Trevor Marshall

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Dr. Trevor G. Marshall
Dr. Trevor G. Marshall
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Trevor G. Marshall (b. 1948, Adelaide, South Australia), is a biomedical researcher. He developed what's known as the "Marshall Protocol" as a possible treatment of a class of chronic diseases, which he argues are caused by L-form or cell wall deficient bacteria. Waterhouse, in a 2007 Townsend Letter article, stated the protocol has been used successfully to treat many chronic conditions, including chronic Lyme disease, Sarcoidosis, Fibromyalgia, and rheumatoid arthritis.[1] It involves the use of low-dose antibiotics, an angiotensin II receptor antagonist (being used as a VDR agonist),[2] and avoidance of sources of Vitamin D such as sunlight, as a possible treatment of a class of chronic diseases.

The protocol's critics state it's efficacy to treat autoimmune diseases has not been confirmed with peer-reviewed data and results by the medical community.[3]

Contents

[edit] Background and Early Work

Trevor Marshall received his PhD in Electrical Engineering from the University of Western Australia in 1984.[4] He also possesses an undergraduate and a masters (1978) degree in Electrical Engineering.[5]

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, where he lectured undergraduate courses on electronic design and production until 1982[6]. 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 design of portable, battery operated programmable pumps for the delivery of pusatile LHRH for treating cryptorchidism, along with both male and female infertility.[7][8]

In 1982, Marshall moved to California. He continued his PhD thesis research while a Visiting Scientist in the Department of Surgery 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 and a paper on insulin infuser technologies.[9]

For 12 years, from 1988 until 2000, Marshall was the Chairman, CEO and principle shareholder of YARC Systems Corporation, a publicly listed corporation based in California which researched, designed and produced printer technology, such as postscript raster image processor software and printer servers. [10]. The The YARC-XP, released in 1997, was the first Internet-enabled Print Server.[11] In 2001 YARC became insolvent and was liquidated.[12].

[edit] Interest in sarcoidosis

Marshall developed sarcoidosis in the seventies and pursued research in biomedical engineering 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 becomes end-stage within one or two decades of diagnosis.[13][14] At this point, sarcoidosis was considered to be a member of a class of diseases with an unclear origin and no curative treatment option.[15]

Some consider sarcoidosis to be an autoimmune disease. Frequently it is treated with immunosuppressive drugs, including the corticosteroid prednisone.[16] 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.[13]

[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 concluded that the vitamin D synthesis caused by incident radiation was playing a crucial role in driving his illness.

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. He started a sabbatical in early 2001 in order to further investigate this reaction.

Marshall concluded that ARBs produce unexpected symptoms in sarcoidosis patients by directly affecting the immune system. Later, in 2006, Marshall performed a study using mathematical modeling and molecular genomics to examine how ARBs are able to modulate the nuclear receptors of the immune system. He concluded that these models show that the vitamin D receptor (VDR) must be activated in order for the body to mount a correct innate immunity response.[17]

Marshall did further studies in molecular modeling in order to understand the precise effect of vitamin D metabolites on the VDR. He concluded 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.[18]

In 2008, Marshall published a paper exploring how, in his words, "lifelong supplementation of the food chain with vitamin D might well be contributing to the current epidemics of obesity and chronic disease."[19]

[edit] Bacteria in sarcoidosis

In 2001, 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.[20]

In 2002, Marshall published a pathogenesis for sarcoidosis followed in 2004 by the paper in Autoimmunity Reviews “Sarcoidosis Succumbs to Antibiotics.” [21]

[edit] Treatment takes shape

Marshall’s 2004 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. 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.

Marshall believes 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.[22] 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 his colleagues named the 'Marshall Protocol'.

[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 aim 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[23]

In March, 2006, Marshall 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.[24] In 2006, he co-authored a chapter about Vitamin D dysregulation.[25]

Marshall is an Adjunct Professor in the School of Biological Sciences and Biotechnology at Murdoch University.[26][27]

[edit] Criticism of the Marshall Protocol

The Marshall Protocol's efficacy to treat autoimmune diseases has not been validated by the medical community. Rosen and Bagwell, in their 2007 review of treatments for sarcoidosis, argue that the Marshalls' 2003 paper, "Antibiotics in sarcoidosis—reflections of the first year" has "serious deficiencies", and the data has not been peer-reviewed nor the results quantified.[3]

[edit] References

  1. ^ Waterhouse, JC. (2007). The Marshall Protocol for Lyme disease and other chronic inflammatory conditions, Part One: overview and implementation. Townsend Letter for Doctors and Patients. Retrieved December 5, 2007 from http://findarticles.com/p/articles/mi_m0ISW/is_285/ai_n19170371
  2. ^ Marshall, TG. "Bacterial Capnine Blocks Transcription of Human Antimicrobial Peptides." Metagenomics 2007. San Diego, CA. 2007 July 11-13. Retrieved 2007-12-07 from http://metagenomics.calit2.net/files/Metagenomics2007Program_lowres.pdf.
  3. ^ a b Badgwell, C & Rosen, T. (2007). Cutaneous sarcoidosis therapy updated. Journal of the American Academy of Dermatology, 56(1): 69-83. Retrieved 2007-12-05 from http://dx.doi.org/10.1016/j.jaad.2006.06.019 PMID 17190623
  4. ^ Marshall, T. G. (1984). Modelling and simulation in diabetes care Unpublished doctoral dissertation, University of Western Australia.
  5. ^ University of Adelaide, School of Electrical & Electronic Engineering. Past Postgraduate Students. Retrieved on 2007-07-20.
  6. ^ http://www.trevormarshall.com/resume.htm
  7. ^ 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. doi:10.1016/S0022-3468(83)80102-X. PMID 6135766. 
  8. ^ 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. 
  9. ^ 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. doi:10.1109/TBME.1983.325181. 
  10. ^ http://web.archive.org/web/19990203091208/http://www.yarc.com/
  11. ^ http://www.trevormarshall.com/resume.htm
  12. ^ http://www.sec.gov/Archives/edgar/data/843650/0000843650-01-500005.txt
  13. ^ a b Autoimmunity Research Foundation (2003). NIH ACCESS study shows that sarcoidosis does not go away. Retrieved on 2006-10-06.
  14. ^ 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. 
  15. ^ Merck Manual of Diagnosis and Therapy (2006). Sarcoidosis. Retrieved on 2006-10-06.
  16. ^ National Heart Lung and Blood Institute. Sarcoidosis -- Treatments. Retrieved on 2006-10-06.
  17. ^ 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. doi:10.1186/1742-4682-3-1. PMID 16403216. 
  18. ^ Marshall TG: VDR Nuclear Receptor Competence is the Key to Recovery from Chronic Inflammatory and Autoimmune Disease. Abstract presentation, Days of Molecular Medicine, Karolinska Institutet, Stockholm, May 2006. Copy available from URL http://autoimmunityresearch.org/karolinska-handout.pdf
  19. ^ Marshall TG (2008). "Vitamin D discovery outpaces FDA decision making". Bioessays 30 (2): 173–182. doi:10.1002/bies.20708. PMID 18200565. 
  20. ^ 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. doi:10.1086/339962. PMID 11930323. 
  21. ^ Marshall TG, Marshall, FE (2004). "Sarcoidosis succumbs to antibiotics - implications for autoimmune disease". Autoimmun Rev 3 (4): 295–300. doi:10.1016/j.autrev.2003.10.001. PMID 15246025. 
  22. ^ Mangin M (2004). "Observations of Jarisch-Herxheimer Reaction in Sarcoidosis Patients". JOIMR 2 (1): 1. doi:10.1016/j.autrev.2003.10.001. 
  23. ^ FDA. "Cumulative List of All Orphan Designated Products." Accessed: August 11, 2007. Available from http://www.fda.gov/orphan/designat/alldes.rtf
  24. ^ 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
  25. ^ 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.
  26. ^ Trevor Marshall, PhD (HTML). Trevor Marshall, PhD (Copyright 1995-2007). Retrieved on 2008-06-01.
  27. ^ Trevor Marshall Adjunct Professor (HTML). Murdoch University (2007). Retrieved on 2008-06-01.

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