Townsend Letter for Doctors and Patients, April 2006 i273 p38(2)
New York's OPMC issues memo on "minority" therapy mainstream media picks up on TNF in Avian flu. (Office of Professional Medical Conduct)(tumor necrosis factor) Marcus A. Cohen.
Full Text: COPYRIGHT 2006 The Townsend Letter Group
Last July, Dennis Graziano, director of the Office of Professional Medical Conduct (OPMC), New York Department of Health, put out a memorandum on the investigation of practitioners using treatments "not universally accepted by the medical profession" (i.e., treatment given by a minority of MDs). The memo endorsed principles currently in place, based on Article 131 of the New York Education Law. In defining the practice of medicine, this article states that its wording "shall not be construed to affect or prevent ... [a] physician's use of whatever medical care, conventional or non-conventional, which effectively treats human disease, pain, injury, deformity, or physical condition."
New York physicians who offer beneficial treatment departing from community practice should be encouraged by the "message" the July memo sent to OPMC investigators and prosecutors. So long as a treatment mode meets the criteria of Article 131, practice or recommendation of that mode does not "by itself constitute professional misconduct." Consequently, it is against OPMC policy and practice to "investigate or charge" a practitioner solely on that practitioner's "recommendation or provision" of such treatment modes.
I interviewed Assemblywoman Nettie Meyersohn (Democrat, District 27, Queens) and Assemblyman Adam Bradley (Democrat, District 89, Middle & Upper Westchester) about the OPMC memo. Meyersohn and Bradley had worked steadily for a year with counsel from Governor George Pataki's office to draft the memo. They had considerable input from Lyme Disease and Complementary and Alternative Medicine (CAM) activists.
Full Size Picture The Lyme activists were concerned that the Governor's veto of Assembly and Senate due process reform bills exposed doctors to disciplinary action for treating persistent and recurrent Lyme patients with long-term antibiotics. Antibiotics are mainstream therapy for numerous bacterial infections, but long-term antibiotic care for Lyme infection can have adverse effects. Insurers are also opposed to extended antibiotic care in Lyme disease (because of its high cost), and some insurers have asked the OPMC to investigate MDs giving Lyme patients lengthy antibiotic treatment, which the insurers contend is an unproven therapy.
Meyersohn and Bradley were aware that protracted IV antibiotics carry a risk, but until safer, effective treatment becomes available, they felt Lyme patients had a right to a therapy that in numerous cases relieves or even resolves the condition. Governor Pataki agreed, Assemblywoman Meyersohn said, hence, his interest in the memo.
I pointed out to Meyersohn and Bradley that the OPMC has a documented history of regarding internal memoranda about its operations as less binding than law. Both were familiar with that history and were taking a "wait and see" position on implementation. Both were looking ahead to the next legislative session and to passage by the Assembly and Senate of a smaller, broadly acceptable package of reforms to minimize due process abuse by the OPMC.
A woman working in Meyersohn's office involved the assemblywoman in Lyme disease issues four years ago. (Meyersohn has been in the Assembly for 28 years.) The woman became infected and experienced difficulty finding a physician willing to administer long-term treatment, if needed. Assemblyman Bradley, a relatively new Assembly member, represents a suburban area with pockets of Lyme infestation.
Click for Full Size Monica Miller, legislative affairs consultant for the Foundation for the Advancement of Innovative Medicine (FAIM), for many years was pleased by language in the memo that went farther than provisions of the 1994 Alternative Medical Practice Act in protecting CAM and other physicians using treatments not widely accepted by mainstream medicine from OPMC investigation.
A day before I submitted this column to the Townsend Letter for publication, I phoned Assemblyman Joel Miller (Republican, District 102, SW Duchess County, including Fishkill, Peekskill, and Poughkeepsie). Half a year had sped by since my interviews with Assembly members Nettie Meyersohn and Adam Bradley, and I wanted a quick "bi-partisan" read on the outcome of their "wait and see" approach to the OPMC memo.
Miller had been a major player in drafting the memo. His Assembly district encompasses endemic Lyme disease areas, and a large number of residents have been infected. He's shown an early and abiding interest in facilitating effective treatment for Lyme patients (in general). He's long supported efforts to curb due process abuse by the OPMC.
Miller felt that the OPMC memo had improved the regulatory environment for New York MDs who use long-term antibiotics to manage persistent Lyme. Like Meyersohn and Bradley, during the current legislative session he's working on an acceptable package of reforms for the OPMC.
More on Media Coverage of Avian Flu Research
Late in 2006, when I drafted my column on Avian Flu and vitamin A (Townsend Letter, Feb./March 2006), I could come up with only one mainstream newspaper report about the research on Avian Flu at the University of Hong Kong that accounted for this strain's high fatality rate: the Ottawa Citizen, on November 12, 2005. I've learned since that wire services, including Reuters (1) and other newspapers, had reported on the Hong Kong research.
On December 16th, The Wall Street Journal ran a feature story on the findings at the University of Hong Kong; it was titled "Avian Flu Death Rate May Be Tied To Overkill By Immune Systems." The Journal reporter, Marilyn Chase, a science writer, interviewed the lead flu researcher, J.S.M. Peiris, on what prompted his team to investigate "overkill" by the immune system. The Journal feature included the following statement:
"'Illness seen in early bird-flu patients in 1997 made us think the immune response might be hyperactivated,' Dr. Peiris says. Among the evidence, he found immune cells called macrophages that normally devour germs and infected cells were instead 'gobbling up everything in sight and killing healthy red cells.'"
The Journal article noted that early investigation, published by the Hong Kong researchers last summer, had indicated that the H5N1 virus strain had caused the macrophages to "spew out excessive amounts of an inflammatory chemical called tumor necrosis factor [TNF]." Further investigation by Peiris' team at the University of Hong Kong (published in the fall), the Journal story said, had revealed "that human lung cells infected with H5N1 churn out more inflammatory substances--such as interferons and interleukins--than lung cells infected with a regular flu virus."
To date, the research at the University of Hong Kong has been conducted on test tube models utilizing human macrophage and lung cells, but the evolving in vitro picture of H5N1 has led some scientists to spot a resemblance between this lethal Influenza A strain and the highly lethal strain responsible for the 1918 flu pandemic. The latter caused hemorrhagic pneumonia and targeted young people with naturally strong immune responses. Bear in mind that 20th-century pandemic was transmissible human to human; H5N1 has not yet mutated into such a form and may never do so. Most of the 135+ cases of H5N1 in humans since 1997 have been attributed to poultry and other infected birds.
What avenues of treatment are medical researchers tobogganing down should H5N1 genetically morph into a strain capable of exploding into a human pandemic? Both the Reuters dispatch and The Wall Street Journal feature on H5N1 point toward drugs that suppress immune response and antivirals like Tamiflu. (Tamiflu is the antiviral of choice at the moment, given with 48 hours of first symptoms).
On the combined antiviral/immune-damping approach, Reuters quoted Dr. Anthony Fauci, Director, National Institute of Allergy and Infectious Diseases (US), and the Journal quoted a medical epidemiologist with the Influenza branch at the Centers for Disease Control and Prevention (US). The CDC epidemiologist cautioned that timely treatment would be a problem. "Patients aren't presenting early in the illness," observed the CDC representative, adding: "If this cytokine storm has already been triggered, antiviral drugs aren't going to turn it off."
I'll conclude this follow-up on my column about Avian flu and vitamin A with another quote from the Journal feature: "Taming the immune response without destroying defenses is a great idea, but we don't know how to do that yet," says flu expert Robert Belshe of St. Louis University. We don't know how to do that? My column on Avian flu and vitamin A detailed a study at the National Health Research Institute in Taiwan (published a month before the first report from the Hong Kong researchers on TNF and H5N1) and a number of earlier studies elsewhere (on lung tissue and Lyme arthritis), all of which indicated that vitamin A (and certain of its metabolites) can protect human lung tissue against hyperinduction of TNF. Without antivirals! Without drugs that destroy immune function! And at a fraction of the cost and time involved in research and development of antivirals and immune suppressors! I should add that vitamin A downregulates, too, other inflammatory substances shown by recent investigation to be churned up during H5N1-induced cytokine storms, most importantly, Interleukin 6.
Perhaps I should e-mail the draft of my column about Avian flu and vitamin A to Journal reporter Marilyn Chase and see if she picks up on the Taiwan research on vitamin A. If she does write about its value in a potential H5N1 human pandemic, I'd wait--without holding my breath--to see if the medical research community and drug companies seriously look into developing a patentable vitamin A compound for bird flu. (A synthetic version would be their most likely response.)
While in an adding mode: In my Avian flu column, I neglected to refer to a 1994 study at the M.D. Anderson Center, Houston, Texas, which found that retinoic acid (an A metabolite) powerfully inhibited TNF production by macrophages. That reference is included among the footnotes here. (2)
Notes
1. Fox, M. Bird flu kills as "storm" hits lungs. Reuters. Washington, DC; November 12, 2005.
2. Mehta, K et al. Inhibition by all-trans-retinoic acid of tumor necrosis factor and nitric acid production by peritoneal macrophages. J Leukocyte Biol. 1994;55:336-42. by Marcus A. Cohen, 8 East 96th Street #1C * New York, New York 10128
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Modulation of Tumor Necrosis Factor by Microbial Pathogens
Masmudur M. Rahman, Grant McFadden*
"In response to invasion by microbial pathogens, host defense mechanisms get activated by both the innate and adaptive arms of the immune responses.
TNF (tumor necrosis factor) is a potent proinflammatory cytokine expressed by activated macrophages and lymphocytes that induces diverse cellular responses that can vary from apoptosis to the expression of genes involved in both early inflammatory and acquired immune responses.
A wide spectrum of microbes has acquired elegant mechanisms to overcome or deflect the host responses mediated by TNF. For example, modulatory proteins encoded by multiple families of viruses can block TNF and TNF-mediated responses at multiple levels, such as the inhibition of the TNF ligand or its receptors, or by modulating key transduction molecules of the TNF signaling pathway.
Bacteria, on the other hand, tend to modify TNF-mediated responses specifically by regulating components of the TNF signaling pathway. Investigation of these diverse strategies employed by viral and bacterial pathogens has significantly advanced our understanding of both host TNF responses and microbial pathogenesis. This review summarizes the diverse microbial strategies to regulate TNF and how such insights into TNF modulation could benefit the treatment of inflammatory or autoimmune diseases."
Proposed mechanisms and preventative options of Jarisch-Herxheimer reactions.
Pound MW, May DB.
Department of Pharmacy Practice, Campbell University School of Pharmacy, Buies Creek, NC 27506, USA.
OBJECTIVE: To review the aetiologies and preventative methods associated with Jarisch-Herxheimer reactions (JHR). DATA SOURCES: Ovid Medline (1966-June Week 1 2004) was utilized to assess biomedical literature; a review of the bibliographies of articles was also performed. DATA SYNTHESIS: JHR often occurs with the treatment of spirochete infections. However, the mechanism by which the reaction takes place is not clearly defined.
CONCLUSION: Studies suggest with conflicting evidence that the JHR is caused by release of endotoxin-like material from the spirochete as well as cytokine elevation in the body. It appears the type of drug and the rate of spirochete clearance from the body have little effect on the incidence of the reaction. Many pretreatment options have been explored with limited efficacy with the exception of anti-tumour necrosis factor antibodies.
Publication Types:
* Review
PMID: 15896248 [PubMed - indexed for MEDLINE]
---------------------------------------------
Neurosci Lett. 2005 Aug 12-19;384(1-2):112-6.
Pathogenesis of Lyme neuroborreliosis: mitogen-activated protein kinases Erk1, Erk2, and p38 in the response of astrocytes to Borrelia burgdorferi lipoproteins.
Ramesh G, Philipp MT.
Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, 18703 Three Rivers Road, Covington, LA 70433, USA.
Lyme borreliosis, which is prevalent both in the US and in Europe, is an infectious disease that may cause local inflammation in numerous organs. We have hypothesized that, as with some neurodegenerative diseases, the pathogenesis of the neurocognitive deficiencies associated with Lyme neuroborreliosis of the central nervous system also has an inflammatory component. Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. Mitogen-activated protein kinases (MAPK) play a key role in the regulation of neuronal development, growth, and survival, as well as that of pro-inflammatory cytokine production. As a model, we explored the possibility that MAPK-mediated lipoprotein-induced apoptosis and gliosis of rhesus monkey astrocytes stimulated in vitro. Lipoproteins are the key inflammatory molecule type of Borrelia burgdorferi, the spirochete that causes Lyme disease, and we had previously shown that lipoprotein-induced TNF-alpha production in astrocytes caused astrocyte apoptosis, and IL-6 enhanced proliferation of these cells. Lipoproteins readily activated p38 and Erk1/2 MAPK, thus enlisting these pathways among the kinase pathways that spirochetes may address as they invade the central nervous system. We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively. Lipoprotein-stimulated IL-6 production was unaffected by the MAPK inhibitors. In contrast, inhibition of both p38 and Erk1/2 significantly diminished TNF-alpha production, and totally abrogated production of this cytokine when both MAPK pathways were inhibited simultaneously. MAPK inhibition thus may be considered as a strategy to control inflammation and apoptosis in Lyme neuroborreliosis.
PMID: 15893422 [PubMed - indexed for MEDLINE]
-----------------------------------------------
But I don't think anyone is treating lyme with anti-tumor necrosis factor antibodies yet.
Posts: 8430 | From Not available | Registered: Oct 2000
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posted
Johns Hopkins used an anti-TNF drug in RA in 2004!!
See this:
�Johns Hopkins Arthritis Center Website (http://www.hopkins-arthritis.org)
Does Reinstituting Anti-TNF Therapy Following Relapse in Remission in RA Have Similar Efficacy?
Summarized by Jon Giles, M.D. and Joan Bathon, M.D.
Approximately one-third to half of patients with established RA will experience deterioration in symptom control in the year following discontinuation of disease-modifying anti-rheumatic drugs (DMARDs). Particularly for older DMARDS, such as parenteral gold and anti-malarials, reinstitution has been suggested to be less effective in controlling RA disease activity.
Though this phenomenon is not as well studied for methotrexate and unstudied for newer cytokines inhibitors, there is concern that reinstating an effective DMARD after discontinuation may not achieve the previous level of efficacy. For this reason, DMARDs are generally continued through long periods of symptom-free remission. Here, Buch et al (Rheumatology; 43, 2004: 243) examine relapse of RA after discontinuing infliximab and efficacy after restarting the drug. METHODS 17 of the 24 subjects enrolled in the ATTRACT (Anti-TNF Therapy in RA with Concomitant Therapy) Trial in Leeds, UK who received infliximab were followed into the extension phase of the trial.
In the first two years of the trial, patients with RA were randomized to placebo or 3mg/kg or 10mg/kg doses of infliximab administered every 4 or 8 weeks (comprising four infliximab treatment groups). Methotrexate of at least 12.5 mg per week was continued in all groups and was continued into the extension phase after infliximab therapy was discontinued.
At 24 months, infliximab therapy was stopped, and subjects were followed for relapse. At relapse, defined as a 20% or greater deterioration in ACR composite score, subjects were restarted on infliximab at 3mg/kg at standard dosing schedule and reassessed at nine months for change in ACR response.
RESULTS All 17 patients flared after discontinuation of infliximab. Mean time to flare was between 13.5 to 20 weeks. A statistically non-significant trend in greater time to flare was observed in the two groups previously treated with 10mg/kg of infliximab compared with the two groups previously treated with 3mg/kg of infliximab. 14 of the 17 patients were retreated with at least 9 months of 3 mg/kg of infliximab after relapse. 12 of these 14 achieved comparable ACR-(n) responses on retreatment as observed on na�ve treatment.
The remaining two patients had a less efficacious response on retreatment. No infusion reactions or drugspecific toxicities were noted on retreatment.
CONCLUSIONS Continuation of anti-TNF therapy is required to maintain remission in established RA. Reinstituting therapy after discontinuation and relapse is of comparable efficacy to response in na�ve subjects.
EDITORIAL COMMENT This small study addresses important issues that have not been previously investigated in the context of TNF inhibitors, namely whether continuous TNF therapy is required in TNF responsive patients and whether discontinuous TNF therapy can achieve the same level of efficacy as continuous therapy. This question has practical implications owing to the cost and toxicities related to TNF therapy. Unfortunately, this imperfectly designed and underpowered study cannot reliably support the stated conclusions.
Importantly, it is impossible to refute an ``induction'' effect with the use of TNF inhibition, since no non-TNF treated patients are included in this extension sub-analysis. In other words, among the members of this subgroup, the two years of initial infliximab may have made latter responses better on retreatment than matched subjects that had not received TNF inhibition during that period. Despite this, these preliminary results are worth noting and suggest areas for further investigation.
Posts: 8430 | From Not available | Registered: Oct 2000
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bettyg
Unregistered
posted
Glad you 2 are enjoying yourselves here.
I couldn't read anything so I'm SOB, scrolling on by.
If you have the time, please edit your long posts to norml looking paragraphs making it easier for us neuro lymies to read, and DOUBLE space between each paragraph.
posted
Don't think it is worth the effort, betty. No one on this forum is likely to be this interested in the science of cytokine regulation, even with small paragraphs. I am just talking to myself. And JimBob isn't looking for anything that doesn't come from the health food store or herbal sources. In his own way, he is as closed to other opinions as is A. Steere and his gang.
This forum leans very far toward alt meds, or at least the people who say the most. So, every now and then I try to pile up some mainstream science on the other side of the balance. Waste of time probably. Too bad the lyme science forum destroyed.
The point of my posts above is that some people think regulating cytokines overproduced because of borrelial influence could be useful in lyme treatment. Cytokines are a product of our own immune systems. This is being done in some cases of arthritis and RA.
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Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
Actually I thought that was very interesting, Lou. Thanks for posting it. Your research skills are amazing. I wish they spent as much energy researching Lyme as RA. I also had to wonder how many of their RA patients really had Lyme.
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
The "side effects" of anti-TNF alpha drugs...
Example: Humira (shots, $$$)
Include cancer and TB.
It does NOT stop osteoporosis.
So let's give Foxamax...it INCREASES TNF alpha (it depletes Mg triggering this...documented) AND it increases CRP...not "heart healthy" and if you need a tooth pulled...watch out for jaw bone destruction.
Okay...next step...Let's try Methotrexate. Guess what it depletes... Choline. Let's deplete choline further and see what happens...
Mg drops "significantly" at the outset of lyme.
Ca influx...protective (most abundant mineral to react with acids to produce hydrogen..to INactivate PFK 1...only glucagon inactivates PFK 2 in the liver) AND high calcium level can be destructive (thyroid),
triggers proteins: TNF alpha (beneficial AND destructive - if too much, esp. eyes),
triggers proteins: angiogentensin II (ditto...protective and destructive), triggers angiogenesis...developing new blood vessels.
(Ticks saliva contains angiogenesis inhibitors.)
Gotta get to the root cause. What nutrient is that pathogen...bacterial, viral, fungal...after/what is it using to lock onto and address those issues...quickly restore the balance.
In the case of Bb it is after choline. It looks to be using a Zn-protein to lock on. So long zinc...hello thymus problems (the thymus is our "seat of immunity"...where "baby" WBCs go to get their "assignments".
In the case of SARS...(virus caused, rapid death from lung complications):
Well...look CLOSELY:
Learning how SARS (severe acute respiratory syndrome) became a deadly threat "possibly teaches us a lesson on how to actively fight so diverse and dreadful diseases as SARS, avian flu or the effects of such biotech weapons as anthrax," said Dr. Josef Penninger of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences.
The research may have wider implications for a type of lung failure known as acute respiratory distress syndrome, Penninger reported in a communication to the journal Nature. It can occur in cases such as sepsis, aspiration of gastric contents, pneumonia and both avian and human influenza.
What those diseases have in common is a type of lung failure. Penninger and colleagues report in Monday's issue of Nature Medicine that, working in mice, they found that angiotensin-converting enzyme 2 (ACE2) is a crucial receptor for the SARS virus.
The result is disruption of the body's protective renin-angiotensin system, leading to respiratory distress syndrome as fluids seep into the air sacks. The renin-angiotensin system uses enzymes to regulate sodium balance, fluid volume and blood pressure.
SARS was first identified in 2003, originating in China and spreading rapidly to Asia, Canada and elsewhere. It killed nearly 800 people and disrupted travel, economics and even some scientific meetings.
The researchers found that the SARS virus binds to the ACE2, Penninger said in a telephone interview.
If disabling ACE2 allowed lung damage to occur, the researchers wondered whether providing more of the enzyme would help. They created more ACE2 and infused it into the mice. The result was to protect mice from the lung failure effects of SARS.
It was effective in two ways, Penninger said. First, ACE2 combined with the virus and prevented it from binding to normal cells. Also, the enzyme protected the mice from acute lung failure.
"We of course need to extend these findings in mice now to humans," Penninger said. "Yet in essence, SARS pointed us to a protein that may help millions of people affected with a previously untreatable disease."
To prevent the binding...well, it looks like Bb is using a Zn+protein to bind to the heparin receptors in the endothelial cells. Heparin helps...to prevent the binding (heparin is an acid) and helps to knock off Bb. But...to destroy the protein part of the Zn+protein...is not a "sugar reducer" because Bb's outer walls do not contain LPS like most other pathogens. It is unique.
It might be that (Zn-DFO) would work.
Once Bb is established...forming a fibrin cloak/biofilm/slime layer...it becomes more difficult, but not impossible.
High doses of Benicar/Crestor (?) (watch CoQ10) or even Mg (cheaper and safer) will help...a LOT.
Bb follows the cholesterol pathway. This is known. To INactivate HMG CoA reductase...halting cholesterol formation in the liver = Mg or Benicar (Crestor too?). VERY high doses.
With Bb using acetylcholinesterase to go after the choline part of acetylcholine...leaving "left over" acetyl CoA -> ketones.
With Bb using the sugar from destroying/breaking down fats...ethanol.
Gotta detox that all that ethanol...does a "number" on the brain cells, not to mention the liver.
The liver, our major "detox" organ is taking a huge hit...fast. This is -> "fatty liver" from a choline deficiency too..."hello" bad metals (bile salts are supposed to remove them. A choline deficiency -> disrupts the Na-K pump. Elastase and fibrin problems (esp. lungs). Elastase is helpful, but if not in check (countered) -> cystic fibrosis.
It is believed the protein, TNF alpha may help to cure lyme (documented). Here are some BENEFITS to this protein:
3. ``one mechanism of action of TNF-alpha ...on thyroid FRTL-5 cells is to inhibit calcium entry.'' PMID: 10092616
4. ``is actually a potent modulator of neurotransmitter interaction.'' hdlighthouse.org/see/immune/tnf.htm
5. ``the body does use tumor necrosis factor-alpha (TNF-alpha) to acutely fight infections. If patients are showing any sign of infectious disease, drugs such as Enbrel (that inhibit the effects of TNF-alpha) are temporarily discontinued.'' www.lef.org/protocols/prtcl-128a.shtml
6. ``After noticing that exposure to the naturally occurring compound TNF-alpha (Tumor Necrosis Factor-alpha) killed malfunctioning immune cells...'' www.diabetesincontrol.com/issue166/item1.shtml
7. ``generally the level of TNF increases with aging. Lactic acid and unsaturated fats and hypoxia stimulate increased formation of TNF. Estrogen increases production of nitric oxide systemically, and nitric oxide can stimulate TNF formation. When oxygen and the correct nutrients are available, the hypermetabolism produced by TNF could be reparative (K. Fukushima, et al., 1999), rather than destructive.'' http://www.ferlowbrothers.com/estrogen_osteoporosis.htm (Original website would not link. Above website says the same.)
8. ``TNF-a is a molecule responsible for activating and proliferating cells of the immune system as well as protecting the body from abnormal cell growth.'' (same source as #7)
9. ``Activity of TNF-a is associated with inflammation, cytotoxicity (destruction of abnormal cells) antiviral activity, and the proliferation of immune cells.'' (same source as #7)
(If you go to the above website, please note the mention of spingolipid metabolites and keep this in mind: syhingomyelinase is Mg dependent)
PMID: 9195931
11. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody'' PMID: 12522038
12. ``The increased bone resorption may be due to an increase in TNF-alpha'' PMID: 14704297
13. ``no detrimental effects on normal neurons and can protect neurons when present in neuronal cultures during in vitro ischaemia...Once TNF's removed, neuroprotection is lost.''
14. ``TNF- a also causes production of sphingosine which can directly block the release of calcium from the sarcoplasmic reticulum and therefore depress cardiac contraction.''
15. ``suppression of insulin action in the liver resulting from TNF-alpha mediated suppression of tyrosine phosphorylation'' Gastroenterology 2004; 126: 840-848,917-919 (Keep in mind insulin ACTIVATES PFK which Bb is dependent on.)
16. ``Total elimination of the TNF-a cytokine apparently creates a less hostile immune environment...Although `Chronic-lyme' is a lympopenic disease, chronic lyme patients do not usually form sarcoid granuloma. Borrelia burgdorferi appears to be a pathogen with insufficient lympopenic activity to proliferate sarcoid granulomas on its own. However, together with other pathogens, it is frequently found as a component of sarcoid inflammation.'' www.joimr.org/phorum/read.php?f=2&I=38&t=38
17. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody'' PMID: 12522038
18. ``Polymerase chain reaction analysis indicated a protection rate of 95% in mice receiving tumor necrosis factor (TNF)-alpha.'' PMID: 8537658
19. These results are in line with previous experiments using cells of the adaptive immune response, indicating that strong T helper type 1 (Th1) proinflammatory responses might be associated with a successful resolution of Lyme disease. PMID: 15958074
But...
TETs = tetracyclines
These results indicate that TETs are not able to act directly on the synthesis of these cytokines, but they may
modulate other pathways that could in turn be responsible for the inhibition of IL-1 alpha and TNF-alpha synthesis.
...evidence of the augmentation of immune responses by tetracyclines...
This is the first study to show an effect of antibiotic therapy on cytokine levels in vivo. PMID: 8331300
They (TETS) alter the body's chosen pathway. OOPS.
I had lunch yesterday with a friend who has RA...very bad. Her hands are very crippled. She is on enbrel...another TNF alpha blocker. Has it stopped her arthritis...naah. She needs surgery for her feet now.
With every drug, evaluate the potential side effects. Weigh them carefully:
Dangerous reactions
More serious reactions to TNF-alpha inhibitors include:
� Infections. TNF-alpha inhibitors decrease the action of the proteins that stimulate the white blood cells in your body, limiting your body's ability to fight infections.
A number of infections have been reported in people taking TNF-alpha inhibitors, ranging from upper respiratory infections to serious infections such as tuberculosis. For this reason, your doctor will ask you about any current or recurring infections you may have and might test you for various infections.
Your doctor will also want to test you for tuberculosis before prescribing a TNF-alpha inhibitor, as well as fungal infections such as histoplasmosis and coccidiomycosis (valley fever), since these infections may worsen and be more severe if you're being treated with a TNF-alpha inhibitor.
Your risk of serious infection increases if you take a TNF-alpha inhibitor along with the interleukin-1 antagonist anakinra. Don't take anakinra if you're taking a TNF-alpha inhibitor. If you develop an infection while taking these medications, you may have to stop the treatment until your infection has been successfully treated.
� Lymphoma. It isn't clear whether TNF-alpha inhibitors in general cause lymphoma -- some studies have found a link, while others haven't. People with rheumatoid arthritis have an increased risk of lymphoma even without TNF-alpha inhibitor therapy. An increased risk of lymphoma has been associated with infliximab (Remicade).
� Autoimmune diseases. TNF-alpha inhibitors have been associated with the development of autoimmune diseases, in which your body's defenses attack both the invading germs and the healthy tissues. In rare cases people taking TNF-alpha inhibitors have been diagnosed with a condition similar to lupus.
� Neurologic and demyelinating disorders. Conditions such as myelitis, optic neuritis, Guillain-Barre syndrome, multiple sclerosis and seizure disorders have occurred in people taking TNF-alpha inhibitors.
� Blood disorders. In rare circumstances individuals taking etanercept (Enbrel) have developed severe, sometimes fatal blood disorders.
What is the underlying CAUSE of the increase in TNF-alpha?
1. "CONCLUSIONS: These data demonstrate a relationship between angiotensin II and intracellular magnesium and calcium. In hypertension, angiotensin II-stimulated calcium responses may be related to simultaneously decreased intracellular magnesium concentrations." PMID: 8390527
Too many free radicals (this is why Vitamin E and A drop in lyme...documented)...too much oxidative stress...happens to our astronauts too. PFK drops, can lead to anemia. Researchers KNOW this...they are trying to figure out how to measure and deliver Mg to our astronauts because it is the SAFEST way to combat oxidative stress.
Saunas trigger acetylcholine release. Bb does NOT want this released. It is an ester.
Far-infrared saunas/trivalent ozone saunas trigger NO (nitric oxide = dilation) which in turn triggers acetylcholine (constriction).
Or...shatter the crystal outer cell wall using highly targeted frequencies...yes, they do work...and now are being used in cancer. They are trying to figure out how to send a mineral into a cancer cell and then heat that mineral up using frequencies. Microwave oven work on frequencies and they do destroy pathogens.
Guess which minerals burn the hottest...with a white light...to ignite other minerals (basis of fireworks). Al and Mg. That should come as no surprise.
Now what drives more Mg INTO the cells...ATP. But the pump has to be working. ATP, acetylcholine, thiamine, melatonin...all of these contain "H16".
Why does our Army have "H16" kits? Why are we:
"NEW MAGNESIUM PEROXIDE-BASED ANTIBACTERIAL AGENTS FOR COTTON AND COTTON BLENDS. Development of environmentally benign ANTIBACTERIAL agents for application to textiles and other materials is necessary and desirable because many of the older, effective antibacterial agents have been or are in the process of being removed from commercial use.
Thus, scientists at ARS, SRRC in New Orleans developed new, environmentally benign antibacterial agents by the reaction of two readily available inorganic compounds: hydrogen peroxide and magnesium acetate tetrahydrate." This activity is retained for 30 launderings on the blend fabrics and up to 50 launderings on cotton fabrics. US Patent 5,656,037.
Acetate..now that's an interesting word...
I hope you realize I am on "thin ice".
P.S. Selenium will help to a degree...it is another "nutrient" in Group 16.
[ 15. April 2006, 10:18 AM: Message edited by: Marnie ]
Posts: 9428 | From Sunshine State | Registered: Mar 2001
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I do not agree that posting mainstream science is a waste of time. It is that mainstrem science broadened and enriched by what are called alternative medicines which is going to save us. As for nobody being interested, dear Lou, you need to think again. Even if one person reads and benefits from what you have to say it is worthwhile.
Further I think we need to rethink the general trashing of the conventional medicine. It is true that it has failed in the area of Lyme disease and failed miserably. But in other areas it has done truly remarkable and wonderful things. Yes there are huge problems, but let us not throw out the baby with the bath water here.
To swap one form of dogma or revealed faith for another is foolish and repeats the same mistake the conventional medical establishment is making. WE need to argue from facts, science and the truth.
As for this business of the immune system, I think this is where the major breakthroughs will come and will benefit not only people suffering with Lyme disease but who know what else as well.
So, as I told Dr. Jones I tell you. Fight the good fight with all thy might!! Don't give out, don't give up and don't give in. We must all develop patience, endurance and courage. Cause we need them. Cheers. Thomas Parkman
-------------------- Thomas Parkman Posts: 341 | From Columbia SC 29206 | Registered: Feb 2003
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I do not agree that posting mainstream science is a waste of time. It is that mainstrem science broadened and enriched by what are called alternative medicines which is going to save us. As for nobody being interested, dear Lou, you need to think again. Even if one person reads and benefits from what you have to say it is worthwhile.
Further I think we need to rethink the general trashing of the conventional medicine. It is true that it has failed in the area of Lyme disease and failed miserably. But in other areas it has done truly remarkable and wonderful things. Yes there are huge problems, but let us not throw out the baby with the bath water here.
To swap one form of dogma or revealed faith for another is foolish and repeats the same mistake the conventional medical establishment is making. WE need to argue from facts, science and the truth.
As for this business of the immune system, I think this is where the major breakthroughs will come and will benefit not only people suffering with Lyme disease but who know what else as well.
So, as I told Dr. Jones I tell you. Fight the good fight with all thy might!! Don't give out, don't give up and don't give in. We must all develop patience, endurance and courage. Cause we need them. Cheers. Thomas Parkman
-------------------- Thomas Parkman Posts: 341 | From Columbia SC 29206 | Registered: Feb 2003
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posted
OK, Thomas. Guess I just feel overwhelmed at times by all the alt med posts. And getting grouchy.
When I say I want more science, it is with the caveat that it should be science I can understand! Marnie leaves me in the dust most of the time. However, here are a few thoughts on the points she raised:
--yes TNF has benefits in disease-fighting and giving anti TNF has drawbacks. I think the possible (not proven, not even tried) benefit of such a therapy would only be for cases of overexpression of cytokines. Possibly only if patients not responding to abx, and if the condition is proven to be auto-immune related. Some lyme docs apparently do think there is an auto-immune component. I am hanging back on this question because it doesn't seem medical science yet has a clear understanding of the interaction of infectious agents and animal tissues.
--yes, it would not be wise to use anti TNF when actual infection still underway, or at least not unopposed.
--I was not suggesting this was a good lyme treatment. But someone unbiased should be looking at it. Thinking that the research done with another cytokine in treating vaccine damaged mice points the way to how this research should be framed.
No one commented. We have some vaccine damaged people on this forum. They should have perked up their ears. Maybe it isn't treatment resistant after all.
Posts: 8430 | From Not available | Registered: Oct 2000
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posted
Here is the important paragraph from an article I cited above, worth repeating:
"This review summarizes the diverse microbial strategies to regulate TNF and how such insights into TNF modulation could benefit the treatment of inflammatory or autoimmune diseases."
If the microbes are regulating tumor necrosis factor (and other cytokines), then this is worth considering in treatment.
And finally, here are a lot more abstracts on the subject:
In one of these abstracts is another important passage:
"Lyme borreliosis, which is prevalent both in the US and in Europe, is an infectious disease that may cause local inflammation in numerous organs. We have hypothesized that, as with some neurodegenerative diseases, the pathogenesis of the neurocognitive deficiencies associated with Lyme neuroborreliosis of the central nervous system also has an inflammatory component. Dysregulated production of pro-inflammatory cytokines such as IL-6 and TNF-alpha can lead to neuronal damage. "
Posts: 8430 | From Not available | Registered: Oct 2000
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sizzled
Frequent Contributor (1K+ posts)
Member # 1357
posted
lou, I ditto cave's reply.
Thank-you for taking the time out to post science.
Thank-you!
Posts: 4258 | From over there | Registered: Jul 2001
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sizzled
Frequent Contributor (1K+ posts)
Member # 1357
posted
double post-deleted
Posts: 4258 | From over there | Registered: Jul 2001
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posted
This is my ten year anniversary of the tickbite and I am not feeling very hopeful about current developments in my case.
Makes me grouchy. Pinning my hopes on lyme research, and there just isn't enough of the good, unbiased kind.
I NEED A VACATION. I NEED TO GET WELL AND DO SOMETHING ELSE BESIDES LYME!!!!!
Posts: 8430 | From Not available | Registered: Oct 2000
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Greatly simplified...
When the minerals drop...Mg, Ca(ultimately it drops too - at late stages), K, P, Zn...
Even WHEN the infection is gone...
the body still thinks it is "under attack" since many pathogens use the minerals and specific acids one way or another (esp. the minerals iron and zinc).
A Mg deficiency alone causes a slew of problems.
("Magnesium is an essential cofactor in many biochemical reactions, and depletion of magnesium destabilizes the Gram-negative bacterial outer membrane (1).
Growth in medium LIMITED for magnesium promotes Gram-negative virulence gene expression (2-4)
suggesting that, at least in part, it simulates environmental conditions that bacteria encounter on colonization of host tissues.")
So...the body keeps pumping out the proteins...acids (antibodies - damaged ones, TNF alpha, and angiotensin II to try to counter = "autoimmune".
This damages the cells...ultimately...esp. the weak hydrogen DNA bonds.
Gotta restore the minerals. Raise the pH.
Cancer ONLY happens in an acidic environment.
How about a handful of almonds...the ones with the brown skin on esp.?
Posts: 9428 | From Sunshine State | Registered: Mar 2001
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posted
You rock Lou,youre a great spokesman for lyme.Almost 5 years for me,about 4 on orals with not much improvement,pushing 6 and a half months IV and some improvement but what a battle.We need some street demonstrations if we hope for some real reaserch.Strength to you Lou.
Posts: 308 | From new bedford,Ma. | Registered: Dec 2004
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posted
You rock Lou,youre a great spokesman for lyme.Almost 5 years for me,about 4 on orals with not much improvement,pushing 6 and a half months IV and some improvement but what a battle.We need some street demonstrations if we hope for some real reaserch.Strength to you Lou.
Posts: 308 | From new bedford,Ma. | Registered: Dec 2004
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Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
quote: With Bb using the sugar from destroying/breaking down fats...ethanol.
From the complete genomic sequence of Bb, it lacks genes encoding enzymes or compounds for tricarboxylic acid cycle and electron transportation. This means that Bb cannot use sugars or fats to generate ATP as its energy supply. It must get ATP from the host.
Posts: 1078 | From Fairland | Registered: Apr 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
"Our initial aim was to isolate LPS from B. burgdorferi, for a potential vaccine use.
Although LPS has been identified in several spirochaetales, such as Leptospira and Treponema, we could not find evidence for its presence in B. burgdorferi, nor were we able to detect markers of LPS such as KDO, Lipid A or 3-hydroxy fatty acids.
However, we isolated and characterized, two major glycolipids from B. burgdorferi, designated as BbGL-I and BbGL-II. These compounds were purified by silica gel chromatography, and analyzed using GLC-MS, MALDI-TOF, FAB-MS, NMR spectrometry, and metabolic labeling.
The structure of BbGL-I was determined as cholesteryl 6-O-acyl-beta-D-galactopyranoside, and that of BbGL-II as 1,2-di-O-acyl-3-O-alfa-D-galactopyranosyl-sn-glycerol. This is the first demonstration of a cholesteryl galactoside in bacteria."
****Function of a cholesteryl galactoside?****
"Spirochetes have a limited metabolism and can only ferment a few types of organic molecules.
They ferment carbohydrates to acetate, ethanol, CO2, and H2 as major end products.
All spirochetes so far examined use the Embden-Meyerhoff-Parnas pathway to take glucose to pyruvate.
Under anaerobic conditions this is converted to acetate and ethanol using common fermentative pathways.
Interestingly, the facultative anaerobes in the group use both oxidative phosphorylation and substrate level phosphorylation in the presence of air and seem to be dependent on at least some fermentation.
The TCA cycle has not been detected in these microbes, and it is unclear how they get their ATP by oxidative phosphorylation.
B. burgdorferi will also move away from ethanol and butanol."
Microaerophiles are microorganisms which are unable to grow when oxygen concentrations reach those found in air (20%) but nevertheless whose growth requires the presence of some oxygen (e.g., 2 to 10%).
"Microaerophiles appear to grow best in the presence of a small amount of free oxygen. They grow below the surface of the medium in a culture tube at the level where oxygen availability matches their needs." (p. 147, Black, 1986)
The enzyme nitrogenase is poisoned by normal atmospheric oxygen levels thus rendering nitrogen fixation nonoperative. Nitrogen fixing bacteria have a consequent growth preference for lower than normal atmospheric levels of oxygen.
Examples: Borrelia burgdorferi Helicobacter pylori Lactobacillus spp. (can also be a facultative anaerobe) Treponema pallidum (can also be an anaerobe)
The in many ways similar Treponema pallidum and Borrelia burgdorferi spirochetes are also both examples of microaerophilic bacteria. Note, however, that Bergey's classifies T. pallidum as "Anaerobic or microaerophilic." (p. 30, 1994, Nineth Edition)
The causative agent of Lyme disease, Borrelia burgdorferi, for example, encodes a vacuolar-type ATPase that is very similar to the one from T. pallidum and also contains a typical Na+-binding motif (data not shown).
Remarkably, the genome of B. burgdorferi does not encode any (known) primary H+ or Na+ pump, except for two NQR subunits, NqrA and NqrB, fused into a single polypeptide chain (BB0072).
Therefore, it appears that this organism uses its Na+ ATPase for ATP hydrolysis and depends on its two NhaC-type Na+/H+ antiporters (BB0637 and BB0638) for the generation of proton motive force.
Carbohydrate utilization by the Lyme borreliosis spirochete, Borrelia burgdorferi.
von Lackum K, Stevenson B.
Department of Microbiology, Immunology, and Molecular Genetics, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, USA.
Growth kinetic analyses of Borrelia burgdorferi indicated that this bacterium can utilize a limited number of carbon sources for energy: the monosaccharides glucose, mannose, and N-acetylglucosamine, the disaccharides maltose and chitobiose, and glycerol.
All of these carbohydrates are likely to be available to B. burgdorferi during infection of either vertebrate and arthropod hosts, enabling development of a model describing energy sources potentially used by the Lyme borreliosis spirochete during its natural infectious cycle.
PMID: 15668016
P.S. This has been driving me nuts:
Do I have the following correct?
Bb has a need for : acetyl-CoA C-acetyltransferase AND choline.
If Bb is taking away our choline and acetyl CoA-C-acetyltransferase, we can't MAKE acetylcholine.
``Levels of the enzyme that makes ACh, choline acetyltransferase, or ChAT, drops in the brains of AD sufferers, leading to a drop in the level of ACh itself.''
Low acetylcholine = no REM sleep...which is when we make proteins. Impact of this on norephin.? One down, other up?
Since acetyl Co A comes from sugars and fats...it looks as though Bb is following the glycolysis AND cholesterol pathways. ``PFK dependent".
[ 17. April 2006, 12:20 PM: Message edited by: Marnie ]
Posts: 9428 | From Sunshine State | Registered: Mar 2001
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Dave6002
Frequent Contributor (1K+ posts)
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posted
If Bb cannot generate ATP, how it get it from the host?
I guess that ATP may not be secreted by cells into blood. Blood might not have ATP avalaible for Bb.
So the only way Bb gets ATP is by intracelluar way: gets into the cell to get ATP and move out.
Posts: 1078 | From Fairland | Registered: Apr 2006
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Jellybelly
Frequent Contributor (1K+ posts)
Member # 7142
posted
As to the queston of mainstream or alternative medicine.......It seems to me that those who are leaning heavily toward alternative treatments are those who may not have been fighting so long. For me, my tick bites were about 37 years ago and I started really getting sick about 25 years ago. I have tried ALL kinds of stuff. I fought taking any kind of drug for much of my life.
As I look back that was many good years of my life wasted on feeling crappy. I used all kinds of vitamins and supplements and they cost me a fortune. On occasion I felt a little bit better, but it never lasted and I continued my downward decent. Finally I started searching in mainstream medicine.
Thankfully I found a doctor who used both mainstream and alternative therapy. FINALLY my heath has turned around. I take a handful of mainstream pills every day, and I also take a handful of alternative supplements. I have used heparin, high concentrations of oxygen, heat therapy as well. It is ALL of these things combined that has gotten me well, or at least so it seems. My handful of mainstream drugs has gotten smaller.
I have even taken Elavil which most people refuse to take, most of all for the fear of gaining weight. I didn't care if I gained wait, because I was so sick, of being sick.
When you are newer at this, I think you are more hopeful that you can do this naturally. Time usually bears out that it is going to take something MUCH stronger.
Those with experience have already been there and done that. Unfortunatly telling people it won't work, won't work either. People need to see for themselves and that just has to be OK, even though it can be frustrating for those getting well watching those trying to get well.
You can lead a horse to water but you can't make them dirnk.
Posts: 1251 | From california | Registered: Apr 2005
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JimBoB
Unregistered
posted
Hi Everyone.
I have not been following this post, even though I posted it as I have been too busy on the house, and such.
BUT I read most of your posts tonight, and I am wondering WHAT ANY of them have to do with the post I initialized on waht appears to maybe there will be some relief for LLMD's, NOT for Lyme sufferers???
I also agree that it is frustrating for those of us who are getting better and trying to help others to get on the road to health too, but they just keep on keeping on with their same old abx, or whatever. Seemingly afraid to at leat TRY something that is working for others.
posted
The reason the thread diverged is probably because this is old news. The memo from the health dept was a brokered compromise after more than five years of effort on the part of lyme patients who wanted a law instead. In fact, a bill was passed by both legislative houses, but the governor vetoed it in the last hour of the last day of the session, so it could not be overridden. And this was a governor who had had Lyme disease himself.
Memos can be revised or changed at any time in the future and are not legally binding. Therefore, not only is this old news, it is not guaranteed protection. The people who want to put LLMDs out of business still want to do this. If you look at Texas, where they had legislative interest and thought their doctors were protected, you will see that the state medical board was only biding their time and found other ways of persecuting the few medical practitioners who would help late stage lymies.
It might be a good thing if newbies would go to the Lyme Times website and read back issues of the newsletter in the archives. It will give them background and improve their understanding of the situation. Assuming, of course, that they wish to have more informed input into the discussion.
Posts: 8430 | From Not available | Registered: Oct 2000
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Where does Bb get its ATP?:
"The existence of glycolysis and absence of a tricarboxylic acid -TCA- cycle in T. denticola
suggests that ATP is generated by sugar fermentation as in the case of B. burgdorferi and T. pallidum,
whereas L. interrogans possesses both a TCA cycle and an electron transport chain -ETC . The lack of cytochromes and quinone biosynthesis genes in T. denticola indicates that it does not possess an ETC for energy production."
The link is long, I will send it via email. For some reason or other, I couldn't include it when I tried to post it, even though I took out the parenthesis in the quote.
JimBob:
The original post said the following...which got us off on another path...
"While in an adding mode: In my Avian flu column, I neglected to refer to a 1994 study at the M.D. Anderson Center, Houston, Texas, which found that retinoic acid (an A metabolite) powerfully inhibited TNF production by macrophages. "
So we started talking about TNF alpha ...and whether or not it is a good idea to block it.
Cave...
"Growth in medium LIMITED for magnesium promotes Gram-negative virulence gene expression (2-4)"
Bb becomes more virulent.
This pathogen is taking from us several nutrients...but the key ones are acetyl CoA (which comes from sugar and fats) and choline.
We respond initially (at the time of the rash) by dumping Mg into the system. Why? For many, many reasons...antibodies need Mg with Ca to be "healthy", Mg INactivates HMG CoA reductase, putting the brakes on the cholesterol pathway...which we KNOW Bb takes...and Mg will chelate zinc...and Bb does have a zinc "finger". This may well be the neurotoxin. We need a little zinc, not a lot. A lot causes way too many problems.
Bb prevents us from MAKING acetylcholine. It takes the nutrients we need to MAKE it. Hence the approach of preventing the breakdown of acetylcholine...keeping more available.
Likely acetylcholine (H16)...is capable of destroying Bb.
So do other things...ozone saunas trigger NO...which triggers acetylcholine release.
HIGH doses of Mg or specific statin/arbs drugs that INactivate HMG CoA reductase...putting brakes on the cholesterol pathway indeed help.
So does Rife, believe it or not.
People have reported "alternative" routes that HAVE been successful when abx. fail.
If someone "reports" that a particular "alternative" therapy helps, I try to figure out HOW this is working and if it makes sense (and is SAFE).
[ 19. April 2006, 08:23 AM: Message edited by: Marnie ]
Posts: 9428 | From Sunshine State | Registered: Mar 2001
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Cave, NO additional zinc!
It appears Bb has a "zinc endoproteinase" . This toxin prevents the release of acetylcholine. In other words, it appears Bb is taking our zinc to use to make its endotoxin (a toxin in the outer cell wall).
While we need a very little zinc for a healthy thymus (the ``seat of our immunity...where WBCs go to be given their specific ``jobs''), etc., this deficiency is harmful and the release of it as the Bb is destroyed is toxic to us if too much too fast.
Too little, not good, too much, not good. Tricky.
A zinc...as well as a Mg deficiency impact many things...NK cells, thymus, etc. A deficiency of zinc and Mg are related to diabetes also. The nutrients have multiple jobs.
The primary nutrients needed include Mg citrate (if Al is not a prob...if it is then Mg malate)+ lecithin (for phosphorus and choline) + B vits. It is the TIMING of smallish doses that is so important.
These are the critical nutrients...then there is a list of "helpers"...probiotics, vit. E, CoQ10, selenium, etc. Each chosen for multiple documented reasons.
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