This is Amy. I write the articles for this site and interviewed Dr. Ewald. I’m very glad that you found his interview inspirational. It’s true - I believe you can reach your goal if you work with passion and integrity.

Good luck!

Amy

thanks always
sierra

It’s good to hear from you. I think I’m finally seeing a light at the end of the tunnel when it comes to my grad school applications. Next in line, I have to write two papers based on my Porto presentation. Hopefully then I can get back to Bacteriality.

I wish I had more time, because I’d love to read Dr. Ewald’s book as well. The question of why bacteria were essentially ignored, particularly during the decades you mentioned, is one I think about often.

I think there may have been a certain degree of denial among the mainstream medical community who wanted to think that the discovery of penicillin and other antibiotics had stopped bacteria in their tracks once and for all.

I chalk a lot of it up to the illusion of accomplishment. And then there was the shiny new toy, genetics, which led people on a different track of thinking entirely.

I still think that, in the future, people will look back into the science from a generation ago and ask why we didn’t capitalize upon the earlier research.

I might actually get the chance to meet Dr. Ewald next week, because he’s lecturing at Cornell, which is very near to where I live. I’ll let you know if he says anything of great interest.

Best,
Amy

Thanks to both you and Paul Ewald for the great interview and information. As a result I just finished his book: “Plague Time How Stealth Infections Cause Cancer, Heart Disease, and Other Deadly Ailments”, and can recommend it as five stars.

It adds more support to the idea that those of us who have been diagnosed with an idiopathic chronic disease can find a cure with the Marshall Protocol.

However, it leaves open the question as to why the medical community essentially ignored the possibility of infection as the cause for many chronic illnesses from the 1950’s through to the 1980’s. The groundwork for infectious causes was established and then it was just ignored. Over thirty years seems like an incredible lost opportunity!

I hope all is going well with your efforts toward grad school but want say your articles and interviews are greatly missed.

Gene

I’m glad you found the interview interesting. Unfortunately, I don’t have the detailed information you are requesting. I would suggest calling up the University of Louisville in order to find out how long Dr. Ewald has been on their staff.

As for his salary etc, that is private information that I certainly don’t have. How did he get into his field of science? In my opinion because he is an extremely bright thinker and an excellent scientist - one who is able to approach disease from a novel viewpoint. He was certainly aided by a PhD education.

Sorry I can’t be of more help,

Amy

Very interesting observations. I agree that there are cases like sickle-cell where the disease offers the host some advantage, but in my opinion, they are few and far between. At least I can’t see any way that having a chronic inflammatory disease like fibromyalgia would offer anyone a survival advantage.

About the fact that any event that weakens the body or the immune system can allow people to more easily acquire the microbiota of chronic L-form and biofilm bacteria at the heart of inflammatory disease (collectively called the Th1 pathogens), I absolutely agree. Stress, lack of sleep, any drug that weakens the body (and particularly immune function!) will not doubt make it harder for the body to effectively fight the pathogens that cause chronic disease. I have definitely heard stories of people developing stronger symptoms after a car accident or a death in the family which certainly correlates with stress.

However at the moment I think most mainstream doctors peg stress as the CAUSE of many of these diseases, when in my opinion, it is an exacerbating factor. A person could be serious stressed out, but if they didn’t come in contact with the Th1 pathogens, I don’t think they would develop an inflammatory disease.

In your girlfriends case, I’m sure her experience with Post Traumatic Stress Disorder put her body in a state that made it much easier to acquire the Th1 pathogens that cause fibromyalgia. Still, she probably harbored Th1 pathogens even before the fibromyalgia symptoms seeing as they are probably what caused her to develop the stress disorder. After all, as 1,25-D rises as a result of the inflammation and VDR blockage generated by the Th1 pathogens, it starts to displace metabolites from the nuclear receptors that control the body’s hormones. The adrenal receptor is definitely affected, and the negative impact of excess 1,25-D on the adrenal receptor could have cause your girlfriend to suffer from such severe stress in the first place.

It’s true that people are having sex at much younger ages and with more partners. I agree that this absolutely fosters the spread of the Th1 pathogens. They can survive in the sperm can definitely be transmitted through intercourse. So it’s quite easy for a young person who has a lot of sexual partners to pick up many different varieties of the Th1 pathogens.

Best,

Amy

1. Ewald left out a catagory of diesease in his calculus - the type which evolves because the harm it causes is outweighed by some other advantage. The most well worn example would be sickle cell anemia, which, when heterozygous, allows a person to survive malaria. Sickle cell anemia is not caused BY a disease, but by a reaction to a disease. Another example of this phenomenon, which doesn’t involve pathogens, is color blindness. If a man is color blind, that means that his mother was probably capable of seeing in 4 channels of color, not just three. Meanwhile, the military uses colorblind men for certain tasks since they rely on different visual cues and are more able to see through camoflage.

2. To reiterate what another poster said; there’s a fair bit of evidence that temporary immunosupression can lead to a chronic inflammatory state. My girlfriend has fibromyalgia, which many related to the MP claim is realted to chronic infection with l-form bacteria. However fibromyalgia is also linked to end-stage Post Traumatic Stress Disorder. So if fibromyalgia really is caused by pathogens, stress may weaken the immune system enough for the infection to establish itself.

Similarly, while the notion that recreational drugs like poppers might CAUSE AIDS has been discredited, HIV seems to establish itself most often in people whose bodies are already immunosuppressed by drugs or pathogens.

3. What hasn’t been mentioned yet (what is, in fact, almost never discussed) is the increase in unprotected sex since the rise of antibiotics, legalization of abortion, and increase in the average age when people marry. As Ewald elucidates in Evolution of Infectious Diseases, such an environment would favor increasingly harmful pathogens. The difficulty of culturing most l-form bacteria strongly suggests that the majority of them are obligate parasites.

Those people familiar with the science that forms the backbone of the MP realize that we are all in a boat headed in exactly the right direction. We don’t even need oars because the boat has a motor.

I can’t really see how the article you posted has any relevance to Ewald’s work or Dr. Marshall’s work.

The MP model for chronic disease does put all factors on the table. A large microbiota of chronic ideopathic biofilm and L-form bacteria generate the inflammation and resulting symptoms that cause most inflammatory diseases. The persistent bacterial forms also dysregulate many of the body’s pathways by binding and dysregulating a variety of receptors.

These bacteria do mutate a patient’s DNA. If fact, they create many mutations that can be passed from generation to generation. Some of these mutations may make it easier for pathogens to infect a particular cell type which may then allow new pathogens to infect the person’s cells with greater ease. This phenomenon is described in greater detail in the following article:

http://bacteriality.com/2007/10/31/family/

When it comes to environmental contaminants, it appears that they are not having much of an effect on causing chronic disease, as those people to finish the MP usually report feeling “better than ever” and have no lingering health problems. That is probably because a bacteria free body with a very strong immune system is very effective at dealing with contaminants in a way that a body weakened by bacteria cannot.

Best,

Amy

For example, pathogens have been around for a long time (and are still evolving), but this toxic soup of low dose environmental toxins is rather new, so this has got to be considered as a co-factor along with the pathogens. I will post an abstract that shows just such an interaction. Also, pathogens are well known to be able to exert epigenetic effects on the host, thru gene expression. So, now we have all three categories possibly involved in some diseases.

Here is the abstract:

Clinical & Experimental Immunology

Volume 150 Issue 1 Page 189-197, October 2007

To cite this article: C. Ekerfelt, M. Andersson, A. Olausson, S. Bergström, P. Hultman (2007)

Mercury exposure as a model for deviation of cytokine responses in experimental Lyme arthritis: HgCl2 treatment decreases T helper cell type 1-like responses and arthritis severity but delays eradication of Borrelia burgdorferi in C3H/HeN mice

Clinical & Experimental Immunology 150 (1), 189–197.
doi:10.1111/j.1365-2249.2007.03474.x

ORIGINAL ARTICLE
Mercury exposure as a model for deviation of cytokine responses in experimental Lyme arthritis: HgCl2 treatment decreases T helper cell type 1-like responses and arthritis severity but delays eradication of Borrelia burgdorferi in C3H/HeN mice

* C. Ekerfelt,*+*Division of Clinical Immunology, +Unit of Autoimmunity and

Summary

Lyme borreliosis is a complex infection, where some individuals develop so-called ‘chronic borreliosis’. The pathogenetic mechanisms are unknown, but the type of immune response is probably important for healing. A strong T helper cell type 1 (Th1)-like response has been suggested as crucial for eradication of Borrelia and for avoiding development of chronic disease. Many studies aimed at altering the Th1/Th2 balance in Lyme arthritis employed mice deficient in cytokine genes, but the outcome has not been clear-cut, due possibly to the high redundancy of cytokines.

This study aimed at studying the importance of the Th1/Th2 balance in murine Borrelia arthritis by using the Th2-deviating effect of subtoxic doses of inorganic mercury. Ninety-eight C3H/HeN mice were divided into four groups: Borrelia-infected (Bb), Borrelia-infected exposed to HgCl2 (BbHg), controls exposed to HgCl2 alone and normal controls. Mice were killed on days 3, 16, 44 and 65 post-Borrelia inoculation.

Arthritis severity was evaluated by histology, spirochaetal load determined by Borrelia culture, IgG2a- and IgE-levels analysed by enzyme-linked immunosorbemt assay (ELISA) and cytokine-secreting cells detected by enzyme-linked immunospot (ELISPOT). BbHg mice showed less severe histological arthritis, but delayed eradication of spirochaetes compared to Bb mice, associated with increased levels of IgE (Th2-induced) and decreased levels of IgG2a (Th1-induced), consistent with a Th2-deviation.

Both the numbers of Th1 and Th2 cytokine-secreting cells were reduced in BbHg mice, possibly explained by the fact that numbers of cytokine-secreting cells do not correlate with cytokine concentration. In conclusion, this study supports the hypothesis that a Th1-like response is required for optimal eradication of Borrelia.