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Posted: Wed Aug 3rd, 2005 06:20 |
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How does Th1 inflammation develop? What is successive infection?
Successive infection
Trevor now says that the disease state one acquires is probably dependant on the sequence, and type of pathogens which infects the body. This is called 'successive infection' or 'infectious cascade' and has little to do with defective human genes or genetic predisposition.
For example, "When one of the nasty bugs arrives, does it find your DNA intact in the cell it invades, or has the DNA already been altered by a previous pathogen? If it tries to act on an altered gene, then the result will be different from if it acts on a 'clean' gene. Nobody is immune to the L-form pathogens. Some eventually get heart attacks or cancer, others get Th1 diseases." This is the process of cell mutation and changed expression of genes due to the bacterial, viral, and bacteriophage, infections we collect during pur lifetime.
Trevor states that, "Prof. Bach's work indicates that the species of infective agent and sequence of infection are quite capable of producing the plethora of Th1 disease diagnoses that we see."
What disease you develop and how quickly you develop it is determined by factors such as exposure (some species are acquired before birth), route of transmission (healthcare workers have a higher incidence of sarcoidosis), CWD species, virulence of the species and external stimuli.
An infant is solely protected by its innate immune system for the first month or so of life. Adaptive immunity (activated lymphocytes/antibodies) take a month or two to develop. This is the period when the newborn is most at risk, and when Vitamin D supplementation, turning down its innate immunity, can do a lot of harm. You might review the discussion at URL
http://www.marshallprotocol.com/forum39/6896.html
Siblings are likely to eventually suffer from Th1 chronic disease, but it may be CFS, FM, Arthritis, Parkinsons, MS, Dementia or some other presentation. It all depends on the pea-soup of pathogens they collect.
It has been several years since we first understood that the Th1 pathogens can all be passed down the maternal line, and two years since we realized Borrelia was also one of those L-form pathogens.
"The presence of high 1,25-D points to an external stimulus as being the culprit behind the original infection." Thus, pregnancy (the placenta generates high levels of 1,25-D) or sunbathing, for example, stimulate bacterial growth and cause disease exacerbation.
Trevor discusses these issues in his "Familial Aggregation" talk on the 'Panel' DVD from the MP Conference in Chicago:
"Look at my "Can I Catch It?" talk on the DVDs, and especially the way the OM85 species innoculated against the diabetes in the NOD mice. Keep playing this talk until the implication sinks in that we might be dealing with symbiotic infective pathogens rather than any one causative species. This would certainly explain why there are no specific genetic susceptibility alleles being isolated, despite intensive genomic studies. The predisposition is not genetic, it is acquired.
We are dealing with a lot of Th1 and autoimmune diseases/syndromes, but then again one would expect a few dominant (successful) genetic adaptations to be shared among species. Indeed, there is one paper showing that the Bet-lactams increase the liklihood of DNA sharing as the L-forms emerge.
So the data is pointing away from the genetic predisposition hypothesis, IMO, and towards the concept of successive infection. Actually our pathogens are likely still 'inherited' though - both from the mother, and from L-Forms accompanying the sperm.
The tendency of medicine to cling to the (1897) postulates of Koch is at the root of the problem. Koch's postulates have already failed in the case of a number of diseases - it is time to throw them away and start thinking about genes, and horizontal transfer of DNA between species of chronic pathogens.
..Trevor..
"My current understanding is that successive infection determines the course of disease. If there is any genetic predisposition, none of the genetic studies have found it yet. In Chicago I stated that it is my conclusion (from looking at the study data we have) that any hereditary component is minimal or non-existent.
In my opinion, anybody can get sick from these Th1 diseases, if exposed to a similar cascade of pathogens. I believe that high levels of 1,25-D (resulting from pregnancy or sun-bathing) (or whatever) are part of the susceptibility process."
A spectrum of symptoms which gradually accummulate
The perspective I have of Th1 disease is that of a spectrum of symptoms which gradually accumulate into a recognizable condition. I myself, for example, exhibited overtly aberrant social behaviors as early as my primary school years. In my case, these receded (into my 20s) as the disease progressed, rather than getting worse.
I see folk with Th1 disease which manifests itself as maybe a little arthritic pain in joints, or slow healing of wounds, all the way through to the most seriously ill subjects in our cohort.
So, although I recognize that most people (including myself) identify a date as the point at which the disease became manifest, I believe they are mistaken in their understanding of the insidious progression of the Th1 syndromes. In my own case, I was convinced that an insect (tick?) bite I received during military training, which caused a 6-week bout of continuous coughing, was probably what gave me sarcoidosis. Yet, twenty years later, when I reviewed the chest Xrays taken well before that incident, the disease is clearly apparent upon them. I was clinically sick, but didn't know it. Nobody around me noticed, including the person who read those initial Xrays. However, hindsight is 20:20, and nobody could review the early Xrays, knowing what happened to me later, without noting the significance of the adenopathy present on them.
..Trevor..
Are the cellular changes permanent?
"These are primarily genetic changes in the nucleus of infected cells. Those cells do not live forever (apoptosis), and so we can expect the effect of the pathogens to become less important as the immune systems 'cleans them up.'
We are seeing very few signs of permanent damage, except for structural damage (fibrosis, scarring), and the body is showing a remarkable ability to even work around the collagen, in any case."
..Trevor..
Can a healthy immune system kill L-form bacteria?
9/10/07 This is a good question. Answer is, we don't know yet. The pathogens must affect the immune system in some way, as cytokines and chemokines are released during all stages of the Th1 infection, including 'healthy aging'. But exactly what happens, and the sequence of events, is unclear. At some point some of the bacteria start to shut down the VDR. But is this fortituous? Which species does this? Maybe a harmless species involved purely in the aging process?
These are all imponderables right now. But excellent questions. One could construct a hypothesis where relatively harmless bacteria living in the intraphagocytic biofilms have for centuries (millenia) gradually shut down the body's hormonal system as it ages. It wasn't until Vitamin D supplementation became commonplace, perhaps, that the hormonal control systems get shut down at a younger age. Perhaps the proliferation of L-forms resulting from the overuse of penicillin and cephalosporin antibiotics during the 1940s caused more L-forms to take advantage of weakened human bodies. Who knows?
We live in interesting times 
..Trevor..
Simple explanation of successive intracellular infection
We ALL get invaded/infected by CWD-bacteria constantly.
These CWD-bacteria alter the genes in the invaded/infected cells (not the human genes/DNA, but only the genes in the infected cells' nucleus).
If you are first invaded/infected by CWD # 1 you may have 70 genes that are altered (this is shown by research).
If you are then invaded/infected by bacteria #2, there will be even more genes altered, as well as the ones that are already altered.
You can see that if you get invaded/infected by more and more species, you can get enormous changes.
You, and also everyone else on this planet will give CWD-bacteria to other people. ~Frans
Th1 vs. Th2 diseases
"The Th1 diseases are defined to be characterized by high levels of Interferon-gamma in the inflamed tissue and it catalyzes production of 1,25-D by the mitochondria of the activated macrophages.
Common mistakes made by those who are confused between Th1 and Th2 include trying to measure the cytokines in venous blood (not in the paracrine tissue), not measuring Interferon-gamma but trying to make inference from something else, and making pronouncements when they don't have a clue about the underlying molecular medicine."
..Trevor..
Related information:
Cell Wall Deficient Bacteria and the Marshall Protocol
Am I contagious?
Babies and bacteria: How pathogens may affect an infact during its first weeks of life
Why has there been a sharp rise in the incidence of Th1 inflammatory diseases?
Bactera vs genes: the spread of chronic disease in families
Interview with evolutionary biologist Paul Ewald
Cognitive dysfunction in women with Chronic Fatigue Syndrome: examining the role of the endometrium, the nuclear receptors, and antimicrobial peptides
Last edited on Fri Mar 14th, 2008 19:08 by Foundation Staff
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Posted: Tue Mar 7th, 2006 06:10 |
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Genetic studies have not yielded any successful treatments
The mistake that all these researchers are making is the assumption that an association between disease symptoms, and mutations in genes, infers that the gene changes lead to the symptoms.
Yet after billions of dollars spent in research, not one gene therapy, not even for the classic genes supposed to be causal for Cystic Fibrosis, not one gene therapy has proven safe or effective.
The reason for this failure-to-perform is that the hypothesis is incorrect. What the researchers are seeing as changes on genes are indeed changes, but they only correlate at low levels of significance because they are due to pathogens. They are due to mutations from chronic infection. Consequently there is no causal effect - only an associative observation.
If you consider that it takes folks on the MP, killing the intracellular bacteria at the fastest rate their bodies can manage, 3 years or more to fully clear the bacterial load in their bodies you can get some idea of the huge amount of pathogenic DNA we are all carrying about. A recent study found 60% of the 'healthy' population are carrying L-forms in their bloodstream.
Part of the problem is that the folks computing the statistics are not the physicians who collected the data, and so there is a disconnect, and two disparate sets of knowledge are not quite meeting when discussing the meaning of statistical certainty. The statistical correlation in every one of these gene studies is very low indeed. Just above the noise.
So once again "the alternate hypothesis" reigns supreme. One that the optimism of modern medicine consistently fails to adequately consider.
..Trevor..
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Posted: Wed Dec 20th, 2006 03:18 |
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Measles makes the cells more susceptible to a secondary infection
(filelink)
Measles Virus-induced Immunosuppression
"MV infection, while inducing lifelong immunity, also suppresses the immune system leading to an increase in susceptibility to other, secondary infections (24, 67, 91). In vitro research has shown that MV infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion (13) "
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Posted: Thu Jan 11th, 2007 00:17 |
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(filelink)
Interspecies microbial interactions may alter the course of disease, the response to therapy and the population structure of bacterial communities
Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19890-5. Epub 2006 Dec 15.
Selection for Staphylococcus aureus small-colony variants due to growth in the presence of Pseudomonas aeruginosa.
Hoffman LR, Deziel E, D'Argenio DA, Lepine F, Emerson J, McNamara S, Gibson RL, Ramsey BW, Miller SI.
Departments of *Pediatrics, Microbiology, Medicine, and Genome Sciences, University of Washington, Seattle, WA 98195.
Opportunistic infections are often polymicrobial. Two of the most important bacterial opportunistic pathogens of humans, Pseudomonas aeruginosa and Staphylococcus aureus, frequently are coisolated from infections of catheters, endotracheal tubes, skin, eyes, and the respiratory
tract, including the airways of people with cystic fibrosis (CF). Here, we show that suppression of S. aureus respiration by a P. aeruginosa exoproduct, 4-hydroxy-2-heptylquinoline-N-oxide (HQNO), protects S. aureus during coculture from killing by commonly used aminoglycoside antibiotics such as tobramycin. Furthermore, prolonged growth of S. aureus with either P. aeruginosa or with physiological concentrations of pure HQNO selects for typical S. aureus small-colony variants (SCVs), well known for stable aminoglycoside resistance and persistence in chronic infections, including those found in CF. We detected HQNO in the sputum of CF patients infected
with P. aeruginosa, but not in uninfected patients, suggesting that this HQNO-mediated interspecies interaction occurs in CF airways. Thus, in all coinfections with P. aeruginosa, S. aureus may be underappreciated as a pathogen because of the formation of antibiotic-resistant and difficult to detect small-colony variants. Interspecies microbial interactions, analogous to those mediated by HQNO, commonly may alter not only the course of disease and the response to therapy, but also the population structure of bacterial communities that promote the health of host animals, plants, and ecosystems.
PMID: 17172450 [PubMed - in process]
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