By: Martin MesicekMany previous studies have indicated a connection between bacteria in the mouth and myocardial infarction, but have yet to find any singular species of bacteria to blame. Now, Norwegian scientists might have a clue why the others have failed.
The scientific project was conducted at the University of Oslo in cooperation with The Institute of Public Health, and published in the Journal of Clinical Periodontol. The results showed that the detection of antibodies from one singular bacteria species could not be associated with greater risk for MI, but when they could detect antibodies from a combination of four bacteria known to cause periodontitis, (Porphyromonas gingivalis (PG), Aggregatibacter actinomycetemcomitans (AA), Tannerella forsynthia (TF) and Treponema denticola (TD), risk for MI increased by 30%. This result was not affected by correcting for other known cardiovascular risk factors. The study concludes: ”No single bacterium, but rather combinations, were related to increasing relative risk for MI (myocardial infarctions) independent of known cardiovascular risk factors” (1).
So what has this to do with chronic autoimmune disease?
First of all, this is another indication of ”Koch’s postulates” failure to fully describe or explain disease and infections from microorganisms. His postulates was published in 1890, yes, you read right, the first two numbers are one and eight, but still doctors and scientists stick to his work when trying to explain that some diseases are not caused by infectious agents. Dr. Trevor Marshall (ph.d University of West Australia, 1984) from Autoimmunity Research Foundation in California, which is the organization that has designed the treatment protocol I have chosen to cure myself from Sjogren’s Syndrome, doesn't give Koch’s postulates much credit when it comes to explaining chronic infections. During his presentation at ”The World Gene Congress 2008” in China last December, he says: “ They (the postulates) caused us to search for a singular pathogenic species, because the postulates of Koch said, “one bug, one disease,” and sidetracked science from understanding the horizontal transfer of DNA within the microbiota”. The human body may consist of as many as 1 000 000 bacterial genes, compared with “only” 25 000 human genes, according to the National Institute of Health’s microbiome project. Furthermore Marshall claims that most of today’s diseases, and autoimmune disease in particular, of unknown etiology can be explained by intraphagocytic microbiota, capable of knocking out our innate immune system and causing chronic systemic inflammation (2).
With Marshall’s science in mind the Norwegian study becomes even more interesting, all though there are different species of bacteria involved in Marshall’s hypothesis, his work focusing on intracellular bacteria, it kind of creates a macro picture anyway. If colonies of bacteria in the mouth can cause heart disease, what kind of diseases can colonies (microbiota) inside phagocytes cause? Maybe the notion of one bacterium equals one disease, isn't the only viable way of infection afterall? Possibly, bacteria that we today know little or nothing about, or have yet to identify, can be the cause of many of today’s mysterious chronic disease. L-form bacteria are one hot candidate. All the subjects in the Norwegian study suffered from periodontitis, a chronic inflammatory condition in the mouth caused by bacteria. That’s funny; because patients using Marshall’s treatment protocol reports that periodontal disease reverses once they have been on the treatment for some years. This might be as a result of their underlying infection being gradually resolved, and their innate immune system being able to fight off other infections as their Vitamin D Receptor starts functioning again (3).
References:
1: Antibody levels to single bacteria or in combination evaluated against myocardial infarction. Institute of Oral Biology, University of Oslo, Oslo, Norway. L. L. Haheim et al, J Clin Periodontol. 2008 Jun; 35(6):473-8.
2: Understanding Human Disease requires study of a Metagenome, not just the Human Genome, presented by Prof Trevor Marshall, Director, Autoimmunity Research Foundation, Des 5. 2008 World Congress of Gene, Fuchan Kina.
Video presentation available:
3: Vitamin D Metabolites as clinical markers in autoimmune and chronic illness, presented by Dr. Greg Blaney (MD) at the 6th International Congress on Autoimmunity, Porto, Portugal 10-14 sep 2008.
Video presentation available:
Transcript: http://autoimmunityresearch.org/transcripts/ICA2008_Transcript_GregBlaney.pdf
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