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Trevor Marshall

From Wikipedia, the free encyclopedia

Trevor G. Marshall, PhD
Trevor G. Marshall, PhD

Trevor G. Marshall, PhD (b. 1948, Adelaide, South Australia), is a biomedical researcher. Over the last few decades, he has developed a medical intervention, dubbed the 'Marshall Protocol', which uses antibiotics, Angiotensin II receptor antagonist, avoidance of bright sunlight exposure and diet to treat a class of chronic diseases, which he purports are caused by L-form or cell wall deficient bacteria. His protocol is being used by physicians to treat diseases such as sarcoidosis, Chronic Fatigue Syndrome, and rheumatoid arthritis.

Contents

[edit] Background and early work in medicine

Trevor Marshall has an undergraduate and master's degree in electrical engineering, and a PhD in biomedical science, for both of which he as done research.

After a year as a tutor in Papua New Guinea, Marshall joined the staff of the Western Australian Institute of Technology (now Curtin University) in 1975. After gaining his Masters by thesis in 1978, Marshall moved to the University of Western Australia, where he commenced his PhD thesis research. During that time, he studied patients suffering from diabetes and infertility at the Charles Gairdner Hospital.

His research involved the description of a novel way of using pulsatile LHRH for treating cryptorchidism, along with both male and female infertility.[1][2]

In 1982, Marshall moved to California. He continued his PhD thesis research with the Biomedical Engineering group at the Hospital for Sick Children in Toronto, which at the time was a leader in pediatric diabetes research. This partnership led to his thesis Modelling and simulation in diabetes care.[3] and a paper on insulin infuser technologies.[4]

[edit] Interest in sarcoidosis

Marshall developed sarcoidosis in 1978, and pursued a degree in biomedicine in order to further understand the processes of the disease. Sarcoidosis is a systemic granulomatous disease, which restricts lung functionality, negatively impacts lymph nodes and other organs, and usually kills within one or two decades of diagnosis. At this point, sarcoidosis was considered to be a member of a class of diseases with an unclear origin and no curative treatment option.[5]

Some consider sarcoidosis to be an autoimmune disease. Frequently it is treated with immunosuppressive drugs, including the corticosteroid prednisone.[6] However, a 2001 study funded by the NIH shows that these steroids will not cure the illness and are only capable of bringing about periods of relative remission.[7][8]

[edit] Vitamin D and sarcoidosis

As early as 1974, while teaching in Papua New Guinea, Marshall began to sense that there was a connection between his exposure to light and flare-ups of his sarcoidosis symptoms. In the decades that followed, he began to “play with the issue of light sensitivity,” concluding over time that the vitamin D present in incident radiation was playing a crucial role in driving his illness.[9]

In 1999, Marshall developed an interest in a class of drugs known as Angiotensin Receptor Blockers (ARBs), specifically the class of Angiotensin II receptor antagonists, after learning that patients with sarcoidosis who are administered these drugs often develop a neurological reaction.[10] He started a sabbatical in early 2001 in order to further investigate this reaction.[11]

Marshall concluded that ARBs produce unexpected symptoms in sarcoidosis patients by directly affecting the immune system. Later, in 2006, Marshall would use mathematical modeling and molecular genomics to show exactly how ARBs are able to modulate the nuclear receptors of the immune system. Particularly important are his models, which show that the vitamin D receptor (VDR) must be activated in order for the body to mount a correct innate immunity response.[12]

Marshall did further studies in molecular modeling in order to understand the precise effect of vitamin D metabolites on the VDR. He discovered that 25-hydroxy vitamin D, which has the actions of a steroid, binds and inactivates the receptor, shutting down the body’s first line of defense against intra-cellular infection.

[edit] Bacteria in sarcoidosis

In 2002, Marshall read a paper by Nilsson, which reported finding genetic material from Rickettsia Helvetica in the granuloma of two deceased sarcoidosis patients. This, along with other papers by Mattman and Wirostko, led him to conclude that intra-phagocytic, L-form bacteria could drive the biochemical processes observed in sarcoidosis.[13]

In 2002, Marshall published a pathogenesis for sarcoidosis[14] followed in 2004 by the definitive paper in Autoimmunity Reviews “Sarcoidosis Succumbs to Antibiotics.” [15]

[edit] Treatment takes shape

Marshall’s 2002 paper concludes that people who are sick with 'autoimmune' diseases possess a correctable defect in innate immunity brought about by a dysregulation of vitamin D.[18] According to Marshall, dysregulation of vitamin D allows slow-growing, mutated bacteria, known as L-form bacteria, to proliferate.

Marshall also concluded that a range of other chronic inflammatory diseases --which he has termed “Th1 illnesses”-- result from the same bacterial pathogenesis as sarcoidosis. Thus, in every Th1 disease, L-form bacteria directly drive the phagocytic biochemistry, causing the release of Th1 cytokines.[15][16]

Marshall found that patients with Th1 illness are capable of restoring innate immunity by using the ARB Benicar to activate the VDR, while at the same time avoiding exogenous sources of vitamin D-- the kinds of vitamin D present in various foods and catalyzed by exposure to bright lights and sunlight. Along with the help of pulsed, low-dose antibiotics, the body’s own immune system is then able to destroy L-form bacteria-- causing a temporary change in a patient's immunopathology.[17] Marshall argues that the release of cytokines and endotoxins generated by this reaction cause an increase in past or present Th1 symptoms. These concepts became the fundamental aspects of Marshall’s treatment plan for Th1 illness which he named the “Marshall Protocol.”

[edit] Study-related web sites

In 2002, Trevor Marshall started the web site, sarcinfo.com to study the use of the Marshall Protocol as a curative treatment for sarcoidosis. As evidenced by members' reported progress, nearly all experience a powerful immunopathological reaction[17] after taking a dose of antibiotics.

With the success and popularity of sarcinfo.com, Marshall pioneered a larger study site, broader in scope, which addresses the growing demand to use the Marshall Protocol on a wider range of Th1 illnesses. Marshallprotocol.com represents one of the largest internet-based medical treatments, and is moderated by a group of volunteer nurses. Members of the site, who have dozens of different medical conditions including Chronic Fatigue Syndrome, rheumatoid arthritis, juvenile diabetes, Lou Gehrig’s disease, and lupus are all experiencing strong, steady changes in immunopathology. As of September 2006, the site has over 3,000 members and 70,000 posts.

A number of patients have claimed the complete resolution of symptoms including Marshall himself. The MP’s record for assisting patients recovering from chronic disease thus far has been chronicled in an abstract given at the 2006 Days of Molecular Medicine Conference.[18]

[edit] Foundation and present work

In 2004, Trevor Marshall founded the Autoimmunity Research Foundation, a California-based non-profit agency. The directors and members of the Foundation have worked to:
1. promote the Marshall Pathogenesis to doctors and patients
2. communicate with researchers in the field of autoimmunity and Th1 disease
3. run the MP's study web sites, marshallprotocol.com and sarcinfo.com
4. gain FDA approval for medications used in conjunction with the MP

Marshall is currently active on the medical-conference circuit and gives periodic continuing medical education presentations to physicians. In March, 2006, he was invited by the Food and Drug Administration (FDA) Center for Drug Evaluation and Review to give a presentation in their "Visiting Professor" lecture series.[19] In 2006, he co-authored a chapter about Vitamin D dysregulation.[20]

Marshall has hosted two conferences on “Recovering from Chronic Disease,” the first in Chicago in 2005,[21] and most recently in Los Angeles in 2006.[22]

[edit] References

  1. ^ Keogh EJ, MacKellar A, Mallal SA, Dunn AG, McColm SC, Somerville CP, Glatthaar C, Marshall T, Attikiouzel J (1983). "Treatment of cryptorchidism with pulsatile luteinizing hormone-releasing hormone (LH-RH)". J Pediatr Surg 18 (3): 282-3. PMID 6135766. 
  2. ^ Keogh EJ, Somerville C, Giles PFH, Mallal SA, Evans D, McColm SC, Parsonage J, Marshall T, Attikiouzel J, Clarke I and Wilson D (1982). "Ovulation induction with pulsatile gonadotrophin releasing hormone (GnRH)". Proc. Endocrine Society of Australia. 
  3. ^ Marshall, T. G. (1984). Modelling and simulation in diabetes care. Unpublished doctoral dissertation, University of Western Australia.
  4. ^ Marshall TG, Mekhiel N, Jackman WS, Perlman K, Albisser AM (1983). "New Microprocessor Based Insulin Controller". IEEE Transactions on Biomedical Engineering BME-30 (11): 689-95. 
  5. ^ Merck Manual of Diagnosis and Therapy (2006). Sarcoidosis. Retrieved on October 6, 2006.
  6. ^ National Heart Lung and Blood Institute. Sarcoidosis -- Treatments. Retrieved on October 6, 2006.
  7. ^ Autoimmunity Research Foundation (2003). NIH ACCESS study shows that sarcoidosis does not go away. Retrieved on October 6, 2006.
  8. ^ Judson MA, Baughman RP, Thompson BW, Teirstein AS, Terrin ML, Rossman MD, (2003). "Two year prognosis of sarcoidosis: the ACCESS experience". Sarcoidosis Vasc Diffuse Lung Dis 20 (3): 204-11. PMID 14620163. 
  9. ^ The Marshall Protocol – Simple Explanations. MarshallProtocol.com (2004-07-14). Retrieved on October 6, 2006.
  10. ^ Marshall TG, Marshall FE (2002-08-29). Valsartan Dosing Regime Modulates Psychotic Events in Two Sarcoidosis Patients. NetPrints. Retrieved on October 6, 2006.
  11. ^ The Marshall Protocol for Treating Chronic Fatigue Syndrome: Interview with Trevor Marshall, Ph.D.. ImmuneSupport.com (2004-07-06). Retrieved on October 6, 2006.
  12. ^ Marshall TG, Lee RE, Marshall FE (2006). "Common angiotensin receptor blockers may directly modulate the immune system via VDR, PPAR and CCR2b". Theor Biol Med Model 3 (1): 1. PMID 16403216. 
  13. ^ Nilsson K, Pahlson C, Lukinius A, Eriksson L, Nilsson L, Lindquist O (2002). "Presence of Rickettsia helvetica in granulomatous tissue from patients with sarcoidosis.". J Infect Dis. 185 (8): 1128-38. PMID 11930323. 
  14. ^ Marshall TG, Marshall FE (2003-01-27). New Treatments Emerge as Sarcoidosis Yields up its Secrets. NetPrints. Retrieved on October 6, 2006.
  15. ^ a b Marshall TG, Marshall, FE (2004). "Sarcoidosis succumbs to antibiotics - implications for autoimmune disease". Autoimmun Rev 3 (4): 295-300. PMID 15246025. 
  16. ^ Marshall, T. G., & Marshall, F. E. (2003, August 3). Antibiotics in Sarcoidosis - Reflections on the First Year. Journal of Independent Medical Research. Retrieved October 5, 2006, from http://www.joimr.org/phorum/read.php?f=2&i=38&t=38
  17. ^ a b Mangin M (2004). "Observations of Jarisch-Herxheimer Reaction in Sarcoidosis Patients". JOIMR 2 (1): 1. 
  18. ^ Marshall TG. (2006 May). “VDR Nuclear Receptor Competence is the Key to Recovering from Chronic Inflammatory Disease.” Poster session presented at Days of Molecular Medicine Conference, Karolinska Institut, Stockholm, Sweden. Retrieved July 28, 2006 from http://AutoimmunityResearch.org/karolinska-handout.pdf
  19. ^ Marshall T.G. (2006) “Molecular genomics offers new insight into the exact mechanism of action of common drugs - ARBs, Statins, and Corticosteroids.” FDA CDER Visiting Professor presentation. FDA Biosciences Library, Accession QH447.M27 2006. Videorecording: http://autoimmunityresearch.org/fda-visiting-professor-7mar06.ram Slide presentation: http://autoimmunityresearch.org/fda_visiting-professor_7mar06_144dpi.pdf
  20. ^ Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G. (2006). High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor — implications of dysregulated vitamin D for diagnosis and treatment of chronic disease. In VD Stoltz (ed.), Vitamin D: New Research (pp 1–23). New York: Nova Science Publishers.
  21. ^ Autoimmunity Research Foundation. Recovering from Chronic Disease. Retrieved on October 6, 2006.
  22. ^ Autoimmunity Research Foundation. Sarcoidosis, Autoimmunity, AIDS & Cancers: Recovering from Chronic Disease. Retrieved on October 6, 2006.
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