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Parasitic co-infections
 Moderated by: Prof Trevor Marshall
 

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dmeal
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 Posted: Sun Jun 3rd, 2007 01:25

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I'm currently writing a book on the etiology of fibroids (uterine leiomyomas) and am very interested in the association of Chagas disease and leiomyomas in South America. One researcher has suggested that the T. Cruzi DNA becomes integrated in the host genome.

"Heritable Integration of kDNA Minicircle Sequences from Trypanosoma cruzi into the Avian Genome: Insights into Human Chagas Disease" Cell, Vol. 118, 175–186, July 23, 2004, Nitz et al.

"kDNA integration represents a potential cause for the autoimmune response that develops in a percentage of chronic Chagas patients which can now be approached experimentally."


(See also "Invasive genes: humans incorporate DNA from parasite" - Science News, July 31,2004 by C. Lock).

I have also been wondering why sarcoidosis would affect the Scandinavians and the Japanese and have come up with a theory based on integrated DNA that may connect these two groups of people.

The Ainu (Northern native Japanese) and the Finnish languages are supposedly related - so this would imply that their cultures are also related. Apparently both of these groups used to worship bears and also ate their livers. Polar bear liver contains Sarcocystis Neurona. So could it be possible that by eating the parasite, it becomes integrated with the human DNA. If so, could this then explain the fibroids and PCOS and cysts etc associated with some people who have sarcoidosis (ie those people descended from the Finns and the Ainu)?

I am not a scientist - so I'd be keen to hear what others have to say about parasite DNA integration, fibroids and sarcoidosis.

Last edited on Sun Jun 3rd, 2007 01:41 by dmeal

Prof Trevor Marshall
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 Posted: Sun Jun 3rd, 2007 01:49

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Part of a scientist's training is the ability to examine the alternate hypothesis. In other words, if your theory is wrong, then where is it most likely wrong?

Trying to study scientific literature without that background, and without the background of having actually worked in a research team yourself, is frought with unforseen traps.

For example, you are making the assertion that Sarcoidosis is more common in the Scandinavian and Japanese nations. Yet the alternate hypothesis says that the rate of disease is the same, it is just that Doctors from different cultures diagnose it at different rates. For example, in Japan the most common sarcoidiosis diagnosis results from eye examinations, in the USA from chest Xrays. So there is a huge difference in understanding of the disease in the two nations, and this is far more likely to have skewed the perceived incidence statistics than any actual rate of disease incidence.

I can assure you that polar bears and language have nothing whatsoever to do with the incidence of Sarcoidosis.

Hutchinson did study many of the national incidence issues for Sarcoidosis (in the late 19th century) and you will find his publications during the early 1900s most illuminating. Unfortunately, you won't find those in PubMed. You will need to go to a University library, and put the material on inter-library loan.


Second, some time ago we published a paper:
Marshall TG, Marshall FE: Sarcoidosis succumbs to antibiotics - implications for autoimmune disease. Autoimmunity Reviews,2004; 3(4):295-3001.
Available from URL http://dx.doi.org/10.1016/j.autrev.2003.10.001
access FullText at author website. You might like to review it.

There have been many papers since then, you might like to review some more at
http://www.trevormarshall.com/papers.htm
There have also been many discussions at this study site, all elucidating the issue of how the pathogens integrate their own genome into the human experience. There are changes in the host DNA (as postulated in the paper you cite), but infinitely many more changes due  modifications of expression of proteins, as many of the bacterial proteins are pretty close in homology to those of homo sapiens, and can substitute for the host proteins in many biochemical reactions.Each species, and there are many involved in chronic infection, potentially produces proteins from 1000-10,000 genes.
 

Please read as much as you can of what this study-site has found. You will get knowledge by observing what works, and why it works, much quicker than by trying to glean info from the isolated scientific studies in PubMed :) Fibroids disappear from folk who are recovering from autoimmune disease by using the protocol we have developed. The liklihood is therefore that they share a common pathogenesis - intraphagocytic, persistent, antibiotic-resistant, biofilm-protected, bacteria.
 
  ps: Don't forget to review the DVDs of our conferences and my presentations - you will find in them a gold mine of information and ideas.
 
 

Last edited on Sun Jun 3rd, 2007 02:16 by Prof Trevor Marshall

dmeal
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 Posted: Wed Jun 20th, 2007 14:14

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Thank you Trevor - I am ordering the DVDs today. Also, I have noticed that the Baltic Gray Seals and the Wild Sea Otters that have fibroids also have associated mycoplasma and granulomatous infections, so the fishermen that are bitten by these creatures (seal finger) need to be treated with tetracyclines or amputation.

Also, these animals have (compensatory?) adreno-cortical hyperplasia, so I was wondering if there is a pineal/adrenal cortical/uterine axis that is being stimulated by the excess 1,25D from the mycoplasma infection. I also have some research on a human hermaphrodite who had a uterine fibroid and benign prostatic hyperplasia, so again, could this be the pineal/adreno-cortical/uterine and/or prostate axis?

And finally, the Amercian veterinarians give their sick ferrets, who have adrenal hyperplasia, ferretonin patches (ie ferret melatonin). Whereas, the scandinavian ferrets who are not spayed do not seem to develop so many adrenal problems.

So I'm trying to understand how the whole pineal - adreno cortical - uterine/prostate axis works with the VDR and excess 1,25D. If one of these organs becomes hypertrophic or hyperplastic due to 1,25D overstimulation, or is removed due to disease, how does this upset the other organs on the axis, and how do they compensate? I'm very keen to understand how this process works, so I've just bought myself some anatomy and biochemistry text books, and will also study your website. I've got some serious catching up to do :) Kind regards.

Last edited on Wed Jun 20th, 2007 16:29 by dmeal

tickbite
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 Posted: Sat Jul 14th, 2007 14:06

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On the topic of parasites, how big a part of the pathogenesis are they? obviously IMO, those of us Th1 sufferers must have heavy parasitic loads too co-infections. I haven't been able to find much (good)medical literature on the subject of immunity and parasitic infection. Can anyone point me to any information on immune system interaction with parasites? and also, will we eventually control these little blood sucking evil creatures?

thanx



____________________
"Lyme","CFS", Meningitis
Phase3 8-2-07, MP on hold 11/2007

Prof Trevor Marshall
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 Posted: Sun Jul 15th, 2007 02:37

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The immune system will look after the parasites for you (Babesia, etc).

The details of how DNA transfers between genomes, and how DNA is integrated by phages into bacteria, and the defenses mounted by the bacteria, were contained in several of the lectures at Metagenomics 2007. Watch for them when they come on line.
http://research.calit2.net/metagenomics/index.php

I particularly remember these two talks:

   Phil Hugenholtz, Joint Genome Institute. "Comparison of two geographically remote bacterial populations reveals global dispersal and local predation pressures"

   Julian Parkhill, Wellcome Trust Sanger. "Metagenomics of single organisms"

as being especially interesting in this regard. It is important to note that although these are bacterial genomes being discussed, similar forces are in play with human DNA. Bacteria are easier to study with precision, and that is why genome scientists are focusing on them at the moment.
 
 


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