Topic: My Theory Of Persistence & Potential Resolution Of Lyme Disease
METALLlC BLUE
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posted
In the Rife thread I discussed a concept that I've been considering for awhile. As I've studied different aspects of human anatomy, physiologly, and microbiology, I've come across some ideas that appear coherent when considered in the context of borrelia infection. Discussing this may be of value, though it is entirely untested, and may contain many intellectual flaws.
See if you can fill in the holes, or if any particular hypothesis can be formulated to simplify a potential application.
My Theory Of Persistence & Therapeutic Resolution
I treat borrelia in cycles with Rife presently. I plan on adding an antibiotic that I know without a doubt has a significant impact on the borrelia, but instead of remaining on the therapy constantly, I plan on using it for two weeks (Until the Herxheimer reaches it's peak) and then I will pull the antibiotic and continue Rife therapy. I will then repeat the cycle in a staggering pattern, such as 2 weeks on abx, 3 weeks off, 2 weeks on, 4 weeks off, 2 weeks on, 5 weeks off.
I believe that the primary reason Lyme Disease continues to cause symptoms is this:
Cause Of Persistence: Avascular sequesteration
I think the problem with Lyme Disease is much like that of other chronic infections. The infection gets into avascular areas (Low/no blood supply) and sequesters itself. It's a simple explanation with no simple solution. Tuberculosis is the same way. I also think the symptoms of Lyme Disease have less to do with "Toxins" and more to do with an sub-clinical inflammatory response as a result of chronic stimulation from the bacteriums organic antigens. This is not true for everyone however, especially the most inactive and debilitated patients with high bacterial loads. The threshold for causing "illness" is probably pretty low, which is why symptoms remain so troublesome even after nailing the infection with heavy antibiotic therapy. The sequestered infection remains unharmed, and when therapy ends, the remaining bacteria begins repopulating the body. The fact that the infection has the ability to adapt quickly by changing it's metabolism and converting into other forms just confirms that even more.
Cycling Antibiotic Therapy
Slow dividing infections with host defense mechanisms that hide in avascular body parts are a pure ***** to kill. Antibiotics will not kill the infection unless those antibiotics are cycled long term and in an "on/off" pattern. I think duration of treatment is far more important than combinations and high doses. For example, if an antibiotic works and leads to a Herxheimer response, I think the antibiotic should be discontinued at exactly the time when the Herxheimer peaks. Then the antibiotic should be removed, enabling the infection to reproduce and resume normal activity. Then therapy is repeated over and over using this pattern.
The Herxheimer Reaction As A Measure
The Herxheimer reaction is the perfect gauge of knowing whether you're killing the infection. Eventually, by cycling, in theory, you gain ground on the infection, surpassing it's ability to repopulate while also encouraging the infection in avascular areas to move out.
This is just a theory of mine.
Overview Of How To Coax Borrelia Burgdorferi Out Of Avascular tissues & alternative forms
A combination of exercise or increased blood flow, cycling of an antibiotic that is "certain" to create a Herxheimer reaction, combined with adequate hydration with trace minerals added, will coax the infection out of these areas of the body. Controlling the inflammatory response will significantly decrease the activity, however to do so I believe the immune system should be mildly suppressed -- which seems counter to what most understand.
How The Immune System Behaves Relative To Borrelia & Symptoms Of Lyme Disease
The immune system is one of the primary contributor to which causes the infection to adapt and move into tissues where it is inaccessible. If the immune response is dampered, then it increases the probability that the infection will become more active. Patients who have used high dose Prednisone add indirect evidence to my theory. The explosive nature in which the infection causes relapse confirms the immune systems role in inducing persistence.
Tri-Combination Therapies At One Time Unnecessary
I also don't believe multiple combinations are required. One or two drug combinations, such as Tetracycline for one routine, or Biaxen/Plaquenil for another routine would be adequate as long as a progressive cycling occurred. Other antibiotic combinations that are simple may work more effectively for other patients, like Minocycline or Doxycycline at higher than standard dosing, but also cycled
Why Pregnancy Alleviates Symptoms & How That Applies To A Solution
I believe this also explains why women who enter pregnancy often experience a drastic decline in symptoms. The dampening of the mothers immune system permits a foreign body (The baby) to develop early on. This leads the infection to become active, but without a normal immune response, the symptoms we typically experience do not generally occur. The moment the mother gives birth, a number of hormones (which we do know with certainty, such as Estrogen, progesterone, HSC (Human Chorionic Somatomammotropin)) or HPL (Human Placental Lactogen), Calcitonin, Thyroxine (T4 & T3), Insulin, Relaxin, Oxytocin, Erythropoietin , Cortisol. Prolactin decline almost immediately, leading to a relapse as the immune system comes back online. Note that a number of these hormones contribute to immunosuppression in the same way transplant supplementation is used to prevent rejection.
This also opposes the concept of bacterial endotoxins playing a major role. In a high load infection, the story is different, but in a low load infection, I don't believe that is the issue.
Immunosuppression: How?
Exercising daily, using aerobics (Which also counters Dr. Burrascano's opinion), combined with other moderate immunosuppression should suffice including the use of steroids or other natural therapies. We understand to some degree how the hormones of Pregnancy alter very specific aspects of the immune system without compromising the mother's ability to survive effectively during pregnancy.
This confirms that we can tease out a method of manipulating immunity while sparing the host from opportunistic infection, which would be more problematic with steroids or other risky suppressants. The cells most engaged in the attack on borrelia clearly are impaired from the hormone combinations.
Disclaimer: Highly experimental, and Risky
I do not suggest anyone attempt this theory unless they are desperate and no other therapy has worked. They should speak to their physician. It is unlikely they will gain support, as the concept is highly theoretical and ignores a number of concepts such as co-infections, as well as the risk of opportunistic infections which take hold during immunosuppression.
Chemotherapy
Someone asked me why Chemo Therapy could not be used to kill borrelia. Cancer patients demonstrate to us that Chemo therapy is "not" an effective method to kill infectious diseases. The risk of opportunistic infections substantially increases while on Chemo Therapy and the damage done to other parts of the body is profoundly unnecessary. Additionally, the infection (borrelia b.) will simply adapt to this new environment as it does any other which threatens it's survival, including antibiotics
Final Note: A number of probiotics also dampen immunity and or modulate it. Plaquenil and other immuno modulators, including hormones considered during pregnancy may be potentially used in men to reduce the symptoms, and in theory, kill the infection more quickly and efficently, though the duration of therapy will still likely be 12 months +
[ 04-23-2011, 10:52 AM: Message edited by: METALLlC BLUE ]
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
posted
Metallic Blue, Are you concerned that the cycling of antibiotics will allow the bugs to become resistant?
-------------------- We really know so little about the body and the microbiome. Posts: 261 | From Southern California | Registered: Jan 2011
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Razzle
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I think there is merrit to your theory. When I was on immune supressive treatment and had to take an antibiotic for a sinus infection (this was before I knew I had Lyme), I tolerated the antibiotic well and felt better than I'd felt in years. Off the immune suppressive treatment, but on the same abx - this time for Lyme treatment, I felt terrible and didn't feel like the abx did much for my Lyme symptoms at all.
But I think the key here is finding a way to reduce inflammation more than to suppress the immune system itself. Granted, there is some overlap here - immune mediators of inflammation are derived from an immune response.
I also really like the pulsing abx idea. I think it does more than just coax the Lyme out from hiding - it also reduces the chance of developing yeast overgrowth and gives probiotics a chance to work between abx pulses.
I seem to remember something about Dr. B saying he found that in some of his sickest patients, he had to let their symptoms get really bad, then he'd hit them with huge doses of abx for a short time. They'd herx severely, then he'd pull them off the abx. Their symptoms would get severe again, so he'd hit 'em again with the big doses of abx for a short time. He did this a few times and then it seemed as thought their Lyme just disappeared. I guess he hit the Lyme when it was most vulnerable by letting them get really sick while not on abx, and then hitting them with the big doses of abx.
Thanks for sharing...this is a most interesting idea.
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4166 | From WA | Registered: Feb 2011
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METALLlC BLUE
Frequent Contributor (1K+ posts)
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quote:Originally posted by 365SunnyDays: Metallic Blue, Are you concerned that the cycling of antibiotics will allow the bugs to become resistant?
No, in-fact I have evidence to the contrary. It is common among Lyme Disease patients to use an antibiotic for a lengthy period of time. The infection initially reacts, producing a Herxheimer reaction. As a plateau is reached, either symptoms subside, or continue (depending on the bacterial load vs the symptom threshold of the individual.
When the antibiotic no longer works, which appears -- based on clinical observations of a wide spectrum of physicians who treat the illness long term, 6-8 months is the point in which the antibiotics lose effectiveness.
If the antibiotic is then discontinued, and restarted 2-3-4 or even 5 months later, the individual will experience a Herxheimer response just as they initially did, confirming that mutation isn't the primary cause of resistance, but rather adaptation physiologically and the ability of the infection to be mobile, finding safe havens where it can continue to survive.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
METALLlC BLUE
Frequent Contributor (1K+ posts)
Member # 6628
posted
quote:Originally posted by Razzle: But I think the key here is finding a way to reduce inflammation more than to suppress the immune system itself. Granted, there is some overlap here - immune mediators of inflammation are derived from an immune response.
Two key points here stood out to me. One: Reducing inflammation. I do not believe that reducing inflammation will coax the infection into an active state. If that were true, most of us would not be suffering even while on antibiotics. The bacterium clearly ignores the inflammatory response, while also contributing to it.
The particular immune system cells, such as Macrophages, Monocytes, Cytotoxic Lymphocytes (Natural Killer Cells), seem to be the primary attackers, which induce persistence.
This is why a shot-gun immuno suppressive concept was presented. We know that Lyme Disease also suppresses the immune system in certain ways, but other immune-cells remain unaffected. These unaffected cells are likely the very cells which aggravate and antagonize the infection, forcing it to alter forms, or remain mobile. It also likely is the cause of why the infection moves from extracellular to intracellular areas. The cells which devastate the infection outside become ineffective. The cells which are known to tag, and read intracellular infection, are suppressed to some degree, such as those which the CD57 Test looks for.
This infection is systematic in it's behavior, and understanding the core mechanisms specifically would provide a successful therapy with minimal risk, but since we don't know the specific aspects of the immune system completely, we can't be certain which are a threat, which are being manipulated, and which are being destroyed. Presently we only know of one particular immune system cell which is reduced substantially. Other cells proliferate, such as Monocytes.
Clearly these cells are not effective of their own accord, but they are the basis for which other immune system cells develop. The branching of the immune system could probably be used to identify which cells antagonize the infection. Reviewing all the studies done on Lyme Disease and it's response to specific cells may provide more specifics. Plenty of studies on these do exist but none have been coherently described in a meta-analysis. A simplified method may be to compare and contrast the pregnancy hypothesis, identifying how the mother's body tolerates foreign material (Both Lyme and the fetus), but then relapses extensively following birth.
The second issue is probiotics and reducing opportunistic infections. Mild immunosuppression will likely still encourage yeast overgrowth in those most susceptible. However, probiotics will aid in suppressing them and should be used during periods where antibiotics aren't used heavily in the cycling period.
Key Point We understand to some degree how the hormones of Pregnancy alter very specific aspects of the immune system without compromising the mother's ability to survive effectively during pregnancy.
This confirms that we can tease out a method of manipulating immunity while sparing the host from opportunistic infection. The cells most engaged in the attack on borrelia clearly are impaired.
If someone is willing to study the immunological changes in pregnant women, and what encourages those changes, the theory may have a more refined basis and be less risky to attempt.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
posted
The amazing nature and resiliency of your brain never ceases to amaze me, Mr. Blue!
Fascinating stuff!
Posts: 564 | From Tick Hell | Registered: Oct 2008
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METALLlC BLUE
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It has been suggested to me that I re-write this in the form of a question and contact Dr. Burrascano and Columbia's Lyme Center. At present he is researching these very topics and may find value in the question.
I am having someone re-write the concepts in a format which is less presumptuous and more appealing.
Does anyone have contact information that is current for Dr. Burrascano?
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
Rumigirl
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Member # 15091
posted
Several issues that were mentioned about Dr. B's guidelines and treating experience that were not completely understood:
He treated patients that needed it for as long as it took to become COMPLETELY free of symptoms for at least two months (even if this took 3-5 years). Then, he had them go off abx.
If they relapsed (and this he did with himself and some patients, not everyone), he waited until they relapsed ALL THE WAY BACK. He said, "don't be afraid to let yourself go all the way down."
Then, he would hit it hard with abx again until they became completely sx free for several months. THen go off abx. And if they relapsed again, the same procedure.
The most people relapsed was 3 times.
On his exercise recommendations: he doesn't say don't do aerobics! He says not to do them for a period of time, say 6 months, while you are building yourself up with strengthening. Then, add aerobics.
I do have his contact info, MB, when you are at that point in this endeavor. I won't be giving it out to everyone, however!
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METALLlC BLUE
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I have narrowed down a substance the achieves the immuno-modulation we're looking for. However immuno suppression would still be required for brief "spikes" of 3-5 days during the therapy I'm hypothesizing.
Read most posts here on this last page for further information:
D Bergy
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Member # 9984
posted
I would guess that the inflammatory state of a Lyme patient is similar to that of someone with an autoimmune disease, like myself.
It exists as the immune system tries to rid the body of the invader. Inflammation is a normal response to a harmful pathogen. The immune system is ineffective in removing the pathogen, so it becomes a vicious cycle of inflammation with no resolution to the problem invader.
It is unproductive inflammation, which in the long term is destructive to your own tissue, if left unchecked.
In the case of Lyme, the pathogen itself weakens, or alters the immune response. With the more typical autoimmune disease, a pathogen may be involved, or not. It is not conclusive at this time.
Heavy metals or other toxins in the body can also contribute to this immune system problem, or at least they do not help.
I think you are more right than wrong in your thinking.
Dan
Posts: 2919 | From Minnesota | Registered: Aug 2006
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Your protocol and reasoning are not that far different than Dr. J in DC....no constant dosing as LYme is slow growth and also the breaks every few weeks for multiple reasons.
Posts: 410 | From Victoria BC, Canada | Registered: Jul 2008
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nefferdun
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I was also going to say that Dr. J pulses abx. It is several weeks on and then one week off. He uses the abx 5-7 days a week so most people are not on it continuously at any time. He pulses the tindamax/flagyl the last few days before the break.
It seems like his idea is to coax the cyst out and then when it is a spirochete, go after it again.
He uses this method for the co-infections too. I have not been to him. This is just what I have read.
I think you (in general) have to know what you are doing. I was feeling pretty well last year and decided to pulse my meds so I could sleep better at least a couple days a week. In one month I took a nose dive and I have not come out of it yet.
But my problem now is babesia. The Bb seems undercover. I can't remember the last lyme flare, which used to come like clockwork every full moon.
-------------------- old joke: idiopathic means the patient is pathological and the the doctor is an idiot Posts: 4676 | From western Montana | Registered: Apr 2009
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RDaywillcome
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FOR REAL?
Posts: 1738 | From over the rainbow | Registered: Jul 2009
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