
Many first-line treatments for chronic disease were developed before it was understood that the death of chronic bacteria necessarily results in an immunopathological response and temporary feelings of malaise. Such treatments are designed to slow the immune response under the mistaken premise that autoimmune disease results when the immune system attacks the body.
According to the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop., bacteria drive chronic disease, and treatments that slow the immune system only appear to “work” because they decrease bacterial death. While this causes a drop in inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. that offers temporary symptomatic relief, bacteria which drive the disease state cease to be targeted and spread easily. The net result is that patients generally become increasingly ill over the long-term.
In essence, feeling better is not the same as getting better.
Anything which makes you feel better, almost always does so because it is stopping the immune system from killing the pathogens. The reason patients remain ill is that one just cannot apply the standard logic of “feeling well” to these chronic diseases. You have to understand the disease mechanism.
Trevor Marshall, PhD
In contrast, treatments that target the root cause of an illness rather than masking symptoms are curative in nature. While patients taking curative treatments may not always feel better during the course of therapy, such treatments have the potential to bring about lasting recovery.
Nevertheless, because palliative treatments that slow immune function are very effective at offering temporary relief, the number of medications, over-the-counter supplements, and fortified foods that work by slowing the immune response have escalated over the past decades. Since the goal of every Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. (MP) patient is to effectively target the bacteria making them ill, such immunosuppressants must be avoided. These immunosuppressants range from corticosteroidsA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate. and TNF-alpha blocking medications to “vitamin” D.
Those substances that aim to cover up disease symptoms but do not succeed at reversing the disease state are palliative in nature. A variety of commonly taken medications, foods, and supplements offer temporary palliation by depressing immune function.
The following is an incomplete list of medications that are immunosuppressive:
Relapse… rarely occurred in patients who had not been treated with corticosteroids in the past. The striking difference in relapse rate between treated and untreated patients suggests that patients with disease that would later be severe and protracted were almost unerringly identified early in their course…. Corticosteroids contribute to the prolongation of the disease by delaying resolution.
Jonathan E. Gottlieb et al. 2)

The almost inevitable gravitation towards foods and supplements that slow immune activity (and diminish a bacterial die-off reaction) appears to be done subconsciously by people who play host to significant numbers of chronic bacteria. These foods and supplements include:
Marshall Protocol patients are generally advised to avoid supplements and to consume any food in moderation. Additionally, MP patients should try to get any vitamin through whole foods.
The Marshall Protocol (MP) is a curative therapy and represents an alternative to therapies which mask or delay symptoms of disease. The MP aims to target the Th1 PathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms., which we now believe are ultimately responsible for chronic inflammatory disease.
One cannot judge the success of any therapy in the treatment of chronic illness by symptomatic improvement over the short term.
Greg Blaney, MD
I believe the unraveling of the complex role of the hormone 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. in the Th1 inflammatory diseases is an important part of Marshall's findings, and much of it is counterintuitive. For example, if I take any drug that protects my L-form bacteriaDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria., I feel better and many markers will indicate my disease has declined - but in fact my disease is actually getting worse. Symptoms are sure to resurface later. This is why most anti-inflammatories (including steroids, which suppress the entire immune system, but permit L-form bacteria to thrive) can make us feel better, but do not cure the disease. This is also why our disease tends to get progressively worse over the years, in spite of these drugs.
Similarly, drugs and diet that kill off the L-form bacteria make Th1 patients feel worse (which we call immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed.), but in fact we are getting better.
DaveW, MarshallProtocol.com