AUTOIMMUNE DISEASES CAUSED BY AN INFECTION?

[shijing]

I was thinking about the last session, and I guess that those who "fit the profile", meaning that they would benefit from this protocol, are those with autoimmune disease (?)

I'd say so -- actually, if you have any of the conditions listed in the recent posts from the last couple of pages, you could potentially fit the profile for a chronic infection.

FWIW, you may also fit the profile for someone who should have their SNPs tested -- Latin America is one area where there are above average numbers of polymorphisms in the population that affect the methylation cycle. As I mentioned on another thread, sulfur sensitivity can be due to a CBS mutation, and polymorphisms tend to "travel in packs" -- meaning that if you have one, you're likely to have others.

 

[Laura]

I'd say so -- actually, if you have any of the conditions listed in the recent posts from the last couple of pages, you could potentially fit the profile for a chronic infection.

It would be more useful to list the conditions and then the varied organisms that could be implicated. I think that listing the organisms and what they can cause kinda makes people go cross-eyed.

 

[shijing]

It would be more useful to list the conditions and then the varied organisms that could be implicated. I think that listing the organisms and what they can cause kinda makes people go cross-eyed.

Sure -- it generates a longer list, but you're right that it's good to put them in this order as well. This is from the rain-tree list a few posts back -- it's probably not exhaustive, but it should have a solid core:

AIDS/HIV: Mycoplasma genitalium, Mycoplasma fermentans, Mycoplasma incognitus and Mycoplasma penetrans, Mycoplasma pirum

ALS: Mycoplasma fermentans

amnionitis: Mycoplasma hominis and Ureaplasma urealyticum

arthritis: Mycoplasma genitalium, Mycoplasma fermentans, Mycoplasma salivarium

asthma: Mycoplasma pneumonia

autoimmune diseases: Mycoplasma fermentans, Mycoplasma pneumonia, Mycoplasma incognitus and Mycoplasma penetrans

cancer: Mycoplasma fermentans

cervicitis: Mycoplasma hominis and Ureaplasma urealyticum

Chronic Fatigue Syndrome: Mycoplasma fermentans

chronic nongonococcal urethritis: Mycoplasma genitalium

chronic pelvic inflammatory disease: Mycoplasma genitalium

CNS disorders and diseases: Mycoplasma pneumonia

Crohn's and IBS: Mycoplasma fermentans

diabetes: Mycoplasma fermentans

diseases of the gingival crevices and respiratory tract: Mycoplasma faucium, M. lipophilum and M. buccale

encephalitis: Mycoplasma pneumonia

endocrine disorders: Mycoplasma fermentans

eye and ear disorders and infections: Mycoplasma salivarium

Fibromyalgia: Mycoplasma fermentans

gingivitis: Mycoplasma salivarium

Guillain-Barr syndrome: Mycoplasma pneumonia

Gulf War Syndrome: Mycoplasma fermentans

heart diseases: Mycoplasma pneumonia

infertility: Mycoplasma genitalium, Mycoplasma hominis and Ureaplasma urealyticum

leukemia: Mycoplasma pneumonia

low birth weight infants: Mycoplasma hominis and Ureaplasma urealyticum

Lupus: Mycoplasma fermentans

Multiple Sclerosis: Mycoplasma fermentans

neonatal conjunctivitis: Mycoplasma hominis and Ureaplasma urealyticum

neonatal pneumonia: Mycoplasma hominis and Ureaplasma urealyticum

non-gonococcal urethritis: Mycoplasma hominis and Ureaplasma urealyticum

pelvic inflammatory disease: Mycoplasma hominis and Ureaplasma urealyticum

periodontal diseases including even cavities: Mycoplasma salivarium

peritonitis: Mycoplasma hominis and Ureaplasma urealyticum

pneumonia: Mycoplasma pneumonia

polyarthritis or septic arthritis: Mycoplasma pneumonia

polyradiculitis: Mycoplasma pneumonia

post-partum septicemia: Mycoplasma hominis and Ureaplasma urealyticum

premature rupture of membranes: Mycoplasma hominis and Ureaplasma urealyticum

psoriasis and Scleroderma: Mycoplasma fermentans

pyelonephritis: Mycoplasma hominis and Ureaplasma urealyticum

Reiter's syndrome: Mycoplasma hominis and Ureaplasma urealyticum

septic meningitis: Mycoplasma pneumonia

Steven-Johnson syndrome: Mycoplasma pneumonia

TMJ disorders: Mycoplasma salivarium

upper and lower respiratory diseases: Mycoplasma pneumonia

urinary tract infections: Mycoplasma pneumonia

urogenital infections and diseases: Mycoplasma genitalium, Mycoplasma incognitus and Mycoplasma penetrans, Mycoplasma pirum

vaginitis: Mycoplasma hominis and Ureaplasma urealyticum

wound infections (C-section): Mycoplasma hominis and Ureaplasma urealyticum

Some of the conditions above are listed in the previous wiki-article with different associations -- that may merely indicate the incidence of coinfections.

 

[Gaby]

Other than rheumatoid arthritis, it seems typical bacteria are clearly linked with CFS, fibromyalgia, Sjogren's disease, multiple sclerosis, Grave's disease and several other problems.

Some highlights from the attached paper "The Pathogenesis and Treatment of Mycoplasmal Infections" by Garth Nicolson.

Mycoplasmal Infections and Respiratory Illnesses

Various respiratory illnesses, such as chronic asthma, airway inflammation, chronic pneumonia and other respiratory diseases, are known to be associated with mycoplasmal infections. For example, M. pneumoniae is a common cause of upper respiratory infections, and severe asthma is commonly associated with mycoplasmal infections. [...]

Certain Mycoplasma species are involved in respiratory tract infections associated with airway inflammations, induction of bronchial hyperresponsiveness (BHR) and asthmatic attacks. At a minimum, M. pneumoniae infections can cause worsening of conditions in asthmatic patients, whose attacks are associated with significant and specific IgA and IgE responses.

Mycoplasmal Infections in Urogenital Diseases

Mycoplasma species are commonly found in urogenital infections. For example, M. hominis was detected in more than 12% of females who presented at gynecological services, and M. genitalium has been associated with acute and nonspecific non-gonococcal urethritis in males but not in asymptomatic controls. This organism is also a common cause of genital infections in women, and it was detectable in 7% of women with sexually transmitted diseases. M. hominis and U. urealyticum have been implicated in a wide variety of urogenital diseases, such as pelvic inflammatory disease, infertility, non-gonococcal urethritis (NGU) and other genital infections, pyelonephritis, Reiter's syndrome, and peritonitis. The appearance of various bacterial species in bacterial vaginosis may be a result of pathophysiological alterations of the vaginal ecosystem, and mycoplasmas appear to play an important role in this process. Mycoplasmas are also known to interfere in pregnancy, For example, U. urealyticum was found to be involved in 11% of patients with fertility problems.

Mycoplasmal Infections in Autoimmune Diseases

Several characteristics of mycoplasmas make them attractive as agents that may be responsible for triggering autoimmune responses. First, during their intracellular replication and release from host cells mycoplasmas can capture antigens from the host cell surface and incorporate them into their cell membranes. This can lead to immune responses against these antigens and possibly autoimmune reactions. Second, mycoplasmal antigens can mimic host antigens and trigger immune responses against these antigens with resulting cross reactivity against host antigens. Third, mycoplasmas can cause apoptosis of host cells with subsequent release of normal host antigens.

Superantigens are potent immunomodulators derived from microorganisms, such as bacteria, viruses and
[...] Mycoplasmal infections have also been implicated in the progression of Kawasaki disease, Graves’ disease, Hashimoto’s disease, Sjögren’s syndrome, systemic lupus erythematosis (SLE) and multiple sclerosis (MS).

Mycoplasmal Infections in Fatigue Illnesses

Chronic fatigue is the most commonly reported medical complaint of all patients seeking medical care. However, the fatigue syndromes, such as chronic fatigue syndrome (CFS, sometimes called myalgic encephalomyelitis), fibromyalgia syndrome (FMS) and Gulf War illnesses (GWI) are distinguishable as separate syndromes that have muscle and overall fatigue as major characteristics, among many other multiorgan signs and symptoms, including immune system abnormalities. Because of the complex nature of these illnesses, many patients are often diagnosed with multiple syndromes. We and others have examined the presence of mycoplasmal blood infections in CFS, FMS and GWI patients and have found that the majority of patients have blood mycoplasmal infections.

 

[Gaby]

10 days of Roximisan (roksitromicin) - I felt much better with this

7 days of Hemomycin (azitromicin) - I felt worse with this

7 days of Doksiciklin - I felt better with this

My replacement GP actually told me that my therapy was wrong and that I should've taken all three antibiotics in the same time and that it had no effect taking it one by one. :/

Taking them all at the same time sounds crazy. It seems to me that the way you did it was a good way to go. You rotated antibiotics, decreasing the chance of resistance. According to these protocols, one needs at least 6 weeks in these antibiotics.

Typical dose of doxycycline 100mg twice per day, Azitromycin 500mg per day for three days, ciprofloxacin 500mg twice per day for one week and so forth.

I hope to get a hold of the researched protocols for mycoplasma species and chlamydia though.

 

[Gaby]

Signs and symptoms of atypical bacteria infection (i.e. mycoplasmas)

IDENTIFICATION AND TREATMENT OF CHRONIC INFECTIONS IN CFIDS, FIBROMYALGIA SYNDROME AND RHEUMATOID ARTHRITIS: SUPPORT FOR ANTIBIOTIC REGIMENS

Chronic Fatigue Immune Disfunction Syndrome (CFIDS) is characterized by a number of chronic (>6 months duration) signs and symptoms that do not resolve with rest. Among these are disabling fatigue, intermittent fevers, joint and muscle pain and loss of joint mobility, impairments in short-term memory, headaches, skin rashes, diarrhea, coughing, nausea and gastrointestinal and breathing problems, diminished vision and other signs and symptoms. Other chronic illnesses, such as Fibromyalgia Syndrome (FMS), Gulf War Illness (GWI), Rheumatoid Arthritis (RA), Inflammatory Bowel Disease, among others, also show many of these same signs and symptoms, suggesting that there may be some overlap in the underlying causes of these conditions or at least in the factors that may result in sickness (morbidity) or illness progression.[...]

As chronic illnesses such as CFIDS, FMS, GWI and RA progress, there are a number of accompanying clinical problems, particularly increases in autoimmune signs and symptoms seen in some patients. These include acquiring most but usually not all of the classical signs and symptoms of Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS or Lew Gehrig’s Disease), Lupus, Graves’ Disease, RA and other complex autoimmune diseases. Although it is not proven, such usually rare autoimmune responses are at least consistent with certain chronic infections, such as mycoplasmal infections, that penetrate into nerve cells, synovial cells in joints and other cell types. It is proposed that these autoimmune signs and symptoms are caused when intracellular pathogens, such as mycoplasmas and other bacteria, escape from cellular compartments. Some microorganisms like mycoplasmas can incorporate into their own structures pieces of host cell membranes that contain important host membrane antigens that can trigger autoimmune responses [1], and they can also mimick host cell antigen structures [3]. Thus patients with such infections may respond immunologically to microorganism antigens as well as their own membrane antigens, producing unusual autoimmune signs and symptoms.[...]

The recommended treatments for mycoplasmal blood infections require long-term antibiotic therapy, usually multiple 6-week cycles of doxycycline (200-300 mg/day), ciprofloxacin or Cipro (1,500 mg/day), azithromycin or Zithromax (500mg/day) or clarithromycin or Biaxin (750-1,000 mg/day). Multiple cycles are required, because few patients recover after only a few cycles [4-6], possibly because of the intracellular locations of the infections and the slow-growing nature of these microorganisms. We now recommend that patients who have been diagnosed with blood infections receive continuous antibiotics for at least 6 months before using the 6-week cycles of treatment. Although patients starting such therapy usually have Herxheimer reactions and feel initially worse due to die-off or release of toxic materials from damaged microorganisms, they eventually stabilize and then slowly begin to recover. Unfortunately, the treatment requires long term therapy and recovery is usually very slow. Patients that have been sick for many years are unlikely to recover within a year of therapy.

 

[shijing]

I was doing a bit of research on my own and found her too, it seems very interesting and she does seem to take viral/bacterial infections seriously, as well as methylation pathways, as you said.

Thanks, Yas, for mentioning that -- I hadn't visited her site recently, and she has two new videos that are very relevant to this discussion which I hadn't seen yet:

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One of the important key points in these videos are that methylation problems create an environment which favors bacterial infection -- this in turn favors the sequestering of heavy metals, both because of the genetic inability to detox the metals as well as the propensity of the bacteria to attach to and utilize heavy metals. In my personal experience, amount of heavy metal burden correlates directly with degree of EMF sensitivity, so it may not be too much of a leap to suggest that EMF sensitivity could indicate both methylation pathway blockage as well as chronic bacterial infection.

One point that Yasko brings up (starting at about 39:00 in the first video) that we may want to research more is that infected individuals (she is talking specifically about H. pylori in this case) respond differently to ketosis than uninfected individuals. It's unclear to me if she is distinguishing clearly between ketosis and ketoacidosis, but it's something that we would want to clarify I think.

 

[RedFox]

One of the important key points in these videos are that methylation problems create an environment which favors bacterial infection -- this in turn favors the sequestering of heavy metals, both because of the genetic inability to detox the metals as well as the propensity of the bacteria to attach to and utilize heavy metals. In my personal experience, amount of heavy metal burden correlates directly with degree of EMF sensitivity, so it may not be too much of a leap to suggest that EMF sensitivity could indicate both methylation pathway blockage as well as chronic bacterial infection.

fwiw you don't need the MTHFR mutation for your methylation pathways to become blocked either, just enough stress, inflammation and toxicity.
Those with the mutation will tend to be like canaries in the coal mine though, and suffer symptoms first. They will probably need support to bounce back too.

 

[RedFox]

I re-watched some MTHFR videos yesterday, and one of the key points I came away with is that those with the mutation methylation pathway breaks down under stress/disease.
Not only does the breakdown of the system lead to chronic disease, but so does chronic disease lead to the breakdown of the system. Catch 22.

The emphasis was in order to get the system working again all burdens to methylation should be corrected (lifestyle, diet, gut health, stress, toxicity etc).

A parasitic or bacterial infestation of the body is going to be the number one problem (when all the above are accounted for) and demand the most from the methylation pathways

Having said that, it needs to be noted that antibiotics and the toxins from pathogens being killed will also have the potential to shut down methylation pathways in those with the mutation.
So again extreme caution should be used with this protocol.

If cortisone is employed and the protocol followed, but health deteriorates a MTHFR mutation should be considered (along with a B12/folate deficiency - so age and how much stress a person has endured in there life should also be considered).
Without that, immune defences will be compromised, toxcicity won't be able to be processed and you will be open to future infection.

Those with the mutation probably should be considered highly likely to have an infection.

I'm going to attempt this antibiotic protocol in the next few weeks, so will update on the results to see if it matches the above hypothesis.

 

[Gaby]

I hope to get a hold of the researched protocols for mycoplasma species and chlamydia though.

I got a hold of them. I'm attaching the most relevant article.

A few key concepts: any treatment lasting less than 6 months will fail. People will relapse sooner or later. Doxycycline 100mg twice or three times per day every other day can be used. After 6 months, 6 cycles with 2 weeks off can be used.

Metronidazol to kill "cysts" can be used at some point.

Nystatin and probiotics other than mitochondrial supplements (alpha lipoic acid, l carnitine, NADH, etc) are useful.

FIR sauna and magnesium baths (2 cups on a bathtub) periodically are most useful too.

I'll study Prof. Garth Nicolson's experience and write up a synthesis. He seems to have a lot of successful case reports and experience, and has published it all in mainstream journals. Any doctor should be open minded to that material.

 

[Yas]

I was thinking about the last session, and I guess that those who "fit the profile", meaning that they would benefit from this protocol, are those with autoimmune disease (?)

I'd say so -- actually, if you have any of the conditions listed in the recent posts from the last couple of pages, you could potentially fit the profile for a chronic infection.

FWIW, you may also fit the profile for someone who should have their SNPs tested -- Latin America is one area where there are above average numbers of polymorphisms in the population that affect the methylation cycle. As I mentioned on another thread, sulfur sensitivity can be due to a CBS mutation, and polymorphisms tend to "travel in packs" -- meaning that if you have one, you're likely to have others.

I was doing a bit of research on my own and found her too, it seems very interesting and she does seem to take viral/bacterial infections seriously, as well as methylation pathways, as you said.

Thanks, Yas, for mentioning that -- I hadn't visited her site recently, and she has two new videos that are very relevant to this discussion which I hadn't seen yet:

Well, I was actually searching about CBS mutation because you mentioned it in the other thread and I had no idea of what it meant :/
So, when I was doing the search, I've found her material and thought it was really interesting. She deals with Autism and other conditions, and she has a protocol as well... I haven't really read the whole thing yet, just scanned through it, but it seems very interesting. Considering that my younger brother has Asperger and my mother also has autoimmune disease and other conditions, I guess that my genetics have something to do with my health problems for sure.

Thanks for the videos, I'll watch them and see if I can read more of her material.

 

[Laura]

I was rather surprised by the list of mental illnesses that are possibly due to pathogenic invasions/infections. However, now that I'm reading this book by Paul Ewald, it begins to make some sense and also may explain some unusual results of my experiment that I'll explain below. He writes:

The issues raised in Plague Time are not stagnantly awaiting resolution. Each week brings new developments in our understanding of the true nature of disease. ... Sometimes key bits of evidence have already been reported but have been overlooked. ...

One such relic was presented to me on a Friday afternoon last April by one of my students, Levi.... He had been doggedly tracking the literature on schizophrenia for two semesters. As he researched evidence familiar to current experts, he also sniffed out older evidence that might have been overlooked or forgotten as a result of inattention or the biases of the times. His goal was to assess whether the entire body of evidence implicated infectious causation. Normally calm and collected, Levi on this afternoon was a bit jittery, a sure sign that he had something interesting in hand. “It’s LSD, or something like it,” he said as he handed over a research paper that had been published a half century ago.

The previous summer, schizophrenia expert Fuller Torrey told me that his research group was finding associations between Toxoplasma gondii infection and schizophrenia, a lead that I passed along in the hardcover edition of Plague Time, and that provided the impetus for Levi’s detective work.

T. gondii is a distant relative of the protozoan that causes malaria, but rather than being dispersed by the bites of mosquitoes, T. gondii is transmitted to cats when they eat rodents, and then transmitted back to other rodents when the rodents lick or eat things contaminated by cat droppings. Instead of being digested by the rodent, the parasite penetrates the intestinal wall and moves to the brain, causing the rodent to behave abnormally in response to important environmental stimuli; for example, when infected rats encounter the smell of a cat they do not seem to appreciate the gravity of their situation—good for the cat (it gets a meal), good for the parasite (it gets transmitted), bad for the rat (it gets eaten). T. gondii encysts in human brains as it does in rodent brains, but this similarity doesn’t mean that T. gondii causes schizophrenia. It would be useful to know whether T. gondii-infected rodents became schizophrenic. But how can one tell whether a rat is feeling paranoid, hallucinating, or hearing voices that are not really there?

The paper that Levi handed to me provided a clue. The authors of the article tested schizophrenics for infection with T. gondii and for the presence of LSD. Over half of their patients were infected with T. gondii, and these infected patients were almost always the same patients who tested positive in the LSD test. The production of LSD or an LSD-like compound in T. gondii-infected schizophrenics strengthens the case for T. gondii as a cause of the hallucinations experienced by schizophrenics, and, more generally, as a cause of schizophrenia.

After Plague Time went to press and while Levi was conducting his detective work, the data collected by Torrey and his colleagues were set in print. In accordance with the study published a half century earlier, almost half of their schizophrenic subjects tested positive for T. gondii whereas only about one in ten of the nonschizophrenic controls tested positive. Mothers of schizophrenics were almost five times more likely to be infected with T. gondii than mothers who did not have schizophrenic children, suggesting transmission during pregnancy as a major route of infection.

This last remark really hit me upside the head, so to say.

For a long time I've been aware of the terrible fact that it seems that I transmitted the genes for autoimmune conditions to my children, each of who manifests a somewhat different disorder. Needless to say, this has horrified me for as long as I've been aware of it because they have really suffered through no fault of their own.

BUT, what if it isn't the genes, but the infection?

We all know that it is generally said that all kinds of conditions are genetic... and that's what this book is about: he says t'aint necessarily so though susceptibility could be partly genetic.

Now, another thing has been on my mind over the last few weeks. Keep in mind that today I'm finishing up my 8th cycle of metronidazole and on this one, have had virtually no reaction that I can detect. What is on my mind, what I have noticed for a few weeks now, is a subtle change in thinking. I don't want to say too much because I need to continue to observe this, but what I will say is that it is like chains are falling off my mind.

In addition to that, there is a different feeling in my legs. I've commented often enough about the fact that my legs have always felt leaden especially when I go up and down stairs. Well, it's too soon for a significant change, but there is enough difference to notice.

At this point, I'm going on the Minocin/doxycycline every other day for the next six months with maybe a single round of metronidazole once a month as Gaby suggests. Our next work here is for those others with the autoimmune conditions (not just my kids) will be utilizing this protocol: starting with the doxycycline for 6 months, and then finishing with 6 to 8 cycles of the metronidazole to take care of any encysted pathogens. That might be considerably less brutal than the other way around.

So, I would say that one doesn't necessarily have to have an autoimmune condition that is obvious to benefit from this protocol: obviously, some mental conditions like OCD, anxiety, and so much more, might be related to a long-term infection. Go back and re-read the list of things that can be related to long-term, slow burning infections. I don't know about you, but for me, having to remember to take medicine for six months, and even enduring a herxheimer reaction is worth feeling better.

 

[RedFox]

Thanks for sharing Laura, this getting really rather interesting.

This last remark really hit me upside the head, so to say.

For a long time I've been aware of the terrible fact that it seems that I transmitted the genes for autoimmune conditions to my children, each of who manifests a somewhat different disorder. Needless to say, this has horrified me for as long as I've been aware of it because they have really suffered through no fault of their own.

BUT, what if it isn't the genes, but the infection?

We all know that it is generally said that all kinds of conditions are genetic... and that's what this book is about: he says t'aint necessarily so though susceptibility could be partly genetic.

This is where my thinking is too - that it's more likely an infection playing off against specific genetics.
Either exploiting a (genetic) weakness or worsening things (so a gentic 'problem' expresses clearly).
And it all goes back to a thread you started in 2006 Toxoplasmosis - The Return of the Puppet Masters

And especially what the C's said (I think we can call this a hit for sure now)

9 August 1997
Q: Next question: is there any relationship between the fact that Roger de Mortimer, the carrier of the last of the line of the Welsh kings, was the lover of Isabella of France, who was the daugther of Philip the Fair, the destroyer of the Templars, and the murder of Edward II, the first of the English Prince of Wales?

A: Templars are a setup, insofar as persecution is concerned. Remember your "historical records" can be distorted, in order to throw off future inquiries, such as your own.

Q: I know that. I have already figured that one out! But, it seems that no one else has made this connection. I mean, the bloodlines that converge in the Percys and the Mortimers are incredible!

A: You should know that these bloodlines become parasitically infected, harrassed and tinkered with whenever a quantum leap of awareness is imminent.

Q: Whenever a quantum leap...

A: Such as "now."

Now, another thing has been on my mind over the last few weeks. Keep in mind that today I'm finishing up my 8th cycle of metronidazole and on this one, have had virtually no reaction that I can detect. What is on my mind, what I have noticed for a few weeks now, is a subtle change in thinking. I don't want to say too much because I need to continue to observe this, but what I will say is that it is like chains are falling off my mind.

In addition to that, there is a different feeling in my legs. I've commented often enough about the fact that my legs have always felt leaden especially when I go up and down stairs. Well, it's too soon for a significant change, but there is enough difference to notice.

That's awesome!

So, I would say that one doesn't necessarily have to have an autoimmune condition that is obvious to benefit from this protocol: obviously, some mental conditions like OCD, anxiety, and so much more, might be related to a long-term infection. Go back and re-read the list of things that can be related to long-term, slow burning infections. I don't know about you, but for me, having to remember to take medicine for six months, and even enduring a herxheimer reaction is worth feeling better.

Agreed.

A few interesting things came up in the health and wellness podcast that are worth mentioning.
The Dr talked about infections of the gut mostly (which would most likely be as problematic). One point was that it will cause the fight or flight (adrenal) system to become chronically activated (i.e. chronic stress).
Another part being that when he works with clients, he focuses on cleaning up digestion (and resetting the gut flora). I don't know if he used antibiotics or similar, but the idea is you need to clean out the 'weeds' or you'll end up feeding those when you start working to repair things.

I figure that applies equally to systematic infections.

 

[Laura]

A few interesting things came up in the health and wellness podcast that are worth mentioning.
The Dr talked about infections of the gut mostly (which would most likely be as problematic). One point was that it will cause the fight or flight (adrenal) system to become chronically activated (i.e. chronic stress).
Another part being that when he works with clients, he focuses on cleaning up digestion (and resetting the gut flora). I don't know if he used antibiotics or similar, but the idea is you need to clean out the 'weeds' or you'll end up feeding those when you start working to repair things.

I figure that applies equally to systematic infections.

Thing is, when you are working on systemic infections, you are killing everything that isn't attached, more or less. So you have to keep up with the probiotics. Plus, you have to supplement since your gut flora will be iffy for the duration and absorption may not be optimal. This new guy who talks about doing the doxy for six months addresses that and I believe that Gaby is sorting out the protocol precisely.

 

[Gaby]

BUT, what if it isn't the genes, but the infection?

We all know that it is generally said that all kinds of conditions are genetic... and that's what this book is about: he says t'aint necessarily so though susceptibility could be partly genetic.

As data to support this hypothesis, from "Mycoplasmal Infections - Diagnosis and treatment in GWS/CFIDS patients" (paper attached):

77% of the spouses and 65% of the children of Gulf War Illness (GWI) patients have developed the same or similar signs and symptoms. Based on the symptom pattern of Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS), we feel that the most appropriate syndrome that characterizes GWI is CFIDS, and this type of GWI/CFIDS is apparently being transmitted to close family members.

In this model, the syndrome is initiated by immune activation and the stimulated release of interferons and cytokines that cause neurotoxicity and other systemic effects. We have proposed that GWI/CFIDS may be initiated by host responses to chronic infections agents....

From our own experience with GWI/CFIDS (our stepdaughter returned from service in a U.S. Army airborne combat unit in Operation Desert Storm wtih GWI/CFIDS, and eventually our entire family presented with CFIDS signs and symptoms), we suggested that most of the CFIDS signs and symptoms could be explained by chronic pathogenic mycoplasma infections... the types of mycoplasmas that we have detected in veterans and their family members are very pathogenic, colonize in a variety of organs and tissues and are difficult to treat.

Several cases are reported and from their experience, a 6 month course of antibiotics is suggested. Although people healed with 6 weeks cycles of antibiotics, some relapsed and later improved if they repeated the cycles of antibiotics. The improvement was so dramatic and the relapses so frequent, that a base of 6 months was established.

Close monitoring is needed to distinguish between an adverse reaction to a drug (very rare), a Herxheimer reaction and if there are no Herx reactions, the addition of other antibiotics or antimicrobials. So even if there is a basic protocol, it will variate according to each individual and their main parasitic infestation. If there are no Herx reactions with the antibiotics, then going with the metronidazol protocol for "cyst" parasites would be the next step.

This is a ray of hope for those who are infested and currently dealing with the parasitic consequences. I wish it was not my case, but I guess the microbes don't mind wishful thinking :/

Very interesting research!