Crohn's disease

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Crohn's disease

Crohn's disease uveitis. Parasitization of vitreous leukocytes by mollicute-like organisms. Am J Clin Pathol. 1989 Mar;91(3):259-64. Johnson LA, Wirostko E, Wirostko WJ. http://tinyurl.com/dh8th\Tinyurl

“Uveitis is a symptom, and has many identified causes and associations at this point. Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with “autoimmune diseases” like Crohns disease and rheumatic arthritis. I suspect that these other cases are due to CWD bacteria. There are several interesting papers that explore this. The researchers found cell-wall deficient bacteria (sometimes called mollicute-like organisms) in the vitreous fluid of patients with sardoidosis, Crohn’s disease, ulcerative colitis, juvenile rheumatoid arthritis, etc.”

See also Crohn's Disease Information

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Mycobacteria avium subspecies paratuberculosis (MAP) is the pathogen suspected of causing Crohn's disease.

Kenc wrote:

This pathogen was suspected in the early part of the last century soon after Crohn's disease was first identified. However, since researchers could not isolate it in Crohn's disease patients they gave up and turned to the concept of Crohn's disease being an immune disorder and so began the big push for immunosuppresive drugs.

Within the last decade there has been a resurgence of interest in MAP. Most Crohn's patients testing positive for MAP (about 45%) have responded well to long term antibiotic therapy in clinical trials (see research by Ira Shafran and by T. Borody). Their response was better than any immunosuppresive drug therapy I know. However, since not all Crohn's patients tested positive for MAP the medical community has remained skeptical of the claim that Crohn's disease is caused by MAP.

I believe the pathogenesis behind the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. includes the infection by one or more types of bacteria. That would account for the other 55% of Crohn's patients who didn't test positive for MAP. Furthermore the MP should work better than an antibiotic treatment for MAP alone since it would help the immune system to eradicate the other types of bacterium that could be present as well along with MAP.

I tested positive for two other types of bacteria other than MAP. One type of these bacterium comes from tics. I did not take a test for MAP. So, my case is evidence that a Crohn's patient can have non-MAP infections as well.

In spite of the increasing evidence for a microbial cause of Crohn's disease, most (>95% I believe) of the research money available for Crohn's disease, including money from charitable organizations, appears to be directed towards the development of immunosuppressive drugs. The latest craze seems to be for TNF-alpha blockers like Remicade.

The most amazing research I've seen was for MS patients. The idea was to kill all the white blood cells in an MS patient and then use stem cells taken earlier from the patient to repopulate the white blood cells. Of course about half of the patients died. This is modern medical research at its finest! It worked out OK for those that survived. Looking at this with MP eyes, I can see this as a drastic way of getting rid of CWD bacterium in the white blood cells - kill all the cells.

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Doctor: Infection is at root of Crohn's disease – Newsday.com

Aussie-native Dr. Thomas Borody, who recently was awarded the Marshall Prize in Australia for innovative scientific research and who will lecture 3/06 on Long Island, has proposed that Crohn's disease, is caused by Mycobacterium avium paratuberculosis (or MAP for short). The microbe is a distant relative of the tuberculosis and leprosy bacteria.

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Targeted Antibiotics Lead to Long-lasting Improvement in IBS Symptoms (filelink)

Source: Cedars-Sinai Medical Center Released: Tue 08-Nov-2005, 14:00 ET Libraries Medical News Keywords IBS, IRRITABLE BOWEL SYNDROME, SIBO

Description Researchers at Cedars-Sinai Medical Center have found that a nonabsorbable antibiotic – one that stays in the gut – may by be an effective long-term treatment for irritable bowel syndrome (IBS), a disease affecting more than an estimated 20 percent of Americans. The findings, which showed that participants benefited from the antibiotic use even after the course of treatment ended, support previously published research identifying small intestine bacterial overgrowth (SIBO) as a possible cause of the disease.

The research was presented at the recent American College of Gastroenterology's annual meeting in Honolulu, HI.

LOS ANGELES (Nov. 8, 2005) – Researchers at Cedars-Sinai Medical Center have found that a nonabsorbable antibiotic – one that stays in the gut – may be an effective long-term treatment for irritable bowel syndrome (IBS), a disease affecting more than an estimated 20 percent of Americans. The findings, which showed that participants benefited from the antibiotic use even after the course of treatment ended, support previously published research identifying small intestine bacterial overgrowth (SIBO) as a possible cause of the disease.

The research was presented at the recent American College of Gastroenterology's annual meeting in Honolulu, HI.

“This study is important as it is the first to show that the use of targeted antibiotics results in a more significant and long-lasting improvement in IBS symptoms,” said Mark Pimentel, M.D., first author on the study and director of the GI Motility Program at Cedars-Sinai. “These results clearly show that antibiotics offer a new treatment approach – and a new hope – for people with IBS.”

The randomized, double blind study involved 87 patients. Those on the rifaximin experienced a 37 percent overall improvement of their IBS symptoms as compared to 23 percent on the placebo. Among study subjects whose primary symptom was diarrhea, those on the antibiotic showed more than twice the improvement of those on the placebo (49 percent vs. 23 percent). Patients received the drug (or placebo) for 10 days and were then followed for a total of 10 weeks. Participants kept a stool diary, took a questionnaire and were given methane breath tests. The positive effects of the drug were shown to continue throughout most of the 10-week study, not just during the actual antibiotic course.

Because the cause of IBS has been elusive, treatments for the disease have historically focused on reducing its symptoms – diarrhea and constipation – by giving medications that either slow or speed up the digestive process. In 2000, Pimentel linked bloating, the most common symptom of IBS, to bacterial fermentation, showing that small intestine bacteria overgrowth (SIBO) may be the causative factor in IBS (The American Journal of Gastroenterology, Dec. 2000).

To show evidence of small intestine bacterial overgrowth, participants in both studies were given a lactulose breath test, which monitors the level of hydrogen and methane (the gases emitted by fermented bacteria) on the breath. In the first study, an abnormal breath methane profile was shown to be 100 percent predictive of constipation-predominant IBS. In the current study, the correlation between the amount of methane and the amount of constipation was confirmed, another key finding.

“We were pleased – but not surprised – with the results of this study,” said Pimentel. “The next step is to start larger, multi-centered studies to confirm the positive results of this study, which suggest that people can benefit from targeted antibiotic treatment for their IBS.”

Irritable Bowel Syndrome is an intestinal disorder that causes abdominal pain or discomfort, cramping or bloating and diarrhea and constipation. It is a long-term condition that usually begins in adolescence or in early adult life. Episodes may be mild or severe and may be exacerbated by stress. It is one of the top ten most frequently diagnosed conditions among U.S. physicians and affects women more often than men.

Other authors from Cedars-Sinai include Sandy Park, B.A., Yuthana Kong M.P.H. and Robert Wade. Sunanda V. Kane from the University of Chicago also participated in the study.

Rifaximin is made by Salix Pharmaceuticals, Inc. Funding for the study was provided by Salix Pharmaceuticals, Inc.

One of only five hospitals in California whose nurses have been honored with the prestigious Magnet designation, Cedars-Sinai Medical Center is one of the largest nonprofit academic medical centers in the Western United States. For 17 consecutive years, it has been named Los Angeles' most preferred hospital for all health needs in an independent survey of area residents. Cedars-Sinai is internationally renowned for its diagnostic and treatment capabilities and its broad spectrum of programs and services, as well as breakthroughs in biomedical research and superlative medical education. It ranks among the top 10 non-university hospitals in the nation for its research activities and was recently fully accredited by the Association for the Accreditation of Human Research Protection Programs, Inc. (AAHRPP). Additional information is available at http://www.cedars-sinai.edu

© 2005 Newswise. All Rights Reserved.

Newswise | Targeted Antibiotics Lead to Long-lasting Improvement in IBS Symptoms http://www.newswise.com/articles/view/515982/\Newswise

PERSONAL:

Members working with their Drs re Crohn's Disease

Crohn's and MP Journey Phase 1 KenC working with his Dr June 2008: I believe I've made some progress on my disease so far. I'm steriod-free and I no longer have significant abdominal pain. One way or the other I will get well.

August 2008: *My dentist is going to take pictures next week so that he has a record of the amazing improvement in my gums - they're growing back! *My optometrist has given me a new lower prescription - 1 diopter less for myopia. *The arthritis in my hands has disappeared. *Most of the psoriasis has disappeared. ~ KenC

Crohn's Success Jeanne

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Posted: Tue Nov 14th, 2006 23:52 Quote Reply

Dr Marshall posted re (filelink) Host Defences - UCSD 2006

University of California-San Diego Frontiers of Clinical Investigation Conference Host Defense 2006: From Bench to Bedside Oct5-7 La Jolla, CA

…one of the presentations was so compelling I have taken the effort to put it online. It explains how the antimicrobial peptidesBody’s naturally produced broad-spectrum antibacterials which target pathogens. (the body's own antibiotics) are employed against the pathogens which cause Crohn's disease.

Many of you have heard me talk about how important it is to get the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. Nuclear Receptor working properly (one of the things Benicar does) because the VDR is responsible for the Cathelicin Anti-Microbial Peptides. It is also responsible for transcribing the genes of the Beta Defensins.

This presentation explains how those, and the other Defensins, are important, and I think that those of you who track the science will find it very interesting indeed.

The 24 Mbyte RealVideo 9 presentation runs for 30 minutes. You can stream it from URL

http://autoimmunityresearch.org/crohns.ram

and the more technically astute can download the whole presentation by right-clicking on this link.

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Posted: Thu Dec 27th, 2007 20:32 Quote Reply

[filelink] Vitamin D and the vitamin D receptor are critical for control of the innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease. to colonic injury.

BMC Immunol. 2007 Mar 30;8:5.

Froicu M, Cantorna MT.Department of Veterinary and Biomedical Sciences, Pathobiology Graduate Program, The Pennsylvania State University, University Park, PA 16802, USA.

BACKGROUND: The active form of vitamin D (1,25(OH)2D3) has been shown to inhibit development of inflammatory bowel disease (IBD) in IL-10 KO mice. Here, the role of the vitamin D receptor (VDR) and 1,25(OH)2D3 in acute experimental IBD was probed. RESULTS: VDR KO mice were extremely sensitive to dextran sodium sulfate (DSS) and there was increased mortality of the VDR KO mice at doses of DSS that only caused a mild form of colitis in wildtype (WT) mice. DSS colitis in the VDR KO mice was accompanied by high colonic expression of TNF-alpha, IL-1 alpha, IL-1beta, IL-12, IFN-gamma, IL-10, MIP-1alpha and KC. DSS concentrations as low as 0.5% were enough to induce bleeding, ulceration and weight loss in VDR KO mice. VDR KO mice failed to recover following the removal of DSS, while WT mice showed signs of recovery within 5 days of DSS removal. The early mortality of DSS treated VDR KO mice was likely due to perforation of the bowel and resulting endotoxemia. VDR KO mice were hyper-responsive to exogenously injected LPS and cultures of the peritoneal exudates of moribund DSS treated VDR KO mice were positive for bacterial growth. 1,25(OH)2D3 in the diet or rectally decreased the severity and extent of DSS-induced 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. in WT mice.

CONCLUSION: The data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunityThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease. and the response of the colon to chemical injury.

PMID: 17397543 [PubMed - indexed for MEDLINE]

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Relationships between vitamin D, parathyroid hormone and bone mineral density in inflammatory bowel disease. (filelink) Silvennoinen J. J Intern Med. 1996 Feb;239(2):131-7. Department of Internal Medicine, University of Oulu, Finland. OBJECTIVES. To explore the relationships between vitamin D intake, serum parathyroid hormone (PTH) and 25-hydroxyvitamin DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. (250HD) concentrations, and bone mineral density (BMD) in inflammatory bowel disease (IBD). SETTING. A university hospital clinic in Finland. SUBJECTS. One hundred and fifty randomly selected patients with IBD from the hospital register and 73 healthy controls. MEASUREMENTS. BMD of the lumbar spine and the proximal femur was measured with dual energy X-ray absorptiometry. Vitamin D intake and serum levels of 250HD and PTH were determined. RESULTS. The IBD patients had a lower serum 250HD concentration (28.4 [SD 12.0] nmol L-1) than the controls (36.1 [16.7] nmol L-1; P = 0.001), whereas no differences in the vitamin D intake or the serum PTH levels were found. The serum 250HD concentrations and the vitamin D intake of the patients with ulcerative colitis (n = 67) were similar to those of the Crohn's disease patients (n = 76). The patients with Crohn's disease of the small bowel had slightly, but not significantly, lower serum 250HD concentrations (25.6 [11.0] nmol L-1) than the other Crohn's disease patients (31.4 [14.3] nmol L-1; P = 0.061). In the IBD patients, the vitamin D intake and the serum 250HD and PTH concentrations were not associated with BMD. CONCLUSIONS. Patients with IBD have lower serum levels of 250HD than healthy controls, but similar serum PTH concentrations and vitamin D intake. Vitamin D intake, and the serum levels of 250HD and PTH are not associated with BMD, and malabsorption is unlikely to be a major factor in the aetiology of bone loss in unselected IBD patients. PMID: 8568480 [PubMed - indexed for MEDLINE]

• too many quotes here; it would be nice if we could convert this into bullet points consistent with the other disease articles