The Marshall Protocol for Lyme disease and other chronic inflammatory conditions, Part One: overview and implementation

Townsend Letter for Doctors and Patients,  April, 2007  by J.C. Waterhouse

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Introduction

A new approach, called the Marshall Protocol (MP), is now achieving success in treating chronic Lyme disease. This protocol was originally developed for sarcoidosis by Trevor Marshall, PhD, of the Autoimmunity Research Foundation. (1,2) The MP's main targets are the treatment-resistant cell wall deficient (CWD, L-form or cyst) forms of Borrelia burgdorferi (Bb) and a variety of other bacterial species--though it also kills spirochetal/classical bacterial forms.

Borrelia burgdorferi can transform back and forth between its CWD forms and spirochetal forms. (3) Thus, CWD bacteria that survive initial treatment can produce relapses by transforming back into spirochetes. In addition, CWD bacteria themselves are also believed to directly affect the immune system in a way that can cause chronic inflammation and debilitating symptoms.

Since development of this protocol in the last few years, the MP has been successfully used to treat chronic Lyme disease (post-treatment Lyme disease syndrome), sarcoidosis, rheumatoid arthritis, psoriatic arthritis, multiple sclerosis, Type II diabetes, uveitis, osteoarthritis, cardiac arrhythmia, Hashimoto's thyroiditis, lupus pernio, Meniere's disease, chronic fatigue syndrome, fibromyalgia, tinnitus, irritable bowel syndrome, bipolar disorder, depression, and various other chronic conditions.

In Part One of this two-part article, an overview of the protocol and the steps involved in its implementation are given. Part Two will provide more details regarding the scientific background of the Marshall Protocol, as well as additional data and case histories of patients with various inflammatory diseases being successfully treated with the MP.

Cell wall deficient forms of bacteria are especially elusive because they are often very small and have developed immune system resistance mechanisms that allow them to hide inside cells in infected patients. (1-3) They even persist inside macrophages, thus resisting destruction by the very cells that are supposed to eliminate them. Many of the antibiotics used to treat Lyme disease are ineffective against CWD forms. Some antibiotics, such as the penicillins and cephalosporins, even promote the transformation of bacteria into their CWD forms. (3,4)

The CWD bacteria are able to resist destruction by the immune system and the usual modes of antibiotic treatment. The MP involves three steps to overcome this resistance: 1. Restricting vitamin D intake to enhance immune function; 2. Taking higher than usual dosages of olmesartan (Benicar), an angiotensin II receptor blocker (ARB), to further enhance immune function and protect organs; and 3. Adding very low "pulsed" doses of a sequence of carefully chosen antibiotics to weaken the defenses of the CWD bacteria. (See Caution, page 88)

New insights on the importance of vitamin D limitation and Benicar have revealed why their immune-modulating effects are crucial to the MP. (1,2) As will be discussed further in Part Two, the success of the MP and recent molecular modeling research have led to a reinterpretation of much of the current vitamin D research (5-10) and a recognition of elevated vitamin D's role in immunosuppression.

The angiotensin II receptor blocker Benicar has been found to protect against inflammatory organ damage in a number of diseases, and higher dosage levels are often required for this effect (5) (e.g., also see references cited in Part Two of this article). Marshall et al. (5) has recently published molecular modeling research pointing to the mechanisms for the immune-modulating effects of Benicar. The Food and Drug Administration (FDA) Office of Orphan Product Development (OOPD) has already approved the designation of two antibiotics for sarcoidosis, and the Autoimmunity Research Foundation has other FDA applications pending for drugs used in the MP for chronic Lyme disease. (2)

This article will give an overview of the MP, but it can not cover all the details (available on the free Internet study site) that are necessary to optimize safety and efficacy. (2) No one should begin applying the MP without thoroughly understanding the guidelines on the study site and being committed to following them carefully. The killing of bacteria necessitates the death of cells (apoptosis) that they parasitize. Severe and even life-threatening immunopathology reactions (sometimes called Jarisch-Herxheimer or "Herx" reactions) can occur if the guidelines are not strictly followed with a level of caution appropriate for the degree of illness.

Vitamin D Metabolites: A Revolutionary View of Their Role in Chronic Disease

The Marshall Protocol is based on revolutionary insights regarding vitamin D metabolites that build upon past studies. The scientific background for these insights will be discussed in more detail in Part Two. (2,6-9) In essence, new research has shown that: 1. Vitamin D metabolite levels can be useful markers of Th1 inflammation and indicate a similar pathogenesis in many chronic diseases; and 2. Elevated levels of vitamin D metabolites can produce immunosuppression by multiple mechanisms.