in that it appears that DMSO seems to take effect within an hour while Melatonin might take a week or so.
At this point approximately half of those trying this are happy with Melatonin and half with DMSO. It is difficult to say in advance whether DMSO or Melatonin will be the best approach for any particular individual. One of the most interesting points is that once an approach does work for an individual, it does not become ineffectual with time.
I want to remind people that this write-up is for information only and is not a recommendation for treatment. I strongly recommend that you discuss this with your physician and read the large amount of information that has been published about both DMSO and Melatonin before taking any action.
Proposed Biochemical Mechanisms for DMSO Mitigating Crohn's Disease
The Proposed Biochemical Cause of Crohn's Disease
I propose that the cause of Crohn's Disease is oxidative attack on the intestine, and not an autoimmune attack. Specifically, the attack follows the Haber-Weiss reaction where ferrous ions catalyze the dissociation of biochemically-produced hydrogen peroxide into highly reactive hydroxyl radicals. The excessively high production rate of hydroxyl radicals then produces cellular damage in the intestine. The reaction goes as follows:
H2O2 + Fe(+2) = Fe(+3) + OH- + HO
hydrogen peroxide + ferrous ions
react to produce
ferric ions + hydroxyl ions + hydroxyl free radicals
This reaction is always taking place in normal cells and can play a constructive metabolic role by helping with the initial oxidation of fats in the peroxisomes. However, for people with Crohn's Disease, it takes place to excess.
The Proposed Mitigation Mechanisms for Melatonin and DMSO
In the book "Melatonin" by Ray Sahelian he states that Reiter, one of the most active researchers on Melatonin, believes that it stimulates the enzyme glutathione peroxidase, one of the body's most powerful antioxidants. The details of how this enzyme operates to remove hydrogen peroxide are discussed in many books on biochemistry, and won't be reproduced here.
Mechanism 1: DMSO can be readily oxidized to dimethyl sulfone. DMSO has one oxygen atom and dimethyl sulfone has two. In the presence of hydrogen peroxide it can be oxidized, picking up one oxygen atom, converting the hydrogen peroxide to water.
Mechanism 2: In the process of carrying out literature searches, I discovered a paper in which it was reported that DMSO increased the number of transferrin receptor sites displayed on the outer membranes of two standard cell cultures with a response time of approximately ten minutes. ("A Rapid Redistribution of the Transferrin Receptor to the Cell Surface of HL-60 Cells and K562 Cells upon Treatment with Dimethyl Sulfoxide Due to Slowing of Endocytosis" D. Vestal et. al., Archives of Biochemistry and Biophysics, Vol. 276, No. 1, Jan. 1990, PP. 278-284) This opens up the possibility of a surprise mechanism for DMSO mitigating Crohn's Disease. Transferrin transports iron in the blood. It picks it up from the intestine and brings it to all the cells in the body that need it.
If we postulate that this same effect occurs when DMSO is applied to the body, it will increase the rate of transport of iron out of the intestine and to other cells in the body. The immediate effect will be to lower the iron concentration in the intestine, and thus lower the rate of production of hydroxyl radicals in the intestine via the Haber-Weiss reaction (catalyzed by iron) discussed above.
It is interesting to note that the measured response time of the cells is fully consistent with the rapid response CD people observe for DMSO mitigating their abdominal pain.
It is also possible to postulate additional, downstream effects.
1) The increased transport of iron will specifically increase its transport to the bone marrow. This could increase production of hemoglobin, reducing any anemia that might exist, which is common with people experiencing a CD inflammation.
2) In normal people, the absorption of iron into the blood from the intestine is actively controlled. If this active control mechanism is sensing on anemia or the lack of it, then (in its simplest conceptual form) the existence of anemia would result in increased iron absorption in the intestinal cells, and the reduction of anemia would have a corresponding reduction of iron absorption. Thus, if the application of DMSO resulted in reduced anemia, it would reduce the rate of absorption of iron (from food) into the intestinal cells while increasing its rate of removal from the intestinal cells by transferrin in the blood, resulting in a two-pronged approach to reducing the Haber-Weiss reaction.
The actual control mechanism for iron absorption is complex and only partly understood. One mechanism that has been demonstrated to regulate the transfer of iron across the mucosal-capillary interface is the synthesis of apoferritin by the mucosal cells. When the host requires little iron, a large amount of apoferritin is synthesized to trap the iron within the mucosal cells and prevent transfer to the capillary bed. As the cells turn over (within a week), their contents are extruded into the intestinal lumen without absorption occurring, thus excreting unneeded iron. When there is a iron deficiency, virtually no apoferritin is synthesized so as not to compete against the transfer of iron to the deficient host. Considering this mechanism, one could postulate that the existence of anemia may prevent the formation of apoferritin. This would result in an increase in free (active) iron ions in the mucosal cells. If this is combined with an ineffectual removal of them into the blood by insufficient transferrin transport capacity, these free iron ions could then be very active in the Haber-Weiss reaction, producing excess hydroxyl radicals, and resulting in cellular damage. DMSO would cause increased transferrin transport capacity, reducing anemia, resulting in increased production of apoferritin in the mucosal cells, reducing free iron ion concentration, and thus reducing the activity of the Haber-Weiss reaction and cellular damage.
A Research Effort to Carry Out Needed Controlled Studies
I would like to strongly encourage the performance of controlled studies to evaluate the DMSO/Melatonin approach to mitigating Crohn's Disease and Ulcerative Colitis so as to place it on a sounder technical basis. The ultimate goal would be to satisfy FDA requirements to qualify one or both of them as approved treatments.
Wednesday, March 23, 2011
1. The herpes simplex virus has been identified as the root cause of Alzheimer’s disease.2. The most promising primary treatment is lysine, a proven treatment to arrest the herpes simplex virus. This attacks the root cause directly. (Google: lysine, herpes).3. The backup treatment is coconut oil. (Google: Alzheimer’s, coconut oil). This was first discovered and demonstrated by Dr. Mary Newport in her effort to find a treatment for her husband’s Alzheimer’s disease. It was profoundly effective. Dr. Newport identified part of the biochemical mechanism and this paper is expanding on it to identify important and useful additional insights.4. Nutrition: Nutritional deficiencies have been credited with causing dementia later in life, which is indistinguishable from herpes caused Alzheimer’s without an autopsy.5. and 6. Glycolysis and Cancer: The Alzheimer’s treatment will profoundly inhibit glycolysis, which should in turn inhibit both Alzheimer’s and cancer.
Tuesday, April 28, 2009
This post is for information only. I wrote it in June 2004. It represents the observations, views and opinions of the author, but is not a recommendation for any particular action other than understanding and acceptance.Motivation for Writing this Post
The public debate about same sex marriages has recently brought the extent of homosexuality in society out of the closet. Even though I am not gay, I believe I have understood its root cause for many years and it appears to have been missed by everyone. Perhaps it is because it takes a chemist to fully appreciate its logic and how technically fundamental, and thus irrefutable, it is. Since it has now become an issue in terms of determining public policy I thought it was time to present it. Perhaps with this deeper understanding of its root cause more humane and insightful public policies will result.
To start with, I found an excellent summary of background information presented in the book "Sex, Time and Power" by Leonard Shlain, (2003) Chapters 16 and 17. I will draw from it that will allow me to be as brief as possible.
Schlain states: "From an evolutionary point of view, homosexuality is a supreme paradox." If it had a genetic cause the trait would quickly go extinct. However, throughout history the rate of homosexuality has remained essentially constant, about 3% for males and 1% for females. It appears in all human societies. Thus even though there are those who are attempting to find a genetic cause, it is obvious that it doesn't exist. This historical data is too solid and profound. It will override any genetic investigations, which are based on loose correlations.
Anyone observing the development of a baby into a child cannot avoid the conclusion that his or her sexual attraction choice is present far before puberty. The program determining it had to be present at birth.
I personally remember being attracted to my mother's form from my earliest memory. I had no such attraction to my father's body. I did not have to learn to be attracted to females. I didn't have a choice. It was not something that I learned through social/environmental interactions and then made a decision. It was extremely powerful and no social interaction was about to change it. Over the years, in the interactions I have had with homosexuals, both male and female, they all told me that they knew they were homosexual from their earliest memory, as very young children. Also, they were no more able to change it than I would have been able to change mine. In contrast to me, many of them had a strong, socially imposed motivation to do so. In spite of this, they were unable to.
The Proposed Root Cause
It is clear to me that our sexual attraction preferences are genetically carried. They are not learned after birth. However, our genes contain two distinctly different sexual attraction programs. One is for females insuring they are attracted to males, and the other is for males insuring they are attracted to females. Both options are available at conception. A selection is made during the development of the fetus. As Schlain states: "The female is the default mode for all mammalian fetuses". We all start out as females. At approximately six weeks after conception a male's budding testes will begin secreting large amounts of testosterone. This shifts the developmental sequence towards a male. When the testosterone secretion does not take place, all the fetuses even those with the male Y chromosome, will develop into females. This is the stage where the different developmental sequences between male and female are set in motion. Subsequent male and female features arise from common anatomic precursors that have the potential to develop into either sex. For example, the tissue destined to become the clitoris in the female will become a penis in a male. Since both options are genetically available, a selection process is taking place. This process selects which part of the genetic code will be expressed and which will be suppressed. Included in this are the genetically carried codes for sexual attraction. At the appropriate stage of development, the sexual attraction program is selected irreversibly. It is as irreversible as the selection between a clitoris and penis. It is not clear exactly what stage this particular selection happens. It is only clear that it does happen. This is the point where an error is made for homosexuals. The inappropriate program is selected.
At this point I revert to being a chemist. All developmental processes are chemical processes/reactions. The selection mechanism is a chemical process composed of a set of chemical reactions. Basically there is a chemical switch that is thrown and the program is selected.
As a chemist, I know that there is no such thing as a chemical reaction that has 100% yield of the preferred product. This is a fundamental prediction of thermodynamics. The yield is always less than 100%. Thus, when it is time for the chemical reactions to select the sexual attraction program, one would expect, from a simple chemical argument, that some fraction would not go the appropriate way. From the observations on the ongoing fraction of gay births, one would conclude that the reaction has about a 97% yield for males and a 99% yield for females. The remaining 3% males and 1% females are destined to be homosexual. Thus, homosexuality has a statistical, chemical yield cause. They are homosexual at birth but there is nothing unusual about their genetic makeup because it does not have a genetic cause. They can have the same fraction of normal children as non-gay people. As far as I know, I believe they do.
It is obviously absurd to judge homosexuals morally. In one sense they can be viewed has having been born with a birth defect even though many homosexuals who have found their path might disagree with that characterization. However, they would agree that it was not a choice they made. It was made for them. They are left with having to plot a course in life that recognizes it, accommodates it, and even exploit some of its special characteristics.
Birth Defect or Birth Difference?
I recently read that magnificent book: "The Da Vinci Code" by Dan Brown. To start with, the genius, Leonardo da Vinci, was homosexual. Chapter 26 presents a discussion of Da Vinci and his most famous painting, The Mona Lisa. Brown states "The Mona Lisa's status as the most famous piece of art in the world has nothing to do with the painting itself but rather because Leonardo da Vinci claimed she was his finest accomplishment. He carried it with him whenever he traveled and stated he found it hard to part with his most sublime expression of female beauty". How could this be? Mona Lisa certainly is not particularly beautiful by today's standards and most likely wasn't in Da Vinci's time either. It also is not a great work of art. There had to be a profound but hidden message that Da Vinci held dear and wanted to convey to those who could recognize and appreciate it. Possibly he thought of it as his most meaningful legacy. What could it be and whom did he want to convey it to?
According to Brown, a computerized analysis of the Mona Lisa and Da Vinci's self-portraits show a congruency in their faces. "His Mona Lisa is neither male nor female. It carries a subtle message of androgyny. It is a fusing of both." Brown also points out that Amon is the Egyptian god of masculine fertility and Isis is the Egyptian goddess of female fertility who was once called l'isa. Convert Amon to Mona and add Lisa and you have the name of the painting. "Gentlemen, not only does the face of Mona Lisa look androgynous, but her name is an anagram of the divine union of male and female."
Why was this so important to Da Vinci and to this discussion? I believe he was communicating his belief that a homosexual is a truly exceptional person due to having the fusion of both male and female in the same body. It is not a defect, but a particular form of perfection. I believe he wanted to communicate this not to everyone, but to other homosexuals who suffered from believing they were defective. Perhaps they would recognize this subtle message and it would help, long after he was gone.
Is this particular form of perfection concept supportable? He had to believe it was a key factor in explaining his recognized, exceptional creative genius. Is it a reasonable premise in general? In support of this, Shlain presents a partial list of others: Socrates, Plato, Aristotle, Tchaikovsky, Newton, Milton, Michelangelo and Nietzche to name a few. We just have to look around us in our present society. On average, gays seem to possess exceptional aesthetic and creative abilities. They have made their mark not only in the arts and literature, but also in architecture, music, religion, science, mathematics and many other fields. Shlain states: "They fill a special niche in society and human culture would be considerably grayer and less sumptuous without them".
I believe Da Vinci wanted to convey the message that homosexuals do not have a defect but rather a special gift with the ability to make exceptional contributions. They should not have to hide their homosexuality. They should be able to carry it with pride. That is the message of Mona Lisa that Da Vinci held so close to his heart and the target audience.
I just received an email from a friend who referred me to the site: http://www.rense.com/general62/pills.htm
This site presents an article titled: Mom's Pills May Turn Daughters Into Lesbians - Study
I would urge everyone to read the entire article. However, it is somewhat summarized in the first three paragraphs:
"Pregnant women’s' use of certain diet and thyroid medications may lead their daughters to become lesbians, new findings suggest.
Researchers said the findings are very preliminary and need confirmation. But if born out, they could put a new perspective on the hotly debated causes of homosexuality.
The researchers, Lee Ellis and Jill Hellberg of Minot State University, North Dakota, questioned more than 5,000 U.S. and Canadian women in an effort to determine the effects of drugs they had taken during pregnancy. They found certain types of pills were associated with a much higher rate of lesbianism among the woman's daughters though not with similarly raised rates of homosexuality among their sons."
My comments: This report is fully consistent with my theory. It seems to validate it. The drugs are probably increasing the testosterone production of the fetus, even though the exact biochemical mechanism for doing that has not been identified. Increased testosterone production would be expected to cause more females to become more male-like. One would then expect an increase rate of Lesbians, but also a lowering of the rate of Gay Males. This lowering of the rate of Gay Males is not mentioned, but may not have been measured or looked for. The results indicate a slightly adjustable chemical yield of normal vs. homosexual children, and provide support for my premise that homosexuals are born that way. They are not created by circumstances that arise after birth.
I originally wrote this post in April 2008 at http://www.krysalis.net This post is for information only. It represents the observations, views and opinions of the author, but is not a recommendation for treatment. Anyone reading it should consult his/her physician before considering treatment.
The successful treatment of the autoimmune disease, rheumatoid arthritis, presented above, is a radical deviation from all other autoimmune disease investigations. It started with the careful postulation of a novel root cause never reported before. This lead to the identification of its best possible treatment. The treatment is unique in that it is not based on suppressing the immune system. It is based on selectively arresting the activity of the trigger, avoiding the negative side effects of immune suppressing drugs.
It is a radically new approach, not only for treating rheumatoid arthritis but also has the potential of being expanded to many, if not most other autoimmune diseases.
A few people (you can find their e-mails on my old web site) wrote to me of success using this approach which might seem unimportant because of the small sample. However, it is very significant because:
- It is based on a well thought out theory.
- The two people to test it on themselves represent 100% of the people to try it.
- They tested it by taking the treatment, relatively large doses of lysine (6-8g/day), years apart from each other and both recovered in the same amount of time, about two months of taking it.
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.
- Both individuals stopped taking the lysine shortly after recovering from their RA and were symptom free for many months.
- 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.
- 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:
- 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.
- 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.
- 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.
- 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.
- 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?
- 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.
- 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.
- 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.
- 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.
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.
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.
Cancer: Viruses are well known to a cause of a variety of cancers. The viruses enter cells and harness the cell’s chemistry to produce more viruses. This disruption of the cell’s chemistry can fragment their chromosomes, sometimes leading to cancer cells. In the case of an autoimmune disease, there will be a repeated herpes attack at the same location. Due to this, one would expect a relatively high correlation of cancer with such diseases. A search of the internet produced:
- A paper published by the University of Florida Shands Cancer Center States, “According to study published in the Journal of the National cancer Institute, the risk of diffuse large B-cell lymphoma (a subtype of non-Hodgkins lymphoma) is elevated among patients with rheumatoid arthritis, Sjogren syndrome, systemic lupus, erythematosis, or celiac disease. Some of these conditions were also linked with marginal zone lymphoma, lymphoplasmacytic lymphoma, and T-cell lymphoma.”
- In a paper titled “Autoimmune Diseases and Cancer Co-Morbidity in the U.S. Elderly 1979 to 2001” by Hai Huang, et al. Duke University, Center for Demographic Studies, February 28, 2006. Briefly, this paper concludes that there is a high rate of death in the elderly where cancer and an autoimmune disease are both present and either has been named as the final cause of death. Like autoimmunity, the wide prevalence of herpes infections in different organs is consistent with the many types of cancer, each named by the organ of initiation. It does hint of a common root cause.
Shingles has been identified as being caused by the herpes virus. A shingles attack is characterized by an eruption of serious pain in specific tissue areas with the specific area changing from person to person. In this case the synaptic contacts of the infected nerves are in the tissue where the pain is. Thus, when the attacks repeat, the pain is always in the same place. I know one person who had such frequent shingles attacks that she could not travel. When she started taking a lysine-vitamin C powder they went away completely and she could travel again.
Fibromyalgia is characterized as having muscular pain in specific locations of the body with no known cause. It has a lot in common with Shingles. I predict that it has the same cause as Shingles with the herpes infected nerves having their synaptic contacts at the pain locations. The herpes induced inflammation happens there and thus the pain. I have been in contact with woman who had fibomyalgia for many years. Pain medications helped for brief periods but then ceased to b effective in a few weeks. Upon learning about my theory concerning herpes and lysine, she started to take the lysine. Her pain ceased in a few days and she has been pain free for several weeks now.
Autism: As I have suggested on my autism web page, I believe that a combination of viruses play a role in causing autism. The role of the herpes virus is to do brain damage. I talked to one mother of an autistic boy who told me that a doctor at Harvard Medical Center had detected lesions in her son’s brain. Other infected nerves could be connected to the duodenum disrupting the digestive system. In particular lesions there could play a role in disrupting the capability of the duodenum cells to make secretin. This disruption is common in autistic children.
Psoriasis, Systemic Lupus, Scleroderma, Systemic Scleroderma, Graves Disease, Diabetes Mellitus Type 1, Pernicious Anemia, Glomerulonephritis, Hashimoto’s Thyroiditis, etc. are all examples of degenerative diseases with the characteristic inflammation associated with autoimmune diseases “with no known cause”. None have been evaluated for response to treatment with lysine. The only way to discover if the analysis presented here would apply is to treat with lysine and observe the results. It is extremely inexpensive and safe. The inflammation associated with many of these diseases can cause some serious tissue damage. It may take many months of treatment to reverse the damage.
Lysine Alternatives: There are a number of proposed alternatives to lysine for treating herpes presented on the internet. I don’t know how they compare with lysine and are commonly suggested as a supplement to lysine rather than a replacement.
Seaweed: I am particularly interested in the claims about Red Marine Algae for treating herpes. Put in context, I have found articles that report that almost all versions of viruses that infect humans can be found in ocean water. Seaweed survives quite well in this environment. Thus, all versions of seaweed, including Red Marine Algae, must have developed defenses against them. Could seaweed provide a broad-range anti-viral treatment/defense? Seaweed is commonly viewed as an exceptionally healthy food. Most think it is because of it’s vitamin and mineral content. Could it’s unusual health benefits be primarily due to its generally unrecognized broad-range anti-viral effects? For these reasons I would consider adding any type of seaweed to the diet as a supplement to the lysine to be a good idea. It is a safe experiment.
Where does this lead?
If you are looking for well-funded studies that evaluate this approach to treating any autoimmune disease, it won’t happen. The treatment is widely available with no prescription needed. It is extremely inexpensive. Studies evaluating the use of lysine to treat any one autoimmune disease would be very expensive and to evaluate the application to a broad range of autoimmune diseases would be even more expensive. It would be impossible to obtain a patent for the treatment and impossible to recover the costs of the studies. The only answer I can see for spreading the information and evaluating the true possibilities is for individuals with the problems testing it on themselves and letting others know the results. The internet becomes the key communication tool. It can take many paths and I would encourage every interested person to use their own creativity to find a way.
Monday, April 27, 2009
I originally wrote this post in 2004 at http://www.krysalis.net. This post is for information only. It represents the observations, views and opinions of the author, but is not a recommendation for treatment. Anyone reading it should consult his/her physician before considering treatment.Rheumatoid Arthritis (RA) affects mainly the joints of the hands and feet, although it can extend to other tissues. Of all the forms of arthritis, RA is most likely to lead to crippling disabilities. It is the most common "autoimmune" disease, affecting three times more women than men. It is characterized by inflammation and destruction of cartilage in the joints, often causing deformities in the fingers. Despite continued research, the cause of RA is unknown. Some researchers believe that an infectious microbe (mycoplasma or virus) is the cause and others believe it is simply the immune system has started to recognize the normal cells as foreign and attacks them ("Microbiology, Principles and Explorations" 5th Edition, by Jacquelyn G. Black, 2002, pg. 495.) In either case, it is recognized that the inflammatory immune response causes the bulk of the damage. In general, the drugs that treat the disease are anti-inflammatories. Since an inflammation response is an immune response, such anti-inflammatories can be viewed as immune suppressants. Some of my friends with the disease have told me that some of the drugs are reasonably effective at keeping their RA in control. However, there are others where the drugs have failed to control the disease. My view is that they may be helpful for many, but are limited in effectiveness because they do not address the root, viral cause.
I have long believed that most if not all autoimmune diseases, where the immune system attacks and damages normal cells, have an infectious agent as the root cause. The immune system is attacking the infectious agent with its usual inflammatory response, which is not very specific to the infectious agent. In doing so, it also damages surrounding normal cells as collateral damage. From the statements from the book referenced above, it appears that I am not alone in this suspicion. The big question is: What is the infectious agent?
For a long time I have been suspicious that it might be a herpes virus. As discussed in the above referenced book, there are a wide variety of herpes viruses that can be responsible for a number of different health issues. I won't attempt to list them here. In general, herpes viruses have the characteristic of infecting nerve cells. Once in the cell, they create a "provirus" that takes up permanent residence in the body of the nerve cell, where the immune system will not attack it. It then serves as a template to produce active viruses. It can be dormant for long periods of time and when triggered, by an unknown cause, it will start to produce active viruses. These viruses will move along the axons of the nerve cells and exit at the terminal synaptic contacts. At this exit point the viruses can damage cells, creating the well recognized lesion which is called a "cold sore" or fever blister" in the case of herpes simplex. The damage can be due to the virus or due to the inflammation response. In other types of herpes infections the herpes damage can be internal and not visible on the skin. Six variations of the herpes virus have been identified so far and that is certainly not the end. The infection usually cycles from dormant to active and back to dormant again.
Upon a closer look, it can be seen how this mechanism of virus production and dispersal serves to protect the source, provirus, in the body of the nerve cell. The immune system's inflammation response will attack the active viruses that are exiting at the synaptic contacts, which are spatially removed from the nerve body. Thus the nerve body, which is the host for the source provirus, is protected from the immune system's inflammation response. Since nerve cells have a long life, a herpes infection does also, essentially the life of the person.
If this is a cause of RA, then there must be infected nerve cells that have axons with terminal synaptic contacts in the joints where the inflammation is observed.
Historically, the common treatment for a herpes virus is the amino acid L-lysine. It appears that the mechanism of the lysine is to encourage the provirus to become dormant again stopping the production of more viruses. There are also drugs designed specifically to attack the herpes virus, which appear to be effective. If it is the cause, I reasoned that L-lysine as well as the drugs targeting the herpes virus should be effective in treating RA.
At this point in my thinking, I was reading the journal: The Scientist, Nov. 17, 2003, V. 17, No 22, pg.8. The article is titled "Natural Is Not Necessarily Better". It is primarily focused on breast milk sometimes transmitting viruses to the infant. As part of the discussion it also states that "A study conducted on patients with rheumatoid arthritis showed that the prevalence of HTLV-1 Tax positivity is at least three times higher in such patients than in healthy individuals." It also concludes that the virus was acquired transplacentally or by breast milk. HTLV-1 is a retrovirus discussed in the above referenced book on pg. 262. Could this be the cause of RA and not the herpes virus? Because it is a retrovirus, it is similar to the HIV virus responsible for AIDS. If that is the case, lysine and herpes drugs may be ineffective. There is no clear evidence that they are effective for retroviruses. Retroviruses are very different than herpes viruses. They are RNA viruses while herpes viruses are DNA viruses so one would not expect them to respond the same to the same treatments.
I then happened to read the book: "The Virus Within, A Coming Epidemic" by Nicholas Regush, 2000. This book mainly addresses HIV and AIDS. As part of this, it was found that, in the case of AIDS, there appeared to always be a co-infection with the herpes virus, Human Herpes Virus No. 6 (HHV-6). The evidence also indicated that HHV-6, not HIV, was the primary cause of cell damage and thus death. It occurred to me that if there was a HTLV-1 infection in RA, similar to HIV, there might also be a herpes co-infection. Similar to HIV, the herpes virus might be the primary cause of cell damage. If this was the case, then herpes treatments might be effective in treating RA.