Sorry for the delayed response. Yes, there are patterns that can predict the severity of immunopathology to a certain degree. The first thing to keep in mind is that bacterial load very often correlates with how long a person has been ill. Generally patients that have been sick for decades have accumulated larger bacterial loads, whereas those who start the MP closer to their time of diagnosis often have lower bacterial loads and thus deal with lower levels of IP.

Patients who have taken large amounts of immunosuppressive medications or steroid medications such as prednisone generally also have bacterial loads that have spread to a greater extent. So such patients usually experience stronger immunopathology. Of course, since dietary vitamin D is a secosteroid in its own right, anyone who has a long history of supplementing with vitamin D can generally also expect to have a higher bacterial load and thus stronger immunopathology when they begin the MP.

Many patient say that the level of their immunopathology doesn’t become too much worse than their disease symptoms in the first place, although there are definitely exceptions. To be more specific, I mean that most people find that if they can work before the MP they can generally still pull off working while on the treatment.

So there are a few clues that might allow you to predict what your immunopathology may be like. However, it’s often very hard for people to estimate bacterial load before the MP. Patients are often surprised that they get immunopathology in areas they didn’t even realize were infected.

So it’s really only after you start Benicar and minocycline that you will be able to get the most accurate impression of the immunopathology and light sensitivity that you will be dealing with.

So I hope you can start the MP soon!

Best,

Amy

Thanks for the detailed response. It does help assuage some of the fears I have about being on medication again. Do you know if any patterns have emerged that might help predict how much immunopathology one might expect to face while on the MP. For instance, is length of illness or severity of debility more likely to impact one’s immunopathology?

Thanks,

Paul

I am glad you are researching the Marshall Protocol. I am extremely confident that Benicar and the antibiotics are not putting people into remission. That’s because during the vast majority of the time that MP patients are take the antibiotics and Benicar they feel worse, often much worse.

If Benicar works as an immunusuppressant, and the antibiotics work in the palliative manner - as they do when taken in high, multi-daily doses - then at atmosphere of relief would be created during the MP. The patient would feel better.

Instead, people on the MP face years of difficult immunopathology before reaching a state of remission. The anti-inflammatory properties of Benicar only help patients manage the bacterial die-off reaction to a certain degree. Instead, Benicar’s primary job is to serve as a VDR-agonist (a drug that strongly activates the Vitamin D Receptor). So it’s main action is stimulating the immune response and facilitating bacterial death.

Immunopathology is very difficult for MP patients. Antibiotics must be ramped over the course of years, often up to five or six years in cases of severe illness so that the patient can manage the die-off. Believe me, there is no palliation going on during the MP.

Furthermore, the MP antibiotics were specifically chosen via molecular modeling data from the Max Plank Institute in Germany so as to be administered at concentrations that essentially null the immunosuppressive effects they possess at high doses. For example, one of the phase II antibiotics is only taken every 10-14 days. That’s very low dosing with little possibility for immunosuppression. This article describes how the MP antibiotics were chosen in greater detail and would be a good read:

http://bacteriality.com/2007/10/11/antibiotics/

Finally, there is absolutely a difference between blocking a substance after it has already been created and blocking the creation of a substance in the first place. Once TNF-alpha has been created and released, blocking it’s actions unfortunately require blocking many other components of innate immunity. Hence the immunosuppression.

But Benicar has a subtle effect that causes less TNF-alpha to be created in the first place. If TNF-alpha is never produced, it never has to be blocked, and the innate immune response never has to be blocked. TNF-alpha is a potent inflammatory cytokine so having a little less of it around thanks to Benicar allows the patient to tolerate their immunopathology a little bit more easily, yet the strength of the rest of their immune response stays the same.

Hope this helps!

Best,

Amy

I really admire Dr. Marshall and I’m considering giving the MP a shot. However, allow me to play devil’s advocate for a moment. How can we be certain that the inherent anti-inflammatory properties of Benicar and the tetracyclic antibiotics aren’t responsible for putting people into remission? Why is blocking the release of TNF-alpha immunosuppressive, but blocking it’s generation (as you state to be the case with Benicar) not immunosuppressive?

I am concerned about this. I was on the tricyclic antidepressant amitriptyline for four years to help with chronic pain. While it did help with symptom control, my health really deteriorated while I was on it. I believe this is because amitriptyline, like many so-called “psychotropic” medications, has rather profound immunosuppressive properties. Like the medications mentioned in this article, it suppresses TNF-alpha release, albeit most certainly to a lesser degree. Nevertheless, I did develop a couple of internal cysts while on it and also had some skin issues.

Thanks,
Paul