 |
| Author | Post |
|---|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Sun Jul 17th, 2005 04:18 |
|
Will the Marshall Protocol treat co-infections?
"Co-infections are not uncommon in persons with Th1 inflammatory diseases. Some people have positive antibody titers for bacterial infections such as borrelia, H. pylori, ehrlichiosis/rickettsia, chlamydia and bartonella. Others have protozoan infections like giardia and babesiosis or a fungal/yeast infection. Some have viral infections (not uncommon in the general population) such as CMV, HHV-6 or EBV These pathogens can be detected in blood, serum or other body fluids. Many folks have tried to cure their chronic Th1 inflammatory diseases with aggressive treatment of these organisms with no success.
The way that the Th1 metagenomic microbiota causes chronic disease, is by disabling the innate immune system. Once that has happened, the body loses its ability to transcribe the genes for many families of antimicrobial peptides, and it becomes realtively easier for co-infections to parasitize the body.
IMO, most of the pathogesn which turn up in Th1 patients' blood are coinfections. That assertion is derived from the pathogenesis, and the knowledge that Sarcoidosis can ONLY be diagnosed when there is no sign of any active infection. None of the folks with a very serious bacterial infection (sarcoidosis) have any unusual antibody activity and no cultures are positive; there are no overt signs of infection. No SED rate. No antibodies. Only the coinfections show up.
But the moment we administer the MP, the SED rate shoots up and antibodies can be found. In sarcoidosis, arguably the most agressive of the Th1 inflammatory diseases, there is no sign of any infection. Yet that disease kills, surely and effectively, while not one single test shows one single parasite, bacterial or protozoan. It isn't until the hidden bacteria start being killed with the Marshall Protocol, that overt signs of infection are detected (elevated SED rate, immunopathology)
The issue is that the infections which can be easily detected in Th1 patients are co-infections, and not the cause of their illness. The Th1 pathogens hide so well that no antibodies are generated, and even PCR has difficulty detecting the traces of DNA from host-phagocyte apoptosis. Why can't CWD bacteria be detected with tests?
When the VDR is not functioning properly, when the innate immune system is ovewhelmed by Th1 pathogens, then it cannot properly deal with coinfections which would otherwise be trivial for it to manage. The antimicrobial defenses of the human body target bacteria, viruses, worms and all the threats a normal healthy body can fight against.
Antibodies may have been present in the past (yielding intermediate Lupus and/or RA diagnoses) but they have all disappeared by the time the sarc infection has taken full hold of their bodies.
The most dangerous and successful pathogens are the ones which are intra-cellular, and therefore do not show up on routine testing. These co-infections are not going to make you as ill as the Th1 pathogens. The immune system is not killing co-infections because it is being over-excited by the intra-phagocytic bacteria which are causing the Th1 diseases.
When your immune system gets rid of the Th1 bacterial load it is able to handle the co-infections, including Babesia, without any problems.
The science behind that is the standard Th2 antibody/toll-like-receptor/phagocyte-recognition stuff you find in any immunology textbook. The key is to get rid of the parasites from the phagocytic cytoplasm, and then the immune system operates as it does in a 'healthy' person. No great 'rocket-science' there 
Take a look at a TEM of an infected phagocyte from one of the Wirostko papers
http://tinyurl.com/haor6
http://autoimmunityresearch.org/wirostko-fig3.jpg
Once those tiny (stained) coccoid forms on the small arrows are killed off, the phagocyte cytoplasm is returned to a functional state, no longer controlled by the biochemistry of the pathogen.
The exact mechanism by which our adaptive immune system retains a memory of past pathogen contacts is not entirely clear. We thought we knew how it happened, but recent research has shown it is more complex than previously thought. You should retain immunity gained from vaccinations, at least as well as healthy folk.
Once your immune system is no longer under challenge, it will be able to cope with opportunistic infections. The MP is designed to allow your immune system to function and eventually kill all chronic infections, no matter what label has been put on any suspected infection. Once the Th1 bacterial pathogens are killed off, the immune system deals with the viruses it couldn't clear while the bacteria were present. That's why folks lose warts, psoriasis, and other things as they recover on the MP.
Wait and see! A healing immune system is no longer 'out of sync' with the world, but copes normally with the various things life throws at it, instead of over-reacting.
..Trevor..
Mar08
Back in 1978 I wrote a paper "Electronic Design Educating for an Uncertain Future" where I was wrote about "tackling .. tasks where the starting data may be vague, or incomplete, and where many alternative solutions may be equally valid."
The Idiopathic diseases present us with a very similar set of disparate and incomplete data. We can detect parasitic genomes, in-vitro, but have little data about whether they are active in-vivo, or what their effects might be, in-vivo. Additionally, there are tantalizing hints that other parasitic entities might be present, even though we can't detect them.
The Wirostko TEM micrographs, for example, showed a microbiota totally unknown to Medicine, yet clearly present in the patients Emil and his group were studying. Similarly, there had been many, many studies linking various known pathogens to Sarcoidosis, and CFS, yet none of them were clearly causal, as none of them were present in every individual.
The CFS patients in Australia, for example, who, if seropositive, were usually so for Rickettsia, suffer identically to those in the USA, who are often seropositive for Borrelia. Clearly neither of these pathogens were causal, and there were factors in play which were unknown, interacting in ways which were poorly understood.
That is why I took a different approach back in 1999. Building on my experience dealing with uncertain data and outcomes, I decided that in-vitro testing, the Gold-Standard of Medicine, just had to be missing something important. Similarly, the animal models were not producing results which were portable to human experience, so they, too, had to be set aside.
Thus, having discarded a century of studies, a century of what was thought to be "knowledge," I started to re-examine chronic disease based on the tools and techniques which had been developed for modern genetic biology. Trying to piece together the clues from a tiny subset of available perceptions and data, into a model which would be rigorous, and which would exactly describe the human experience. By its very nature, this study dealt largely with the philosophical. Only in later years did the science fall together into the rigorous mechanistic model we now have elucidated.
It is meaningless to focus on a virus, fungus, or bacterium which can be easily observed. Otherwise the pathogenesis of chronic disease would have been described decades ago. Being able to culture pathogen, or detect it with PCR, gives no clue as to whether that pathogen is causal in the disease process, or just present as a result of the immune system being weakened by an underlying disease process.
I know how tempting it is to apply the lab techniques of yesteryear to the imponderable problems of today. But one needs to start thinking, instead of focusing on observations. The fundamental problem with observational science is that unless you know what you are looking for, you don't know how, or why, to observe it. What is needed in modern medicine is the discipline of Planck and Einstein, the discipline of working with dilemma which defy description, and puzzle out, by sheer philosophical discipline, what the inter-relationships might be, in order that the data can then be experimentally observed, ranked, and the model verified.
..Trevor..
From CELL WALL DEFICIENT BACTERIA AND THE MARSHALL PROTOCOL:
When the body is weakened by these Th1 diseases co-infections are very common, as the immune system is 'busy' dealing with the pathogens which have parasitized the phagocytes and can't deal as effectively with the opportunistic infections. Co-infections that have been resistant to treatment, will likely be eliminated by the immune system as its proper function is restored with the Marshall Protocol.
There is definitely a variation in the effectiveness of various antibiotics in patients. The factors seem to be:
1. Patient's prior exposure to the antibiotics
2. Strength (or weakness) of the patient's own immune system
3. Species of bacteria present
4. Concomitant health problems - eg kidney failure
5. Concomitant infections - eg fungal, viral
6. Medications being taken by the patient
Note: Your doctor may determine that you have an acute bacterial infection which needs immediate treatment with a non-MP antibiotic. Please see:
I need to take a different antibiotic for awhile.What should I do?
(Scroll down for info on specific co-infections)
Last edited on Fri Jun 13th, 2008 08:37 by Foundation Staff
|
Aussie Barb Research Team

| Joined: | Thu Jul 22nd, 2004 |
| Location: | Australia |
| Posts: | 19547 |
| Status: |
Offline
|
|
Posted: Thu Jun 15th, 2006 22:55 |
|
(filelink)
Viral infections
Viral infections are not uncommon in the general population. Many folks have tried to cure their chronic Th1 inflammatory diseases with aggressive antiviral treatment with no success.
"IMO, most of the pathogesn which turn up in Th1 patients' blood are coinfections and not the cause of their chronic illness." ..Trevor..
As the body heals on the MP, and its anti-microbial peptides start to be produced again, the immune system eventually takes care of viral co-infections.
Herpes
Shingles (herpes zoster) is a localized viral infection resulting in a skin rash (blisters) that is caused by an outbreak of the same virus (Varicella zoster) that causes chickenpox. A person with shingles can pass the virus to individuals who have never had chickenpox, but these individuals will develop chickenpox, not shingles.
Shingles occurs in people of all ages who have had chickenpox but most commonly develops in those over 60. The virus that stays in the body after a case of chicken pox usually is kept inactive by the immune system. Typically, but not always, shingles occurs in people who are in a stressful situation such as illness, chemotherapy or immunosuppression. It is important to realize that just because a person develops shingles, the entire immune system is not necessarily having problems.
The two methods of diagnosing shingles are by clinical presentation or laboratory confirmation.
Shingles' symptoms are usually vague or nonspecific at first. Before the classic rash appears, the patient may notice several days to a week of numbness, tingling, itching, extreme sensitivity or burning pain in or under the skin.
In the pre-eruption stage, diagnosis may be difficult, and the pain can be so severe that it may be mistaken for pleurisy, kidney stones, gallstones, appendicitis, or even a heart attack, depending on the location of the affected nerve.
The shingles rash starts as a band of raised dots that develop into small, fluid-filled blisters (reminiscent of chickenpox) on a red base, with new blisters continuing to form for 3-5 days. The blisters follow the path of individual nerves that comes out of the spinal cord. The entire path of the nerve may be involved or there may be areas with blisters and areas without blisters. Generally, only one side of the body is involved.
The rash may affect any part of the body, including head and limbs. It may appear as a band or a half belt around one side of the chest or abdomen, or down an arm or leg. It may affect any part of the head including face, palate, ear and scalp. If a person gets shingles in the upper cheek, the forehead region, eye or tip of the nose, an emergency evaluation with an ophthalmologist is crucial, since this can indicate eye involvement and the potential loss of vision.
Seek medical advice as soon as possible if your rash is:
-painful
-located in a band on one side of the body only
The severity and duration of an attack of shingles can be significantly reduced by immediate treatment (within 72 hours of appearance of the rash) with antiviral drugs, which include acyclovir, valcyclovir, or famcyclovir. Antiviral drugs may also help stave off the painful after-effects of shingles known as postherpetic neuralgia. This post shingles condition is relatively rare but it can have a devastating impact on quality of life since the nerve damage and pain is incurable and may require long-term opioids.
However, antiviral medication can be hard on the liver. If you have (or think you might have) liver inflammation, talk with your doctor about the risk/benefit of taking an antiviral for shingles. We have not had anyone on the MP report a case of postherpetic neuropathy without antiviral treatment but postherpetic neuropathy is a rare occurance and our cohort is relatively small.
MP meds may be continued while taking an antiviral for shingles but if you are miserable with shingles symptoms, be sure to minimize immunopathology symptoms during the duration of treatment for shingles.
The pain associated with shingles can be intense and is often described as "unrelenting." To relieve the pain of shingles, the doctor may recommend over-the-counter analgesics (pain-relieving drugs), such as, ibuprofen and naproxen, or prescription drugs, such as indomethacin, all members of a class of medications known as nonsteroidal anti-inflammatory drugs (NSAIDs). A Lidocaine patch may also be prescribed. If pain is severe, doctors may add stronger analgesics, such as codeine or oxycodone.
Eventually, the blisters pop and start to ooze. The area will then crust over and heal. Zostrix-HP is a cream that can be directly applied to the skin once the lesions have crusted over. When applied to the skin, Zostrix-HP has been shown to reduce levels of substance P—a neurochemical involved in transmitting pain impulses to the brain. Calamine lotion can also help to soothe the area. Keep the area clean and avoid scratching to prevent a secondary bacterial infection. You may feel ill with fever, chills, headache, exhaustion, achiness or stomach upset. Get plenty of rest and drink adequate fluids. Persons who have not had chickenpox should avoid contact with the rash or contaminated materials.
The shingles attack may last longer than chickenpox, and you may need medication for pain, but the MP has given the body has the inner resources to fight back. The lesions heal, the pain subsides within 3 to 5 weeks, and for most patients the blisters leave no scars.
Zostrvax (shingles vaccine)
This article explains the pros and cons regarding the new vaccine to prevent shingles. In addition, the long-term effects of this vaccine are not known and any injection has the potential to introduce new L-forms into your body.
Genital herpes (herpes simplex)
Oral anti-viral medication, usually acyclovir (Zovirax), is used to decrease pain and speed the healing of sores or blisters in people who have first-time or repeat outbreaks of genital herpes. Zovirax ointment may be used to treat infections of the skin and mucous membranes. It is okay to use this medication while on the MP.
Cold sores (herpes simplex)
Zovirax cream is used for herpes cold sores on the lips and face only. It is okay to use this medication while on the MP.
This article lists some alternative medicine cold sore treatments that may be helpful for intolerable cold sore symptoms.
Persistent viral outbreaks
There is evidence that the ratio of the amino acid arginine to lysine in the diet affects the replication of Herpes simplex virus (and may also affect the virus that causes shingles). If your viral outbreaks are chronic, minimizing arginine containing foods (nuts are particularly high in arginine) and/or balancing the arginine with suppplemental lysine (particularly when under stress), may help prevent a reoccurence.
Members have reported that eliminating foods high in arginine and taking 500-2000mg lysine has been helpful in treating and preventing various viral outbreaks.
Nuts and plant based proteins (like rice protein powder) have the most arginine relative to lysine and dairy products have the lowest. Meats are in between and the higher protein foods will be the ones to pay the most attention to since they have the highest concentrations arginine and lysine.
List of foods high in arginine
Members' experiences
-I, too, have had herpes simplex/cold sores as an IP rxn. I used to get these somewhat frequently as an adolescent, but had not had any for many years. Now, I have had three in as many months. For me it is part of a constellation of "lesser" symptoms, as overall I am, at last, feeling much better. ~Carol
See also:
Pain Control
I’ve developed a rash. What should I do?
Last edited on Mon Mar 24th, 2008 06:44 by
____________________ Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 25th, 2006 05:51 |
|
(filelink)
Helicobactor Pylori
Dr Marshall wrote:
H.Pylori is often attacked via its 70S ribosome, using Clarithromycin, which is a subset of the approach we use to target the 70S ribosome in the MP. The pulsed dosing we use will impair therapeutic effectiveness somewhat against blood-borne bacteria, but there are ways to restore that. I would be happy to chat with Doc about these options.
But, in a word, yes, the MP antibiotics will (slowly but surely) target H.pylori. If Doc wants to add Clarithromycin, it is unlikely to affect your herx very much.
....................
The problem with these Th1 diseases is that the pathogens which are making you sick are not usually the ones which appear in clinical testing. That is why these diseases have remained unsolved for so long. The bacteria which are making you chronically ill are evading your immune system, and will not necessarily show up in antibody testing or lab cultures.
So the question I would ask is "are you sure that the Helicobacter pylori is actually making you ill?" When the body is weakened by these Th1 diseases co-infections are very common, as the immune system is 'busy' dealing with the pathogens which have parasitized the phagocytes and can't deal as effectively with the opportunistic infections.
H.pylori was probably just a co-infection, something which could be measured in the lab. I doubt it was making you so ill.
Kiling the bacteria causing these chronic diseases is a very difficult task, and that is why the MP is not just a simple "take these pills for 5 days" routine.
The MP antibiotics are wide spectrum, and, by the time you get to phase 3, are capable of killing just about any bacterium you might have accumulated in your body. H. Pylori translates its proteins with a 70S ribosome, and so is just as susceptible as all the other species of bacteria.
Frankly, the antibiotics you have been given over the last few months have been shown in the lab to kill H.pylori, yet you yourself have found that they are not killing the H.pylori in your body.
The antibiotics we use in the MP are designed to inhibit bacterial growth and defenses by inhibiting Ribosomal protein synthesis. All bacteria need to manufacture a variety of proteins in order to survive. The MP is designed to make that task progressively harder.
There is a major failing in the specialty of Infectious Diseases which will have to be addressed as we start to understand more about the bacterial genomes, and exactly how the infectious process works. The pragma and 'old-science' being used to get rid of your H.pylori is apparently just not working. Understanding that fact is job#1, and figuring out what to do follows from that realization. Growing bacteria in the lab (in-vitro) and in the body (in-vivo) are two different, and not necessarily equivalent things You need to focus on understanding what is making you ill, and it may not be the clinically obvious pathogen...
All of these bacteria cause the release of nitric oxide as they die, this is not unique to H.pylori.
Your doctor should be aware that Minocycline is effective aganist H.Pylori, and that eventually the MP will get rid of the H.Pylori infection too. The issue your Doc has to evaluate is whether your H.pylori infection needs urgent treatment, or not.
Most people harbor H.pylori for years with few ill effects. You must remember that the sarcoidosis will kill you, the H.Pylori will generally not do that. You might print out this paper for Doc:
http://tinyurl.com/6tfsg
Helicobacter Pylori is one of the L-forms which are pathogenic in Sarcoidosis. Your MP phase 3 regime will be killing H.pylori and that is probably why antibodies were found in the lab tests.
I see no reason to aggressively go after any specific species now. The failure rate of the treatment regime Doc is suggesting is high, in any case.
Why did Doc do the antibody testing in the first place? I can guarantee that there are other species he would have found, if he had looked. That is the nature of the Th1 disease. The better test would be a culture, which would also tell Doc what antibiotics the bugs would be susceptible to.
Doc should feel free to call me
..Trevor..
If you test negative but have ulcer symptoms
Ulcer bug may be responsible for 'unexplained' intestinal ulcers
By Mark Cowen,14 February 2008 Am J Gastroenterol 2008; 103:55-61
Many patients diagnosed with 'unexplained' ulcers in their small intestine, called the duodenum, may actually be infected with the ulcer-causing bug Helicobacter pylori, and can be successfully treated with antibiotic therapy, researchers have found.
Dr Antonio Pietroiusti, from Tor Vergata University in Rome, Italy, and colleagues explain that stomach tissue samples, or biopsies, are usually used to identify Helicobacter pylori infection in people with ulcers in their duodenum.
If these tests prove negative, such patients are given treatment with stomach acid-suppressing drugs, instead of the antibiotics used to eradicate Helicobacter pylori.
However, they add that some studies have suggested that duodenal ulcer patients who test negative for Helicobacter pylori infection with the stomach biopsy method often respond well to antibiotic treatment, indicating that stomach biopsies do not always identify infection in the small intestine.
For the current investigation, the team studied 608 patients with duodenal ulcers. Using the stomach biopsy method, 42 of these patients tested negative for Helicobacter pylori infection.
However, further tests on tissue samples taken from the patients' duodenums, combined with breath tests, revealed that 18 of these 42 patients had Helicobacter pylori bacteria in their small intestines, but not in their stomachs.
These patients then underwent Helicobacter pylori eradication therapy with antibiotics and most of their ulcers healed.
Dr Pietroiusti and team conclude: "In this study, we show that a substantial proportion of duodenal ulcer patients who should be classified as H. pylori negative on the basis of the findings of gastric [stomach] biopsies carry the organism in the duodenum, and that eradication treatment induces persistent healing of the ulcer in the vast majority of them.
"This finding may change current views in the management of these patients."
Members' experiences:
Janna's gastric ulcer biopsy shows H. pilori
-I read about H pilori. In fact, in 2001 or 2002, I read the whole of Pizzorno & Murray's Encyclopedia of Natural Medicine, and very successfully cured my gastric ulcer (and H pilori infection) with their recommendation: cabbage juice. (Some say it is the glutamine in the juice, and some say it is the S-methyl-methionine. Whatever it was, it was very effective.) On top of this, I read that lots of people and animals live with H pilori and do not suffer ulcers! And that those who eat broccoli (as I do now) don't get ulcers even if they have H pilori in their stomach!
-In Janna's case, her ulcer is too painful, and she just won't drink cabbage juice or eat broccoli. So, she'll have to try the conventional therapy for 2 weeks.
Fortunately I found a solution in the Proceedings of the National Academy of Sciences: http://www.pnas.org/cgi/content/full/99/11/7610
Per this article, (broccoli’s) sulforaphane is superior to antibiotics for battling against intra- and extra-cellular H. pylori. And I found standardized sulforaphane as “Broccoli Sprouts” (extract made into tablets) by Source Naturals. I suppose that since broccoli doesn’t interfere with the MP, the above-mentioned “nutritional supplement” should not interfere with it either. Janna will be able to resume the MP in a week or two rather than a full month. Hope other H. pylori ulcer sufferers can benefit from this discovery as well.
Moderator note: Normally, we discourage the use of concentrated food products but, in this case, broccoli sprout extract tablets seem better than amoxycillin or cephalexin.
-Because of her ulcer problem, Janna had temporarily discontinued the MP and started aciphex, amoxycillin, and clarithromycin
Because of her antibiotic-induced migraines, Janna replaced the beforementioned antibiotics with cipro, and resumed benicar. She felt well after that. Last couple of days, to aciphex and cipro she added a supplement containing the amount of sulforaphane found in roughly a pound of broccoli. So far, she continues to do well: No ulcer pain, no migraines and no immunopathology
-She is doing well with aciphex, benicar, cipro, and Natural Sources 's "Broccoli Sprouts" with 1 mg sulforaphane per tablet (3 tabs per day). No ulcer pain, and no migraines. Her only complaint is dizziness, which she attributes to cipro. ~Benk
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:17 |
|
[filelink]
Fungal infections
Do not use any of the antifungals unless it is absolutely 100% necessary.
Candidiasis (yeast infection)
Dr. Marshall wrote: "Maybe what was diagnosed as a 'yeast problem' is actually a problem caused by "those tiny, tiny bacteria, smaller even than yeast spores, called Cell Wall Deficient or L-forms. The immune system is not killing co-infections because it is being over-excited by the intra-phagocytic bacteria which are causing the Th1 diseases. As you return to health, these problems disappear.
The bacterial protein-synthesis-inhibiting antibiotics clear up the condition you are all describing as 'yeast'. That does not necessarily mean the condition is a yeast infection secondary to CWD, although it certainly could be. It could be a misdiagnosis of 'yeast'.
We are dealing with a very complex and interwoven set of issues, and I want to emphasize that they must be looked at as part of a larger 'whole' and that we should not force labels like 'yeast overgrowth' onto them and consider them solved.
In any case, 'yeast medications' only temporarily help the condition - again a sign of misdiagnosis, IMO. Deal with the CWD and the 'yeast' symptoms disappear. Mine did. Half a century of 'jock itch' disappeared in just a few months."
See Immunopathology (Herx) .... What is it?
Remember that 100% of the reason your immune system cannot deal with the 'Candida' results from the actions of the Th1 pathogens.
Cutaneous fungal infections
Athlete's foot (tinea pedis) is a parasitic fungal infection of the epidermis of the human foot. Several different fungi can cause tinea pedis. Moreover, a fungi species that causes athlete's foot can also cause, for example, jock itch (tinea cruris). It is typically caused by a mould (but in some cases a yeast) that grows on the surface of the skin and then into the living skin tissue itself, causing the infection. It usually occurs between the toes, but in severely lasting cases may appear as an extensive "moccasin" pattern on the bottom and sides of the foot.
ALL THE ANTIFUNGALS PROFOUNDLY AFFECT THE HOST IMMUNE SYSTEM.
That includes:
IV Amphotericin B (oral use is poorly absorbed)
Sporonox (itraconazole)
Diflucan (fluconazole)
Fulvicin (griseofulvin)
Nizoral (ketoconazole)
nystatin
all other antifungals
Do not use any of the antifungals unless it is absolutely 100% necessary.
Generally, you must have a positive culture (even though sensitivity testing on isolates tells you virtually nothing about how to treat the infection in the human host).
Many Th1 pts appear to have 'Candida' (etc) when it is actually only the Th1 bacteria in the surface layers of the skin.
" fluconazole (Diflucan) is sometimes prescribed to treat fungal (candida) infections. It directly inhibits the enzyme CYP27B1, which is needed for the mitichondria in the macrophages to convert 25-D to 1,25-D. With a lower generation of 1,25-D in the inflammation folks will feel better - for a while - and then relapse worse than ever.
This is also the action of ketaconazole applied the skin. The keratinocytes in the skin still convert 7-dehydro-cholesterol to 25-D but ketaconazole tends to block the conversion of the 25-D to 1,25-D.
Azoles affect the operation of the D-metabolites, and/or the VDR but they do it in a manner which is not dose-controllable, as Benicar does.
..Trevor..
Flagyl (metronidazole)
Flagyl profoundly affects the human Vitamin D metabolism, and all the enzymes associated with it. Patients might think they are 'herxing' but they are just being sick. See Borreliosis
Bottom Line:
1. Forget all you have read about anti-fungals. They all have a profound effect upon the host, as well as on the infection. They work a lot of their 'magic' by suppressing host immune defences. Fluconazole is particularly bad, hitting several of the key CYP enzymes, and Ketoconazole directly antagonizes the VDR. The manner in which they kill fungi, in-vivo, is still essentially unknown. Unlike the MP medications, these are not harmless drugs, and their use carries significant risk to the pt.
IMO Probably more likely that those with candida infection have a more severely compromized innate immune system at presentation. ...look at the video presentation on Crohn's which I posted....? That explains how the VDR is closely linked to the gut via beta-Defensins and Cathelicidin anti microbial peptides.
http://www.marshallprotocol.com/forum39/7489.html
I think the linkage drawn between probiotics and fungal infection is incorrect, and I think it arose because medicine did not understand how active the innate immune system is in GI function. Stimulating that innate immune system with pathogens (probiotic 'flora') might well increase the production of 'immune system stuff' which would reduce the likelihood of a secondary fungal infection. Once the MP has gotten your immune system back into balance I would doubt that probiotics would have any useful function to play. See Should I take probiotics?
You need to understand that anti-fungal treatments can kill Th1 patients. I spoke with one mother of a Lyme patient whose daughter had been paralysed for months by a single dose of antifungal given her for Chronic Lyme. Please don't go down that pathway. The Lyme community has already been there...
Your 'candida' will disappear as you go through the MP and your innate immune system is restored to operation. In any case, much of what folk call 'candida' is actually the microscopic Th1 pathogens in the skin, and not a fungus.
..Trevor..
'Yeast infection very often not the real thing
Wed Sep 19, 2007
NEW YORK (Reuters Health)
By Anne Harding
Only one in every four women who seeks treatment for persistent yeast infections actually has one, a new study suggests.
Women will frequently treat suspected yeast infections themselves with over-the-counter (OTC) products, but the findings show that most of the time this won't help. In fact, using such medications repeatedly may even cause harm, Dr. Susan Hoffstetter, the co-director of the SLUCare Vulvar and Vaginal Disease Clinic at Saint Louis University, told Reuters Health.
"We treat ourselves because we want our problems to go away quickly," Hoffstetter pointed out, adding that this isn't only the fault of patients. "We in medicine also do a lot of treating over the phone just to keep women from having to come in."
Hoffstetter and her colleagues looked at the medical records for 150 women visiting the clinic for the first time who reported persistent yeast infections.
Lab tests showed that only 26 percent of the women were infected with Candida -- the fungus responsible for yeast infections. Other causes of vaginal itching can include sexually transmitted infections, dry skin, or inflammation, Hoffstetter noted, which won't respond to OTC antifungals and could even be aggravated by these products.
Overuse of OTC yeast infection remedies can alter the normal flora of the vagina, which can lead to other health problems, the researcher pointed out. And, she added, drug-resistant strains of Candida are becoming increasingly common.
If a woman experiences pain during sex, burning sensations in the vaginal area, a thick white discharge, and pain during urination, she may indeed have a yeast infection, Hoffstetter said. And it's probably okay for women to self-treat if they experience these symptoms rarely, and they get better with OTC medication, she added.
But women who think they are suffering from yeast infections that never go away are likely to have some other problem, Hoffstetter said. In such cases, she advised, it's important for a woman to actually see a doctor or nurse practitioner and have a pelvic exam and lab tests, if necessary, rather than just getting medical advice over the phone.
Toenail fungus
The fungal (yeast) infection in toenails is quite common. It is usually just unsightly and difficult to treat because the infection is deep within the nail....sometimes toenail removal is required when the nail is so deformed it is painful.
Oral antifungals such as itraconazole (Sporonox), fluconazole (Diflucan), griseofulvin (Fulvicin), and terfinabine (Lamisil) are, reportedly, successful in about 60% of cases. But they must be taken for many months and they are hard on the liver and heart. Most important, they interfere with the immune system and should be avoided.
Home remedies such as Vicks Vaporub applied to the toenails sometimes works.
Members experiences
-Pre-MP I tolerated nystatin but the diflucan shut down my liver function. I never saw big improvenments in my health with the nystatin, so I don't think the yeast was a major part of the underlying problem with me. Diet changes as you know should go along with any possible course of nystatin. As the immune system kicks in on the MP the yeast infections seem to be much less frequent or stop altogether. ~P.Bear R.N.
-My yeast isfection I guess was not a yeast infection becasue I am havin like no symptoms of that anymore and would rate it as a 1. ~Shandy
Related FAQs:
Won't I develop a yeast infection if I'm on antibiotics long-term?
I have a yeast infection. What should I do?
The use of antifungals for borreliosis
Last edited on Wed May 21st, 2008 08:35 by Foundation Staff
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:23 |
|
[filelink]
BCG
BCG is a real problem. It is an intra-phagocytic pathogen (Mycobacterium bovis). Australia stopped using BCG back in the 1970s, once it became linked as a causative agent of disease. You should wipe out any remnant bacteria during the MP.
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:29 |
|
[filelink]
Borreliosis
"In my opinion, treating the co-infections, and not the primary infection (intracellular bacteria), will only make you more ill in the long run. Lymies being treated with the MP, who are having serial Bowen-titre-testing, show a monotonic decrease in titre as they progress on the MP. We have no reason to doubt that the Borrelia titre will (eventually) disappear. When you treat the primary intracellular infection with the MP and return to health, these co-infections disappear."
"Neither Borrelia or Chlamydia are sole pathogens behind Th1 disease. No single species has the ability to wreak the havoc of Th1 disease. In the most simplistic analysis, to infect the heart and lungs requires an aerobe (oxygen-loving); to infect the dense organs requires anaerobes.
In my conference presentations I have described what we are dealing with - successive infection and successive mutation leading to a genetic symbiosis which can evade phagocytosis."
Borrelia is one of the co-infections in Sarcoidosis which has been noted before in several studies. Look for example at URLs
http://tinyurl.com/k2luo
and
http://tinyurl.com/galms
I would suggest you focus on getting rid of the pathogens causing the disease. The Borrelia will disappear too, as time goes by. In any case, MP is the only game in town whether you are looking to cure Chronic Lyme or Sarcoidosis.
ELISA and WB antibodies are not fully specific. A single antibody can react to many different things. At the Budapest autoimmunity conference in 2004, a group from Stanford showed dozens of molecules which reacted with a single antibody. That is why the CDC test requires a set of ELISA antibody reactions to be present. If that whole set is not present then the observed bands might be resulting from interactions with proteins other than the target organism. Igenex bends the rules by making interpretations from additional bands found to be present, an extension which, IMO, is on fairly shaky ground.
Igenex could insist on follow up of their positive ELISA and WB tests with their own PCR or even a bacterial Genome identification test, which produce more certainty. But they usually don't do that.
Maybe there are fragments or plasmids of Borrelia which are involved in the pea-soup mix, but certainly not the active infection known as Lyme. You will find many people here with positive Rickettsia serology, and no Borrelia whatsoever. Yet they have essentially the same symptoms as other folk who test positive for Lyme, and their recovery follows a similar trajectory. Consequently, one can safely assume that Borrelia is not the causative pathogen.
(note: Susan's presentation at the LAX 2006 conference DVD 'recovery' session)
Trevor Marshall, PhD
April 08 "Please stop fixating on 'Lyme'. Borrelia is a co-infection, not what is primarily making you ill. It is the Th1 pathogens in the intraphagocytic microbiota which are stopping your body from getting rid of the remaining vestiges of Borrelia. You would be just as ill if there were not a trace of Borrelia in your body. By blaming all your syndromes on Lyme you make your task of recovery much more complex." ..Trevor..
Flagyl
Flagyl profoundly affects the human Vitamin D metabolism, and all the enzymes associated with it. Patients might think they are 'herxing' but they are just being sick. They get some relief, sometimes, because it takes the body a while to try and get the innate immune system working again after Flagyl has totally shut it down. This is a dangerous drug, in the doses it is used in Lyme therapy. I have spoken to the mother of a Lymie who was paralyzed by it - for weeks.
Member's experience
Lonestartick: Late stage Borrelia with co-infections: Success
Related info:
Post Treatment Lyme Disease Syndrome
Last edited on Wed Apr 30th, 2008 08:24 by Foundation Staff
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:31 |
|
[filelink]
Rickettsia and mycobacteria
One of the most difficult dilemmas I had to resolve, and even more difficult for some patients to come to grip with, is that the infections thought to be causing them to be ill are likely to actually be co-infections, unwitting bystanders at the scene of the crime. These infections are easily observed, but are not necessarily contributing to the illness...
You see, when the innate immune system becomes weakened by the Th1 pathogens which attack the VDR, it can no longer clear viruses, and other infections. Rickettsia and Mycobacteria can be very nasty pathogens indeed, but their mode of action is different from the Th1 pathogens, and they evade the immune system differently. As the body heals, and its anti-microbial peptides start to be produced again, the immune system eventually takes care of fungal, viral and bacterial co-infections.
It is safe to say that these pathogens are more effective against a weakened immune system than a fully functioning immune system.
One paper exploring the mechanisms used by Mycobacteria can be found at
http://tinyurl.com/2wrtpr
with commentary at Nature.com (free access, registration required)
http://www.nature.com/nrmicro/journal/v5/n8/full/nrmicro1728.html
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:33 |
|
[filelink]
Bacteria
Bartonella
If the bartonella co-infection is chronic it can be presumed to be intracellular and the MP will be an effective treatment. Other pathogens causing chronic disease will be successfully eliminated by the immune system once it isn't overwhelmed fighting a losing battle against intracellular bacteria.
Staph
This paper, by Burke Cunha, who wrote a number of textbooks on antibiotics, points out that Minocycline is effective against MRSA ('staph infection')
http://www.postgradmed.com/issues/1997/04_97/cunha_1.htm
C. difficile
Clostridium difficile is a commensal bacterium of the human intestine in a minority of the population. Patients who have been staying long-term in a hospital or a nursing home have a higher likelihood of being colonized by this bacterium. In small numbers it does not result in disease of any significance.
It's really not the use of antibiotics that cause a bacterial infection such as Clostridium difficile, but antibiotic use can trigger a change that may allow the bacteria already present to flourish.
Clostridium difficile bacteria are found in two forms: the active form that causes infection and spores, which are inactive. These spores can be picked up virtually anywhere, are ingested by humans and then lie dormant in the colon until they are activated by some change in that environment. The spores are resistant to killing, which is why people can have infection relapses.
Use of wide-spectrum antibiotics can change the colon's environment by killing off numerous bacteria normally present there. Once this bacterial balance is upset, C. difficile spores there can "come to life again" by changing into infectious bacteria; however, according to this source, use of tetracyclines is considered a rare trigger for this activation. In fact, the researcher in this study concluded that use of tetracyclines was protective against this infection.
People can develop a C. difficlle infection without antibiotic use. Other drugs, such as proton pump inhibitors that change the acidity of the digestive system, have been considered a trigger. Surgery or chemotherapy may also be triggers.
Healthy people do not get sick from C. difficile because they have antibodies that protect them from the toxins produced by this bacteria. The combination of overgrowth of C. difficile and toxins produced by it are what cause damage to the intestines and wreck havoc on the body. Lab tests for C. difficile toxins in the stool are used to diagnose. The test can produce a false positive in some circumstances.
Clostridium difficile is an infection usually acquired in a hospital setting following standard dosing of broad-spectrum, macrolide antibiotics. The MP antibiotics are given at very low doses and are very unlikely to cause C. difficile.
Treatment of C. diff is stopping current antibiotics and commencing specific anticlostridial antibiotics, e.g. metronidazole.
"Yes, there currently are epidemics of various antibiotic-resistant bugs, including C.difficile, and we have argued that they are due to the increasing prevalence of Th1 disease resulting from ill-advised Vitamin D supplementation. We have not seen a high incidence of C.difficile in folk on the MP." Dr. Marshall
See Should I take probiotics?
Last edited on Thu Jun 12th, 2008 18:53 by Foundation Staff
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:37 |
|
[filelink]
Protazoan parasites
Babesia
I have said many times that I believe that a Babesia co-infection is merely that, not the main infection(s) causing the Th1 disease but something which looks spectacular on the microscopy and which gives a physician something to hang their diagnosis upon.
Doc can see that babesia is present, but cannot see the intra-cellular pathogens which are actually making the patient sick.
However Babesia populate (primarily) red-blood cells which don't have a nucleus, and therefore cannot emit the mRNA which causes the Th1 cytokines that are making folks so sick in these diseases.
IMO, the babesia has taken residence because the immune system has been hijacked by the Th1 intra-cellular bacteria, who have down-regulated the lymphocytes and therefore down-regulated the immune system's ability to kill off the babesia.
The immune system will look after the parasites for you (Babesia, etc).
One sure indicator of a protozoan illness is a low 1,25-D (below 12 pg/ml). Is yours that low?
..Trevor..
Flagyl
Flagyl profoundly affects the human Vitamin D metabolism, and all the enzymes associated with it. Patients might think they are 'herxing' but they are just being sick. They get some relief, sometimes, because it takes the body a while to try and get the innate immune system working again after Flagyl has totally shut it down. This is a dangerous drug, in the doses it is used in Lyme therapy. I have spoken to the mother of a Lymie who was paralyzed by it - for weeks.
..Trevor..
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Sep 3rd, 2007 09:39 |
|
[filelink]
Viruses
"Everybody with a serious Th1 infection has HHV-6 and EBV (well, nearly everyone). The really nasty viral co-infections are things like active HIV and Hepatitis. There is usually no point in sweating the typical viral titres. They do not cause illness, despite what you read."
As for viruses - they cannot cause Th1 disease. The genome of the opportunistic viruses generally doesn't have a Ribosome - it has to rely on the host or upon bacteria to turn its DNA into proteins. It is some of those proteins which cause 'autoimmune' disease. The viruses can't do it on their own and they just hang around as co-infections because the weakened immune system in Th1 patients can no longer kill them. The viruses were part of the pathogenesis, but once the phagocytes become parasitized the bacteria drive the primary disease process.
The common viruses have become suspected of causing Autoimmune diseases because they are easily observed after the immune system, weakened by the Th1 pathogens, has been unable to eliminate them. But they do not cause the underlying disease.
Something like "being seen at the scene of the crime" but not actually committing it. The viruses are only co-infections, because the body's immune system has been weakened by the Th1 pathogens, and is unable to fight the viral infection.
See, for example:
GB virus-C - a virus without a disease: We cannot give it chronic fatigue syndrome
and:
We are actually dealing with a chronic polymicrobial infection, one where the DNA is horizontally mobile, and where the postulates of Koch are no longer relevant. I discussed this at our 2005 and 2006 conferences, and I certainly had it in my Karolinksa presentation, and have discussed it here too - with reference to Bacillus cereus picking up plasmids from Baclillus anthracis and becoming pathogenic.
Just search this MP database for what I have written about "plasmids" and "polymicrobial" and you should find more detail. ...You find Epstein-Barr Virus (EBV), for example, in all the Th1 diseases - search PubMed you will find folks saying it causes just about all of them. But it is most likely a bystander, throwing its plasmids into 'the infectious soup'.
The real answer lies in the genomics, in the DNA (and RNA) and the intermixing thereof, and it is possible we may never know the totality of species involved.
..Trevor..
West Nile Virus
People with Th1 disease should take the recommended precautions to prevent exposure to mosquitos in areas where West Nile Virus is present. Symptoms of West Nile Virus are virtually indistiguishable from Th1 disease symptoms.
See My doctor thinks I have an upper respiratory infection. What should I do?
See also: Shingles
Member's experience
I originally thought of myself as having a viral onset because I really began getting fatigued and started my downhill course after what seemed like a bad flu-like illness that was never identified. Later, I came to realize that the virus (assuming that is what it was) was probably just the straw that broke the camel's back, but that the bacteria had been growing in my body underneath all along. I'm not sure what role the "virus" played but I know the MP is helping me improve more than anything else I have tried over 20 years of being ill (and I've tried a lot of things).
. ~Joyce WaterhouseLast edited on Thu Feb 21st, 2008 08:11 by
|
Foundation Staff .

| Joined: | Sat Jul 10th, 2004 |
| Location: | |
| Posts: | 17283 |
| Status: |
Offline
|
|
Posted: Mon Apr 28th, 2008 19:15 |
|
[filelink]
Intestinal parasites
Autoimmune/inflammatory diseases are not caused by worms. The parasites persist because the immune system is weakened. One can take medication to try and kill parasites, but they will continue to recur at least until the immune system is strong enough to prevent them from doing that.
The Th1 pathogens form a microbiota which are part of the human existence. Everybody carries them. If they don't cause disease when a person is young, they will ultimately cause the diseases of the aging, and the processes of aging. They are in our food, our water supplies, and in the air we share with others. They cannot be seen under a lab microscope, they cannot be cultured, yet they have been the bane of mankind since at least Neolithic times. They have evaded detection for at least a century because medicine has largely focused on things which can be seen under a microscope. This approach has to change if we are to prevent the ongoing slide towards epidemic chronic disease, which, with its perversion of mans' cognitive and neurological processes, might well threaten the very existence of Homo sapiens itself.
..Trevor..
Roundworms
This article states "The prognosis for recovery from roundworm infections is good for most patients." and "The definite diagnosis is based on the results of stool or tissue tests. and "Blood tests cannot be used to differentiate among different types of roundworm infections, but the presence of eosinophilia can help to confirm the diagnosis."
Treatment for 3 types of roundworm is anthelminthic medications. There is no treatment for the fourth type of roundworm but "symptoms usually resolve in one to two weeks when the larvae die."
You may want to complete roundworm treatment to resolve any symptoms caused by roundworms before you begin the Marshall Protocol or reduce immunopathology during the MP while you are undergoing this treatment.
See Intestinal parasites.
Flagyl
Flagyl profoundly affects the human Vitamin D metabolism, and all the enzymes associated with it. Patients might think they are 'herxing' but they are just being sick. They get some relief, sometimes, because it takes the body a while to try and get the innate immune system working again after Flagyl has totally shut it down. This is a dangerous drug, in the doses it is used in Lyme therapy. I have spoken to the mother of a Lymie who was paralyzed by it - for weeks.
..Trevor..
|
 Current time is 15:06 | |
|
|
 |
|