AUTOIMMUNE DISEASES CAUSED BY AN INFECTION?

dugdeep

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I'm wondering if something like activated charcoal, bentonite clay or some other natural chelator could be taken in conjunction with the protocol in order to lessen the herxheimer reaction. They'd have to be taken away from the medications and supplements, which may be problematic given the schedule, but I'm thinking it might mitigate some of the suffering you guys are undergoing.

Just a thought.
 

Laura

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dugdeep said:
I'm wondering if something like activated charcoal, bentonite clay or some other natural chelator could be taken in conjunction with the protocol in order to lessen the herxheimer reaction. They'd have to be taken away from the medications and supplements, which may be problematic given the schedule, but I'm thinking it might mitigate some of the suffering you guys are undergoing.

Just a thought.

Wouldn't make much sense. If you try to buffer the meds, you reduce the efficacy. If you take it later, you don't need it and it doesn't really do anything to clean anything out of your system as far as I can tell.

It’s normal for the body to generate an immune response when challenged by foreign matter such as microbes and allergens. Research has led to the hypothesis that this reaction in chronically ill patients is triggered by cell wall deficient, polymorphic L-form microbes. It is believed these intracellular bacteria have learned to live inside the macrophages (phagocytes) of the immune system. Apparently, they fail to be destroyed by the phagocytes which are supposed to kill them because they have adapted mechanisms to prevent being identified by the immune system.

When the intraphagocytic bacteria are killed by the immune system, the cells they lived in also die (apoptosis). As the immune system tries to clear up this cellular debris, it releases a host of inflammatory molecules which, along with the toxins released by the bacteria as they die, cause a rise in symptoms in the area in which the bacteria are being killed.
 

Laura

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This popped into view today:
http://www.ncbi.nlm.nih.gov/pubmed?term=Is%20Multiple%20sclerosis%20caused%20by%20a%20silent%20infection%20with%20malarial%20parasites%3F%20A%20historico-epidemiological%20approach%3A%20part%20II

Is multiple sclerosis caused by a silent infection with malarial parasites? A historico-epidemiological approach: part II.
Kissler H.
Abstract

The comparison between the old map of malaria and the later distribution of multiple sclerosis (MS) first carried out in the USA (Part I) is continued in Europe. The Italian 'dilemma' (Kurtzke), meaning the disappearance of the north-south gradient in Italy by recent surveys, can be solved when considering the dependence of malaria transmission in relation to the altitude. Further, the high prevalence of MS in earlier times in Mississippi, Louisiana and in the former province of Lucania in Italy can be explained by preceding epidemics of malaria. Brickner's therapeutic trial with quinine in cases of MS patients is reevaluated, and by this the Jarisch-Herxheimer reaction is shown to exist in MS too. The possible significance of the old and rather forgotten provocative methods for the diagnosis of latent malaria is discussed.

Copyright 2001 Harcourt Publishers Ltd.

And this:
http://www.ncbi.nlm.nih.gov/pubmed?term=[Whipple%20disease%20associated%20with%20pulmonary%20arterial%20hypertension.%20Jarisch-Herxheimer%20reaction%20after%20antibiotic%20therapy]

[Whipple disease associated with pulmonary arterial hypertension. Jarisch-Herxheimer reaction after antibiotic therapy].
[Article in French]
Peschard S1, Brinkane A, Bergheul S, Crickx L, Gaudin B, Morcelet M, Levy R.
Author information
Abstract
BACKGROUND:

Pulmonary hypertension is an uncommon feature of Whipple's disease and the underlying pathophysiological mechanism remains a subject of debate.
CASE REPORT:

A 57-year-old woman was hospitalized for exploration of migrating joint pain that had developed for 5 years. Histologically proven Whipple's disease was diagnosed on duodenal biopsies. The lung angiogram performed to explore signs of right heart failure demonstrated pulmonary hypertension and ruled out pulmonary embolism. Abundant pericardial effusion developed progressively. Antibiotic therapy using sulfamethoxazole-trimethoprime led to a systemic Jarisch Herxheilmer reaction. The pulmonary hypertension resolved rapidly, the pericardial effusion more slowly.
DISCUSSION:

The pulmonary hypertension in this patient appeared to be directly related to Whipple's disease, probably via vascular infiltration by Tropheryma whippeli.
 

Gaby

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[Whipple disease associated with pulmonary arterial hypertension. Jarisch-Herxheimer reaction after antibiotic therapy].
[Article in French]

When I first studied that disease, it sounded like it was fairly frequent. At least more than what was usually expected. The prospect was frightening... Just how many symptoms at long-term could be due to an infection years before. Worse, practically speaking, doctors forget that these infections exists.

To think that this is what we are actually dealing with, not necessarily and specifically Whipple's, but the analogy serves well.
 

Laura

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Gaby said:
[Whipple disease associated with pulmonary arterial hypertension. Jarisch-Herxheimer reaction after antibiotic therapy].
[Article in French]

When I first studied that disease, it sounded like it was fairly frequent. At least more than what was usually expected. The prospect was frightening... Just how many symptoms at long-term could be due to an infection years before. Worse, practically speaking, doctors forget that these infections exists.

To think that this is what we are actually dealing with, not necessarily and specifically Whipple's, but the analogy serves well.

Yes.

While Ewald doesn't even suggest a profit motive for the turning away from the right path in the late 40s, early 50s, it sort of comes through between the lines that the funding was for research that would lead to answers that could make lots of money. He calls a given set of "risk factors" not much better than what the ancients postulated as the cause of disease: miasma. "Risk factors" are really rather ridiculous when you think about it because few people will have all of them, and many people - maybe even half - will have a disease with NONE of the "risk factors" in play.
 

stellar

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Gaby said:
Yas said:
Ok. Changes done.

The Metronidazole and Ganciclovir and Allopurinol, instead "1 hour later", it should be after lunch time or a meal.

If it doesn't fit, don't worry. I think that with the basic instructions and the monthly plan, it is clear enough :)
Would the protocol be advisable for people on very low carb but not necessarily on a strict keto diet?
 

Laura

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stellar said:
Would the protocol be advisable for people on very low carb but not necessarily on a strict keto diet?

Why do you want to do it? Do you have a condition?

I think that most of the people reported doing it in the various papers we've cited here were NOT on any special diet. Some of the professionals supervising such protocols do recommend some dietary changes, others do not. I try to stay low to no carbs most days, but occasionally encounter a carbageddon that must be navigated.
 

Laura

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Something else to examine in terms of healing the gut during and after the protocol - cross-posted from the keto diet thread:

Carl said:
Following up to the recent radio show on Methylation and genetic defects, I was very interested in Dr. Rostenberg's initial gut healing methods.

I think that my gut is nowhere near healed as I would like it to be. I still can't tolerate many, many foods, and at a recent gathering some chocolate, tapioca, fruit/honey was enough to leave me feeling inflamed for days.

It turns out that he has a protocol simply laid out on his site (10 Day gut healing protocol), which basically consists of HCL/Enzymes, probiotics, botanical anti-microbials and heroic doses of L-glutamine. The other key aspect to the program is eating multiple small meals of only ONE food at a time (something that I've never heard of before).

It is available here: http://beyondmthfr.com/10-day-gut-repair/

It struck me as odd and counter-productive that he would use anti-microbials and probiotics at the same time I posted a comment and here is his reply:

Hi Carl,

Thank you for your comment! Yes, at first it can seem illogical to kill microorganisms while taking probiotics. The key to remember is that we are killing mainly pathogenic organisms – parasites of various kinds, yeasts/fungi, biofilm, bacteria, etc. This is all accomplished with the essential oils and berberine complexes. The other ingredients in the protocol are simultaneously rebuilding the gut wall and providing an optimum environment for the new probiotics to take root. It works very well to do this all at once. The body responds better to frequency, intensity, timing, duration, and quality. In other words, doing something intensely for a short time beats the slow and steady approach in practically every case. Remember too that the probiotics that Metagenics uses are known to produce their own form of antibiotics, helping to rid the gut of pathogens.

I found his reply interesting, as personally I've experimented with many different slow approaches over the years and haven't gotten very far.

I already have a few of the supplements and plan to try this out when I get hold of some others
 

Mikey

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Laura said:
The above may be the explanation for why some do so well on keto and others get sick in one way or another. I guess it depends on what kind of critters are using you for their food supply. Because, in the end, that IS what it is about: we are food and colonies for critters whose main aim is to make more colonies.

I'm still astounded as to how deep the rabbit hole goes regarding these things.

This reminded me of Gurdjieff's (intentionally?) cryptic remark that humans are "food for the Moon", where the term 'Moon' is more or less left undefined. Ouspensky gives more infomation about the System of Octaves, and there it is curious that the 'Moon' is placed one step below 'Earth'. For me, this always was a bizarre statement and a puzzling contradiction: How can humans be food for something that is 'lower' in terms of evolution? Now, the details provided in this thread just might shine more light on this. And if the body including critters is indeed "a battlefield of the wargames of the mind" -- if these critters, semi-critters and chemicals are indeed a kind of 'interface' to the 'mind' and 'emotions' or even 'higher levels' as is discussed beginning here and subsequent posts (excerpts from The Wave) --, then yes, I suspect the rabbit hole would be complex and go very deep.
 

stellar

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Laura said:
stellar said:
Would the protocol be advisable for people on very low carb but not necessarily on a strict keto diet?

Why do you want to do it? Do you have a condition?

I think that most of the people reported doing it in the various papers we've cited here were NOT on any special diet. Some of the professionals supervising such protocols do recommend some dietary changes, others do not. I try to stay low to no carbs most days, but occasionally encounter a carbageddon that must be navigated.
I am still trying to wrap my head around all the info in this thread and it is slow going. I need to understand a little better whether I need to do something like this. The Keto diet and initial detox did wanders for me so I am worried about opening a can of worms that I am not knowledgable about in knowing how to handle it.

I do have a spondylosis condition of my lower spine, the flaring up of which has been significantly ameliorated with the diet but past several months it has been flaring up again. Stiffness, pain, tiredness and feeling like it is spreading higher.

Also my reactions to sugars and gluten that may be hidden in food that I'm not aware of or on occasion doing it knowingly, I come down with such severe hay fever symptoms that I can hardly breathe for a couple of days. So is this protocol for me, not sure yet.

I did want to share this info with a few people that may find it helpful to look into. My son is one of them. He is finishing his degree in naturopathy and has interests in much deeper research than what mainstream is offering at his college including rewriting one or two of their curricula texts. In view of that I was hoping he could explain to me in more simple terms the workings of these critters and what tests he has available that I can do.
 

Gaby

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More possible clues in the following article.
The Relationship between Tourette’s Syndrome and Infections
_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514747/

Open Neurol J. 2012; 6: 124–128. Daniela L Krause* and Norbert Müller

Abstract

Increasing evidence shows that infections and an activated immune status might be involved in the pathogene-sis of tic disorders. Studies discuss the influence of neurotrophic bacteria and viruses on different psychiatric disorders. In addition, signs of inflammation and immunological abnormalities have been described especially in schizophrenia and Tourette’s syndrome (tic disorder). Neuroimaging studies revealed increased microglial activation in psychiatric diseases; indicating an inflammatory state of the CNS.

However, it still remains unclear what the underlying mechanism is of how infectious agents could contribute to tic symp-toms. One hypothesis is that not only one particular infectious agent causes directly to the disease; instead different (chronic) infections influence the immune balance and are therefore involved in the pathology. In tic disorders, infections with group A streptococci, Borrelia burgdorferi or Mycoplasma pneumoniae seem to be associated with symptoms of the disease. Studies have shown that immunologic treatment improves and prevents the re-occurrence of clinical symptoms in Tourette’s syndrome. Also post-infectious events by cross-reactive antibodies(against M-protein) and an altered dopaminergic(noradrenergic) neurotransmission as well as inflammatory/immunological dysregulations were considered as possible mechanisms to cause symptoms. Another contributing factor to the pathogenesis of these diseases could be an activation of the tryptophan catabolism through infectious agents. Tryptophan functions as a precursor for neurotransmitters like serotonin and becomes degraded to products that can modulate the neurotransmitter balance.

A deeper insight into the precise mechanism of how infectious agents influence immune parameter, tryptophan metabolism and the resulting neurotransmitter availability could help finding new therapeutic strategies. [...]

INFECTIONS AND TOURETTE’S SYNDROME

These specific movement abnormalities with the clinical phenotype of poststreptococcal tics and obsessive–compulsive disorders are termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) [...]

PANDAS are characterized by the following criteria: 1. prepubertal onset; 2. chronic tic disorder or obsessive–compulsive disorder; 3. sudden periods of severe exacerbations (‘‘saw tooth’’)—relapsing-remitting course; 4. temporal association of onset and one or more exacerbations with clinical evidence of a streptococcal infections; 5. the presence of subtle neurological findings such as reduced fine motor coordination or increased motor hyperactivity (but not overt chorea) [...]

Two case reports revealed that Mycoplasma pneumoniae might be associated with tic symptoms [19, 20]. This assumption was strengthened by a study that compared 29 Tourette patients to healthy controls regarding the Mycoplasma infection rates. The study found significantly more elevated antibody titers against Mycoplasma pneumoniae in TS patients as compared to controls [21]. Furthermore, an association between herpes simplex virus 1 and the exacerbation of tics was stated [22]. Also an acute infection with Borrelia burgdorferi presenting as TS was reported [23]. Our own group also identified infectious agents as contributing factors in TS: A significantly higher rate of TS patients had elevated antibody titers against Chlamydia trachomatis as compared to controls and trend towards a higher prevalence in the Tourette’s group was shown for Toxoplasma gondii [24].

Unitl now, none of these infectious agents has been linked consistently with TS. Thus a hypothesis is that infections do not directly cause symptoms of the disease, instead they could contribute to TS by triggering an immune response. Therefore the observations of a dysbalanced immune system will be discussed for TS.

[...]

A probable mechanism of how infections can influence the cerebral immune balance could be the activation of the tryptophan catabolism via infectious agents and elevated proinflammatory cytokines [9]. In the CNS tryptophan degradation takes place especially in microglia (also partly in astrocytes and neurons). The essential amino acid tryptophan gets degraded either to serotonin or over the kynurenine pathway (KP) to other products [10], which function either as a NMDA- receptor agonist or antagonist and control the neurotransmitter availability [11]. The activation of this KP has been shown to play an important role in the pathophysiology of neuropsychiatric disorders (e.g. schizophrenia) [38]. Also for TS, Behen et al. have identified in an imaging study that TS patients have an abnormal tryptophan metabolism in the cortical and subcortical area [12].

Considering the involvement of neuroinflammation in the course of TS, it strengthens the association between infectious agents activating the tryptophan breakdown either directly or through resulting pro-inflammatory cytokines and therefore influencing the neurotransmitter balance.

Elevated kynurenine levels have been observed in this disorder.
 

Gaby

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Infectious Agents are Associated with Psychiatric Diseases

_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4253361/

Ment Illn. 2012 Jul 26; 4(1): e10. Daniela Lydia Krause,corresponding author1 Elif Weidinger,1 Judith Matz,1 Agnes Wildenauer,1 Jenny Katharina Wagner,1 Michael Obermeier,1 Michael Riedel,2 Hans-Jürgen Möller,1 and Norbert Müller1

Introduction

In some psychiatric disorders environmental factors are involved in the pathophysiology of the diseases. Especially in schizophrenia and Gilles de la Tourette’s syndrome (TS) the precise underlying pathophysiology is yet unknown, however epidemiological studies have revealed different environmental factors in the pathogenesis such as winter and spring birth, birth in an urban area and complications during pregnancy.1,2 Moreover it has been suggested that infections might also be involved in the aetiology of some cases of schizophrenia.3 While until now different microbial agents have been proposed as risk factors for schizophrenia, many recent studies have focused on members of the viral family of Herpesviridae,4 Borna virus,5 intracellular bacteria like Chlamydia as well as the protozoan organism Toxoplasma gondii.6,7 Reasons for focusing on these agents include their ability to establish persistent infections within the central nervous system as well as the occurrence of neurological and psychiatric symptoms in individuals infected with these agents.8

Many pathophysiological parallels have been identified between schizophrenia and TS, which is characterized by multiple motor and vocal tics.9 Both disorders overlap in the clinical symptomatology and treatment strategies.10 Also some genetic parallels between the two diseases were identified: three out of five copy number variants were found to be implicated in TS and schizophrenia.11 However, these findings represent just a subgroup of patients and with the current literature the genetic association between TS and schizophrenia is far from generally proven. From a biological point of view, especially dysbalanced neurotransmitter systems seem to be a major cause of psychiatric diseases. For schizophrenia and TS many similarities have been found in these systems: Imaging studies favour an important role of the dopaminergic system in TS pathophysiology.12 Also in schizophrenia, dysregulations in various neurotransmitter systems -including dopamine, glutamate and acetylcholine - have been described.13-15 Serotonergic abnormalities have also been reported in TS and schizophrenia,16,17 possibly reflecting a disturbance within the tryptophan catabolism and the immune system in both diseases.18,19

As well as in schizophrenia, recent studies have revealed that infections could also contribute to a subtype of tic disorders. Group A β hemolytic streptococcal infections are a possible contributing factor of neuropsychiatric and movement disorders. At present, the clinical syndrome of post-streptococcal tics and obsessive-compulsive disorders in children is termed PANDAS (paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection).20 In addition to streptococci, several other infectious agents have been proposed to play a role in the pathogenesis of TS: two case reports revealed that Mycoplasma pneumoniae might be associated with tic symptoms.21,22 This assumption was strengthened in a study that compared 29 Tourette patients to healthy controls regarding the Mycoplasma infection rate and found significantly elevated antibody titers against Mycoplasma pneumoniae in TS patients.23 Also viruses were investigated and an association between herpes simplex virus 1 and the exacerbation of tics was stated.24 Moreover, Riedel et al. reported about a case where Lyme disease presented as Tourette’s syndrome.25

Considering all these findings, it still remains controversial, which of the neurotrophic infectious agents are involved in the pathogenesis of schizophrenia and TS and which ones are just present ubiquitously. In order investigate this issue we searched for overlapping infection rates in both diseases that might help to identify relevant infectious agents that are associated with schizophrenia and TS. However, with the present study design conclusions in regard to the pathophysiology of these diseases cannot be made. In this study we investigated whether there are differences in the distribution of antibodies to infectious agents that establish a persistent central nervous system infection in healthy controls, schizophrenic and Tourette patients.

[...]

Discussion

The present study revealed that the rate of positive antibodies against infectious agents differs between schizophrenic and TS patients. We showed that there is a higher prevalence of seropositivity for viral infections in the schizophrenic group as compared to TS, because antibodies against herpes simplex virus and cytomegalovirus were overrepresented in schizophrenia. In total, Tourette patients showed lower rates of different antibodies to infectious agents then schizophrenic patients. When the two diseases were compared to healthy controls a strong trend towards a higher rate of Chlamydia trachomatis was found in schizophrenia and TS. These findings are in line with previous studies studies that concluded that Chlamydia infection represents one risk factor for schizophrenia.27

To our knowledge, so far no study has investigated the comparison of TS and schizophrenia regarding the antibody distribution. Even so, the two diseases TS and schizophrenia show parallels in the underlying pathophysiology their different, but in total elevated vulnerability to infectious agents, might be explained by alterations within the immune status. One possible explanation for the varying disposition of antibodies between the two groups is that there might be a shift within particular immune parameters. As the toll like receptor family plays a fundamental role in virus/ bacteria recognition and activation of innate immunity these TLR might qualify to be further investigated in TS and schizophrenia. The present study found some indications that could point to a disturbed immune system in these diseases: we have seen mainly IgG and not IgM or IgA antibodies to be elevated. IgG antibodies are involved in secondary immune responses and IgM antibodies appear already early in the course of an infection and usually reappear. This finding could indicate that the infections have progressed to dormant infections with a persistent immune response.

Recently the involvement of the immune system in the pathophysiology of psychiatric diseases has gained broad attention: the international schizophrenia consortium has demonstrated an association between the major histocompatibility complex and schizophrenia, implicating aetiological mechanisms involving autoimmunity and infections.28 Numerous studies have identified the important role of immunologic parameters in schizophrenic patients.29 An immune disturbance in schizophrenia was suggested because of elevated levels of interleukin-1β, tumour necrosis factor-α and a higher nuclear factor-κB (regulates the cytokine system) activation.30 Furthermore signs of inflammation were found in the brains of schizophrenic patients.31

Also for TS evidence for the important role of immune parameters in the disease’s pathophysiology is emerging: support for this immunologically based hypothesis of TS comes from studies investigating the prevalence of different immunogenic cells: Kawikova et al. found that TS patients have a decreased number of CD4+CD25+ regulatory T cells and their number correlated with the severity of symptoms.32 On balance, these results suggest that both innate and adoptive cell mediated mechanisms may be overactive in TS.

A probable mechanism of how infections can influence the cerebral immune balance could be the activation of the tryptophan catabolism via infectious agents and elevated proinflammatory cytokines.33 The essential amino acid tryptophan gets degraded either to serotonin or over the kynurenine pathway to other products,34 which function either as a NMDA-receptor agonist or antagonist and control the neurotransmitter availability.35 The activation of this kynurenine pathway has been shown to play an important role in the pathophysiology of schizophrenia.36 Also for TS, Behen et al. have identified in an imaging study that TS patients have an abnormal tryptophan metabolism in the cortical and subcortical area.37

There are also some limitations to our study: first, it is known that antipsychotic medication influences the immune system and therefore also the infectiousness might be affected.38 In this study, only the schizophrenic patients were unmedicated considering antipsychotic drugs. The TS patients received in 70.2% antipsychotic treatment at the time of study inclusion. As TS patients usually get diagnosed during childhood, patients at our hospital have started treatment already several years before. A second limitation is that it was not possible to evaluate the rate of sexual activity in patients and controls. This seems important as Chlamydia trachomatis is a sexually transmitted disease. Though the groups were age matched, it is likely that their sexual activity might resemble. However, there are studies showing that schizophrenic patients suffer from sexual dysfunction and of less social activity and have therefore an impaired sexual life.39 Third, the sample size was rather small and therefore the statistical power might be slightly restricted.

In summary infectious agents might influence the cerebral neurotransmitter balance via activating on the tryptophan catabolism. The precise mechanism, how an altered metabolism of tryptophan might contribute to the pathogenesis of schizophrenic symptoms and tics is not yet fully understood. On the one hand it could reflect a state of immune activation; or on the other hand it might be possible that kynurenine and its neuroactive metabolites (e.g. quinolinic acid) cause directly a toxic effect in the basal ganglia and the CNS. So far the association of infections and the kynurenic pathway seems promising as this finding could have therapeutic implications: at present inhibitors or enhancers of certain metabolites of this pathway are available and being currently tested for different neuropsychiatric conditions.40

Conclusions

The outcome of this study emphasizes on the association between infectious agents and psychiatric diseases (schizophrenia and TS). It highlights the differential distribution of seropositivity to these agents in both patient groups. Future studies with larger sample sizes are needed to investigate the precise role of infectious agents as possible contributing factors to psychiatric diseases.
 
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