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bar Jonah
October 1st 2004, 06:35 PM
Crohn's disease, sick cows and contaminated milk
October 1, 2004
By Chris Bennett
© 2004 WorldNetDaily.com
http://worldnetdaily.com/news/article.asp?ARTICLE_ID=40722

For issues that affect public health, it shouldn't matter who leads the government.

When research uncovers the cause of a disease, or shows where our food technology is no longer adequate, public health agencies under the leadership of either party should step forward.

When the agencies don't act, the effect is chilling. In the short term, some special interests are protected, some companies make short-term profits. In the long term, we all lose.

But by far the biggest losses are experienced by new patients diagnosed with a disease that, arguably, should not have happened.

Over 20 years of independent research links a common disease in humans - characterized by chronic diarrhea and severe abdominal pain - with sick cows and contaminated milk.

We're not describing a disease process on another continent, or another era. I'm sad to say that we're talking about the United States in 2004.

According to the U.S. Department of Agriculture, from 20 percent to 40 percent of U.S. dairy farms have sick cows. These cows aren't mildly ill, they're infected with Mycobacteria paratuberculosis, which produces massive diarrhea and incredible weight loss. But on factory farms, sick cows still provide commercial milk. Milk from sick cows is pooled with milk from healthy cows. The result: contaminated milk and, apparently, a whole lot of sick people.

It's not a pretty picture - for the cows, or the humans. And like most medical matters, the story is not simple. I hope you'll stay with me.

Think of the worst stomach flu you ever experienced. Then imagine trying to live with that every day.

That's Crohn's disease.

Crohn's disease was virtually unknown before 1940. But by the 1950s, the number of confirmed cases doubled. And then it tripled, and then quadrupled. Today, the disease affects somewhere between 1 to 2 million people in the United States alone, and the number of new patients increases every year. Many are children. According to epidemiologists, Crohn's disease is advancing into epidemic levels.

This is a disease characterized by pain and extreme embarrassment. Those who have it, don't talk about it.

Many Crohn's patients plan their day so that bathrooms are always available. In order to go to work, some drive RVs instead of cars. Some simply stay home 24x7. The direct costs of treatment are now estimated at more than $2 billion per year in the United States alone. The secondary costs to the economy in lost wages and productivity are many times that. The costs in human misery are immeasurable. It's not an exaggeration to describe Crohn's disease in the United States as a health emergency.

Crohn's is classified by U.S. medicine as an autoimmune disease, treated by a variety of anti-inflammatory drugs, including steroids. As the disease progresses, many patients suffer the surgical removal of diseased portions of their digestive system.

But what makes it unimaginably worse is compelling research, mostly from Europe, which reveals this horrible disease is not autoimmune at all.

Compelling evidence links Crohn's disease with Mycobacteria paratuberculosis.

And the most likely source of the infection? Milk.

That's right, milk. According to published research, susceptible individuals are consuming literally millions of pathogenic bacteria while drinking off the shelf, pasteurized, in the carton, highly subsidized ... milk.

Crohn's disease

Crohn's was unknown until the early 1900s when two very similar diseases were described: one in domestic animals called Johne's disease and one in humans named after the physician who first wrote about it, Dr. Burrill Crohn.

Dr. H.A. Johne was the first to describe the disease in cattle. What became know as Johne's disease is characterized by profuse and intractable diarrhea, severe weight loss and diagnostic changes in the lining of the small intestine. In diseased cattle, the intestine has so many ulcers, the surface of the intestines, normally smooth, is described as having a cobblestone appearance.

Untreated Crohn's disease is also characterized by profuse and intractable diarrhea, severe weight loss and diagnostic changes in the lining of the small intestine. In diseased humans, the intestines are also described as having a cobblestone appearance.

By the 1930s, Johne's disease was found to be caused by an odd bacteria named Mycobacteria paratuberculosis. This organism is in the same family with bacteria which cause tuberculosis and leprosy.

M. paratuberculosis produces disease by over stimulating the immune system. The bacterium lives inside the cells of the host, where it divides only once about every 2 to 12 hours. (By way of contrast, the bacteria in the gut divides about once every 20 minutes.)

There are no toxins or poisons produced by the bacteria. Disease happens when the immune system recognizes the "foreign" proteins of the bacteria, even inside a living cell and mounts a furious attack. The immune "attack" focuses on the infected cells in the mucosal layer of the digestive system. Massive inflammation results, as well as ulcers, diarrhea and weight loss.

The disease is known to pass from cow to calf, as infected cows shed millions of active bacteria into their milk. The infected animals also pass the infection to healthy animals by food contaminated by diarrhea. Factory farming methods where larger and larger herds are grazed on smaller and smaller plots of land further increase the potential for infection.

Infected animals are known to lose over 300 pounds per week, mostly from massive diarrhea. Fecal material from infected cows contain as much as 1 trillion bacteria per gram. Infected cows spray fecal material everywhere, including over their udders and on nearby cows where the material contaminates milk. Infected cows also pass the bacteria directly into milk in millions of bacteria per gram.

Sadly, in today's factory farms, milk from sick cows and milk from healthy cows is pooled together and then trucked to the milk processor, where it is piped into cartons and then sold at the local market.

A 1997 USDA study showed that that the number of herds infected is increasing, and that at least 20 percent - and as many as 40 percent - of U.S. dairy herds were positive for M. paratuberculosis.

Interestingly, the incidence of Crohn's disease is also increasing, at roughly the same rate as Johne's. The United States now has the highest incidence (new cases) of Crohn's disease in the world.

M. paratuberculosis and Crohn's disease

In the 1930s and 40s, Dr. Crohn was convinced that the human disease was virtually the same as the disease in cattle. But despite repeated trials, he couldn't isolate m. paratuberculosis from human tissue. Also, the bacteria could not be detected in diseased human tissue using a light microscope.

In cattle, the bacteria grows a special cell wall which is easily stained and readily visible in microscopy. In infected cattle, researchers could see swarms of bacteria under the microscope. In humans, they could see none. Even though the progress of the two diseases was extraordinarily similar, without an organism they could either see or culture, Dr. Crohn and other researchers were forced to conclude that the Crohn's disease was caused by an unknown autoimmune process.

The mystery was resolved in 1984, when a microbiologist at Brown's University, Dr. Rodrick Chiodini, demonstrated that m. paratuberculosis sheds its cell wall in humans, and takes a new form, called a spheroblast. In a landmark study, Dr. Chiodini cultured Mycobacteria from children infected with Crohn's.

Dr. Chiodini's effort was extraordinary. Mycobacteria are very difficult to cultivate. Special media are required and months of incubation, since the organism divides only once or twice a day. M. paratuberculosis is in the same family with the organisms which causes leprosy and tuberculosis. In the case of Mycobacteria leprae, the organism which causes leprosy, the only way to grow the bacteria (believe it or not) is in the foot pads of a special species of mice or in the nine banded armadillo. It just won't grow in outside of a very narrow band of living hosts.

Even with the difficulties in cultivation, labs were able to isolate M. paratuberculosis from Crohn's patients in California, Texas, France, The Netherlands, Australia, England and the Czech Republic.

In 1987, using DNA probes similar to the techniques used to identify forensic cases, researchers in England looked at tissue samples from Crohn's patients and compared them with patients with ulcerative colitis. Sixty-five percent of the samples from Crohn's patients were positive for m. paratuberculosis, compared with 4 percent of the control. Dr. Herman-Taylor, who led the research effort, was convinced at the time that with better lab technique, over 90 percent of the samples should have been positive.

In 2002, Dr. Herman-Taylor performed a similar survey, with a larger group of samples, and with improved lab techniques. This time, 92 percent of the samples from Crohn's patients were positive for M. paratuberculosis.

Further establishing the causative link, M. paratuberculosis isolated from Crohn's patients was found to cause a similar disease when fed to farm animals.

I wish I could report that the Food and Drug Administration, the USDA and the U.S. Animal Health Association is responding to the health implications of contaminated milk, but to date, there has been little funding and minimal response from agencies of the U.S. government, whose main responsibility is the health and welfare of its citizens.

Despite convincing evidence (only a small portion is presented here), the agencies tasked with funding research and advocating disease treatment are essentially ignoring advocates for bacterial Crohn's, even while dramatic increases in the number of new cases are occurring, especially in those under 30, and a coincident increase in the number of very sick cows infected with paratuberculosis are seen in factory farms.

Universally contaminated milk = epidemic Crohn's disease

As mentioned previously, cows infected with Mycobacteria paratuberculosis shed literally trillions of bacteria, most of it from diarrhea, but some excreted directly into milk.

OK, Bennett, that's certainly disgusting, but why write about it?

The reason is simple, and equally disturbing. M. paratuberculosis is strongly - even conclusively - associated with a nasty disease in humans called Crohn's disease, a disease characterized by extraordinary pain and unchecked diarrhea, a disease currently reaching epidemic levels.

The infection rate of M. paratuberculosis in U.S. dairy herds is beyond epidemic. As reported by the USDA. as many as 40 percent of the nations dairy herds have sick cows, infected with and actively shedding M. paratuberculosis.

The response by the milk lobby and the USDA: No problem here.

The disease in cows is called Johne's disease, and in humans, Crohn's disease. For most of us, the possibility that pathogenic bacteria might exist in the milk supply is difficult to believe. After all, milk is pasteurized, and pasteurization is advertised as a complete protection against any potential pathogenic bacteria.

Sadly, this is not the case with M. paratuberculosis.

Pasteurization in the United States is accomplished predominately by the HTST (high temperature short time ) method, where milk is exposed to 72 degrees centigrade (165 degrees F) for 15 seconds, as milk streams through the pasteurization coils.

In the laboratory, 72 degrees C. for 15 seconds doesn't kill M. paratuberculosis. In fact, 90 degrees (194 F) for 15 seconds doesn't kill the bacteria. Part of the reason is that the organism is concentrated in pus cells in milk which protect the bacteria from heat damage during pasteurization. Again, sadly, the USDA allows the highest number of pus cells in commercial milk in the Western world.

Of all the available milk products on the shelf, only ultrapasteurized milk was found to be free of live M. paratuberculosis.

OK, that's the lab ... what about store-bought milk?

In Ireland in 1998, researchers bought 31 cartons of milk from 16 retail outlets and tested them for M. paratuberculosis. Six (19 percent) grew out live cultures of the bacteria.

The results were widely publicized in the United Kingdom, but singularly ignored by the major press in the United States. Responding to public pressure, the British government initiated a 1,000-sample survey of milk, finding in 2000 that over 3 percent of the milk sampled grew live Mycobacteria . The detection levels were higher than the 1998 Irish study. In order to be labeled positive, a sample of milk had to be contaminated with over 1 million bacteria.

The USDA initiated its own study in 1998, but curiously ignored the established techniques to isolate Mycobacteria . It has been reported that the milk samples tested by the USDA were first frozen (known to weaken Mycobacteria ), then the samples were exposed to high frequency sound waves. Finally the samples were grown on media which is considered inadequate to culture Mycobacteria . In contrast with accepted protocols, the cultures were incubated for only three months. It is widely accepted that the minimum time required for M. paratuberculosis culturing is four months. Not surprisingly, the cultures were all negative.

Other countries have not been so cavalier. Milk studies continue in Europe, among them a study from Switzerland in 2003, where 1,384 bulk milk samples from different regions were tested for M. paratuberculosis using DNA probe methods. Some 19.7 percent were positive for the bacteria. Intriguingly, the cows from Swiss farms were predominantly asymptomatic – they were apparently ill, but not producing the massive diarrhea that characterizes the latter stages of M. paratuberculosis infection.

Laboratories independent from the USDA have been examining milk for the last 10 years. Anecdotal evidence from around the United States indicates that over 10 percent of milk products surveyed by these labs are positive for m. paratuberculosis.

It has also been reported that independent researchers are nearing publication of a long-term study which concludes that random commercial milk samples from a Midwest state are more than 10 percent positive for live Mycobacteria .

Unfortunately, contaminated milk is not the only avenue of infection. Eventually, even factory farm cows become too sick to be useful. These cows are culled from the herds, slaughtered and made into hamburger, which is also sold in stores. Sadly, the same process which contaminates milk, also contaminates meat.

The USDA, however, does not consider these very sick cows to be any health risk whatsoever.

Antibiotic treatment for Crohn's disease

Forefront physicians across the world have been treating Crohn's patients with a cocktail of antibiotics specially formulated to be effective against M. paratuberculosis. The results have been stunningly successful.

In Florida, Dr. Ira Shafran published a study (self-financed) where 77 percent of the patients treated with antibiotics were markedly improved. In Australia, Dr. Tom Borody is conducting a 2-year study on the effects of antibiotic therapy on Crohn's. The results will be published within months, but Dr. Borody states that the early indications are strongly positive. Within his own practice, Dr. Borody told WND that more than 70 percent of his patients eventually reach remission. Approximately 15 percent of his patients are considered healed - having no symptoms for four or more years.

In 1997, in England, a treatment trial was published where 52 patients with severe Crohn's disease were treated with two antibiotics for almost one year. Six of the patients were unable to tolerate the drug therapy and dropped out. Of the remaining 46, 94 percent were in remission at the conclusion of the trial.

Dr. Herman-Taylor, who continues to research and treat Crohn's patients told the press: "I've seen people without hope get better like magic. I've been a doctor for 40 years, and this is the best thing I've ever seen in medicine." Another researcher was quoted: "If this were cancer, we'd be calling these long remissions a cure."

While not 100 percent, no other treatment available today even comes close.

Given the harsh realities of an epidemic disease, you'd think that all of medicine would enthusiastically welcome a new treatment model based on state-of-the-art research under which more than 70 percent of Crohn's patients were able to resume normal lives.

If you thought that, you'd be wrong.

Medicine in the United States has a sad history of hanging onto foolish disease paradigms, despite compelling evidence to the contrary. In the recent past, gastroenterologists waited as long as 15 years before recognizing that ulcers are not caused by stress, but are actually caused by another unusual slow-growing bacteria - Helicobacter pylori.

In the United States, the engines for change in medicine are the drug companies, university medicine - funded by various government agencies, and research demanded by political pressure - AIDS research and breast-cancer research for example.

Drug companies sell the current view of Crohn's disease as an autoimmune disease and are unlikely to shake the paradigm. No single drug company would "own" the treatment of Crohn's, should its bacterial origins become commonly known. There is little profit motive.

In fact, there is arguably a negative profit motive, since at present, a patient's steroid and anti-inflammatory treatments never end. When ulcers were found to be caused by H. pylori, drug companies lost millions. It's a terrible pun, but for the drug companies, Crohn's is a cash cow.

In the case of government funding, the Cleveland Free Press reported that over 25 of Dr. Herman-Taylor's grant proposals for projects associating M. para with Crohn's were summarily rejected. Other researchers suffered similar reactions. The reasons are complex and are arguably related as much to the milk lobby as they are to forefront medicine.

According to the milk lobby, one of the most powerful in Washington, there is absolutely no reason to suspect that there could be anything wrong with the U.S. milk supply. In the face of increasingly convincing evidence, a spokesman for the U.S. milk lobby compared those who are trying to publicize the evidence to those who believe in flying saucers.

Where do we go from here?

Clearly the United States lags the rest of the world in recognizing the link between Mycobacteria paratuberculosis and Crohn's disease.

Equally clear, Americans will not long tolerate out-of-date treatment protocols and disinformation.

If the research is correct that the disease in cattle and the disease in humans are the same, the U.S. government needs to address this right away.

Dr. William Davis, a professor of veterinary microbiology and pathology at Washington State University, and a member of the National Academy of Science's Johne's Disease Committee, has stated that the research linking M. paratuberculosis with Crohn's disease is intriguing, but that the numbers of patients cited in existing research are not large enough.

Dr. Davis told WND that a conclusive study would involve a significantly large group of patients and would proceed under strict controls. He also admitted that funding for M. paratuberculosis is not deemed a high priority at the National Institute for Health, and that the exhaustive research that he would like to see is unlikely at the present.

It has been reported that the United States currently spends less than $4 million per year on Mycobacteria paratuberculosis research. Consider that a typical medium-sized downtown office building costs more than $100 million. For a disease that costs over $2 billion per year in direct treatment costs, $4 million in research funding is woefully, even criminally inadequate.

To contrast Crohn's disease with breast cancer: 2.8 million women in the United States are estimated to have breast cancer, approximately equal to the upper estimate of Crohn's patients. In 2003, from the National Cancer Institute alone, $550 million was allocated to breast cancer research.

Medical professionals correctly warn patients against betting the lives of their loved ones on some off-the-wall treatment program trumpeted on the Internet and sold in a foreign country. Most reasonable people know this and agree whole heartedly.

But in the case of Crohn's disease, many professionals, including physicians, whose children have been diagnosed with this disease are actively seeking antibiotic treatment, in many cases without the endorsement of traditional gastroenterologists. Anecdotal evidence has parents educating their own physicians and then begging them for antibiotic treatment.

Without adequate research and a responsive government, the sad reality is that across the country, literally hundreds of thousands of children cry themselves to sleep every night, because when they eat it hurts so bad, and sometimes even the steroids don't work.

Can we live with that?

http://worldnetdaily.com/news/article.asp?ARTICLE_ID=40722

yxboom
October 1st 2004, 06:50 PM
you have crohns?

bar Jonah
October 1st 2004, 06:56 PM
No, it just seemed very newsworthy. Especially after something Anthrogirl said in the Dairy-Alternative thread.

Esther
October 1st 2004, 09:41 PM
Thank you for posting this, RI. I know four people with Crohn's, one of whom was recently diagnosed. I'm going to print this out for them or email it. I think I understand now why ag could psychosomatically become ill after ingesting milk. :puke:

chickenman
October 1st 2004, 10:49 PM
1: Am J Gastroenterol. 2004 Aug;99(8):1539-43. Related Articles, Links
Click here to read
Bacterial DNA within granulomas of patients with Crohn's disease--detection by laser capture microdissection and PCR.

Ryan P, Kelly RG, Lee G, Collins JK, O'Sullivan GC, O'Connell J, Shanahan F.

Alimentary Pharmabiotic Centre; and Departments of Medicine, Histopathology, Microbiology, and Surgery, University College Cork, National University of Ireland, Ireland.

OBJECTIVES: We previously reported the use of laser capture microdissection (LCM) and PCR to detect the presence of Mycobacterium paratuberculosis DNA in granulomas of patients with Crohn's disease. While this does not imply a cause-effect relationship, it may influence the disease process because bacterial DNA has immunomodulatory effects. The aim of this study was to determine whether DNA from nonmycobacterial commensals, such as Escherichia coli, is also increased in the granulomas of Crohn's disease. METHODS: Archival tissue from 15 surgical cases of Crohn's disease and 10 non-Crohn's granulomatous bowel disease controls were examined. Granulomas were isolated using LCM, and the extracted DNA was examined for presence of E. coli DNA by nested PCR amplification of a 135 base-pair segment of the uidA gene. RESULTS: E. coli DNA was detected in microdissected granulomas in 12/15 Crohn's disease patients and in 1/10 non-Crohn's control granulomas (p < 0.001). Also, E. coli DNA was detected in 8/15 Crohn's full-thickness sections and in 4/10 control full-thickness sections. CONCLUSIONS: E. coli DNA may be detected more frequently in Crohn's granulomas than in other non-Crohn's bowel granulomas. This may indicate a tendency for lumenal bacteria to colonize inflamed tissue, or may be due to increased uptake of bacterial DNA by gut antigen presenting cells. In light of previous detection of M. paratuberculosis DNA in Crohn's granulomas, the nonspecific nature of the type of bacterial DNA present in granulomas is evidence against any one bacterium having a significant causative role in Crohn's disease. Copyright 2004 American College of Gastroenterology
so is M paratuberculosis a cause or a complication of the disease?


1: Am J Gastroenterol. 2004 Jun;99(6):1134-40. Related Articles, Links
Click here to read
NOD2/CARD15 genotype and phenotype differences between Ashkenazi and Sephardic Jews with Crohn's disease.

Karban A, Waterman M, Panhuysen CI, Pollak RD, Nesher S, Datta L, Weiss B, Suissa A, Shamir R, Brant SR, Eliakim R.

Department of Gastroenterology, Rambam Medical Center, Haifa, Israel.

OBJECTIVE: NOD2/CARD15 has been identified as a major susceptibility gene for Crohn's disease (CD). Three mutations, Arg702Trp, Gly908Arg, and Leu1007fsinsC, are associated with CD. The incidence and prevalence rate of inflammatory bowel diseases is two- to four-fold higher in Ashkenazi Jews as compared to non-Jewish Caucasians. The aim of this study was to determine the significance of the NOD2/CARD15 mutations in Jewish CD patients in Israel, and more specifically, to compare the significance of the mutations to the expression of CD in the Ashkenazi and Sephardic Jewish populations. METHODS: Allele frequencies of the mutations were determined in 180 Jewish CD patients, 73 ulcerative colitis patients, and 159 ethnically matched controls. Variants were detected using allele-specific PCR and restriction enzyme digestion assay. Demographic and phenotypic characterizations of the CD patients were determined. RESULTS: The carrier rate of the three mutations in the entire Jewish Israeli CD cohort is 41.1% versus 10.7% in controls (p < 0.0001). The Ashkenazi Jewish CD patients have an increased carrier rate compared to Sephardic Jews (47.4%vs 27.45%, p= 0.034). Association analyses in Ashkenazi Jews reveal odds ratios of 10.5, 9, and 4.8 for carriage of Gly908Arg, Arg702Trp, and Leu1007fsinsC mutations, respectively. Significantly higher rates of smoking, family history of inflammatory bowel diseases, and extraintestinal manifestations were found among the Sephardic CD patients. CONCLUSIONS: NOD2/CARD15 CD-associated mutations confer increased risk mainly to the Ashkenazi Jewish CD patients in Israel. This suggests that NOD2/CARD15 mutations could contribute to the higher incidence and prevalence rates of CD among Ashkenazi Jews.

PMID: 15180737 [PubMed - indexed for MEDLINE]


1: Lancet. 2004 Sep 18;364(9439):1039-44. Related Articles, Links
Click here to read
Culture of Mycobacterium avium subspecies paratuberculosis from the blood of patients with Crohn's disease.

Naser SA, Ghobrial G, Romero C, Valentine JF.

Department of Molecular Biology and Microbiology and Biomolecular Science Center, Burnett College of Biomedical Sciences, University of Central Florida, Orlando, FL 32816, USA. nasers@mail.ucf.edu

BACKGROUND: Crohn's disease, a form of inflammatory bowel disease, resembles some aspects of tuberculosis, leprosy, and paratuberculosis. The role of Mycobacterium avium subspecies paratuberculosis (MAP) in Crohn's disease is controversial. METHODS: We tested for MAP by PCR and culture in buffy coat preparations from 28 individuals with Crohn's disease, nine with ulcerative colitis, and 15 without inflammatory bowel disease. FINDINGS: MAP DNA in uncultured buffy coats was identified by PCR in 13 (46%) individuals with Crohn's disease, four (45%) with ulcerative colitis, and three (20%) without inflammatory bowel disease. Viable MAP was cultured from the blood of 14 (50%) patients with Crohn's disease, two (22%) with ulcerative colitis, and none of the individuals without inflammatory bowel disease. Current use of immunosuppressive medication did not correlate with a positive MAP culture. Sequencing of PCR products from MAP cultures confirmed the presence of the MAP-specific IS900 fragment. Among 11 MAP isolates assessed, we identified nine strains that were not identical. INTERPRETATION: We detected viable MAP in peripheral blood in a higher proportion of individuals with Crohn's disease than in controls. These data contribute to the evidence that MAP might be a cause of Crohn's disease.


1: J Clin Microbiol. 2004 Mar;42(3):1129-35. Related Articles, Links
Click here to read
Population-based case control study of seroprevalence of Mycobacterium paratuberculosis in patients with Crohn's disease and ulcerative colitis.

Bernstein CN, Blanchard JF, Rawsthorne P, Collins MT.

Inflammatory Bowel Disease Clinical and Research Centre, Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. cbernst@cc.umanitoba.ca

There is renewed enthusiasm for exploring the possibility that Mycobacterium paratuberculosis may be causative in Crohn's disease (CD). We aimed to determine whether CD subjects are more likely to be M. paratuberculosis seropositive than controls. Using our population-based University of Manitoba Inflammatory Bowel Disease Research Registry, we recruited CD and ulcerative colitis (UC) subjects between 18 and 50 years of age for a study involving detailed questionnaires and venipuncture. We accessed the population-based databases of Manitoba Health (single provincial health insurer) to get age-, gender-, and geography-matched controls to our inflammatory bowel disease (IBD) population. We asked enrolling IBD subjects for potential nonaffected sibling controls. We used an enzyme-linked immunosorbent assay (ELISA) for serum antibodies to M. paratuberculosis initially developed for cattle but adapted for human use. The rate of positive ELISA results, based on previously published interpretation criteria, was significantly higher for all study groups. There was no difference in M. paratuberculosis seropositivity rate among CD patients (37.8%; n = 283), UC patients (34.7%; n = 144), healthy controls (33.6%; n = 402), and nonaffected siblings (34.1%; n = 138). For siblings, there was no correlation between M. paratuberculosis serological status and that of the corresponding IBD affected sibling. None of the demographic or questionnaire variables studied were predictive of M. paratuberculosis status. Subjects with CD and UC were less likely to have ingested unpasteurized milk and less likely to have had a non-tap water source as a primary water source. In conclusion, in this population-based case control study, the M. paratuberculosis seropositivity rate was approximately 35% for all groups and there was no difference in rates between CD patients, UC patients, healthy controls, or nonaffected siblings. The much higher rate of seropositivity for subjects from Manitoba, Canada, than for those from Denmark or Wisconsin cannot be obviously explained. While these data seem to refute any association of CD with M. paratuberculosis, the high seroprevalence in Manitobans raises the possibility that the high rates of CD in Manitoba could be related to high exposure rates for M. paratuberculosis. Hence, the possibility of an association between M. paratuberculosis and CD remains inconclusive.

PMID: 15004064 [PubMed - indexed for MEDLINE]


seems the jury is still out on this one, I don't think the mycobacterium hypothesis really explains the extra-intestinal manifestations of crohns either

anthrogirl
October 1st 2004, 10:53 PM
pearls for a great post, RI

thanks for the info...

my best,
ag

yxboom
October 1st 2004, 11:26 PM
so is M paratuberculosis a cause or a complication of the disease?

...

seems the jury is still out on this one, I don't think the mycobacterium hypothesis really explains the extra-intestinal manifestations of crohns either

interesting articles chickenman.


The thing that bothers me about RightIdea's article is that it consistently argues that crohn's disease is not an autoimmune disorder. While it makes some attempts at backing this claim. The big gaping hole in that argument is 2 fold. One, the most effective treatment to date for crohn's is
remicade (http://www.remicade.com/) which is a treatment specifically used for autoimmune disorders such as rheumatoid arthritis. Two, crohn's patients and rheumatoid arthiritis patients both share the uncommon production of the protein TNF-alpha. I'd imagine these two factors alone cause a sufficent problem in the autoimmune claim made by worldnetdaily in making a conclusive statement that crohn's isn't autoimmune. I would echo what chickenman posted, simply that the jury is still out on this since it isn't known if crohn's is caused by bacterial, viral or genetic means. Whether the abnormalities are a cause or effect of the disease is still unknown.

yes i know someone with crohns.

Esther
October 2nd 2004, 08:27 PM
Here's an idea. Doctors of Crohn's patients could allow them to try the suggested testing and course of treatment. What do they have to lose? This is a circumstance in which it appears that the only thing to be lost is money.

chickenman
October 3rd 2004, 02:16 AM
well, its not just money when the treatment in question is antibiotics, because antibiotic resistance is an issue - especially with this particular regime (the anti-tuberculosis one)

tuberculosis is on the rise, as is antibiotic resistance in tb strains

yxboom
October 3rd 2004, 09:16 AM
Here's an idea. Doctors of Crohn's patients could allow them to try the suggested testing and course of treatment. What do they have to lose? This is a circumstance in which it appears that the only thing to be lost is money.

There is some speculation that antibiotics are linked to the onset of crohn's disease. Article. (http://www.ama-assn.org/amednews/2004/03/01/hlsc0301.htm)

Either way, the article documents enough to show that crohn's patients are recieving antibiotics (whether it is believed to be a causing factor or a result of symptoms) and they are not finding a remedy for their condition. Again this goes to show that the jury is still out on the issue of what causes crohn's

Esther
October 3rd 2004, 01:28 PM
There is some speculation that antibiotics are linked to the onset of crohn's disease. Article. (http://www.ama-assn.org/amednews/2004/03/01/hlsc0301.htm)

Either way, the article documents enough to show that crohn's patients are recieving antibiotics (whether it is believed to be a causing factor or a result of symptoms) and they are not finding a remedy for their condition. Again this goes to show that the jury is still out on the issue of what causes crohn's

From the article:

ADDITIONAL INFORMATION:
Which comes first?

Objective: To determine if antibiotic use is linked to the development of Crohn's disease.

Participants: Patients with and without Crohn's who had five years' worth of data in Britain's General Practice Research Database.

Method: Data were extracted based on smoking status, drug prescriptions, age and sex. Logistic regression was used to investigate the relationship between Crohn's and antibiotic use.

Results: Seventy-one percent of those with Crohn's had used antibiotics in the previous five years, compared to 58% of controls. Those with the disease had twice as many antibiotic prescriptions than those without.

Conclusion: There is a statistically significant association between antibiotic use and Crohn's disease, although it is unclear whether this is the cause of the disease or a result of seeking treatment for symptoms.

Source: Gut, February

The problem is that this article doesn't specify which antibiotics were used, what they were used for and if, in fact, they already had Crohn's at the time they took the antibiotics or if they had recently been diagnosed. It speculates that they may have taken the antibiotics to fight the Crohn's symptoms but it doesn't say for sure. This doesn't say they developed Crohn's within that 5 years, just that they already had it and took more antibiotics than the non-Crohn's subjects. People who are in a weakened condition are going to get sick more often and probably require more antibiotics. I think the conclusion is misleading because it only allows for two options. I would think someone with Crohn's, like the 58% in the control group, could get sick from unrelated causes and need antibiotics but that doesn't seem to be a consideration in the study.

In any case, I hope the medical community steps up the research on this disease.

anthrogirl
October 3rd 2004, 08:04 PM
I'm not sure that an overwhelming recognition of the dangers associated with ingesting animal secretions will ever come to fruition. The National Dairy Councel spends hundreds of millions of dollars each year on advertising. They are also federally subsidized.

Dairy business is BIG business...no doubt about it.

ag

matt2454
April 20th 2005, 01:23 PM
Hey, I have some responses to some of your ?'s guys. Crohn's is defitely caused by MAP guys. I can prove it. The reason why antibiotics are linked with crohn's is bc when u take them, they destroy healthy flora which protect your body from foreign enemy bacteria. When u take antibiotics these are destroyed, and guess what, ur defenses are down. Also, flora have been shown to boost your entire immune system anyways. and for gods sake, stop fighting over genetics vs autoimmune vs bacterial. Its all the above except the autoimmune bull[color=red]EDITME[/color][color=red]EDITME[/color][color=red]EDITME[/color][color=red]EDITME[/color] hahha. Reason: ypur body is attacking the MAP right, but cant kill it -maybe this is genetic too, ppl with TB dont get the disease most times right, and TNF alpha is produced, no [color=red]EDITME[/color][color=red]EDITME[/color][color=red]EDITME[/color][color=red]EDITME[/color] stopping this protein will stop inflammation, same with stopping the entire immune reaction with 6 mp. This doesnt stop the disease but it stops ur immune cells from attacking the gut. Guess what again, Nod2 gene defect makes u more vulnerable to infection thats what the gene regulates-foreign proteins on enemy bacterial. crohn's is both genetic and bacterial. why does leukine work then huhu huh???? it boosts ur immune system morons and many docs said OMG this is like putting oil on fire, hhahhaha they are stupid as hell. how come 92% of crohns patients have live viable map in their guts-hermon-taylor. the dna might be the same but who cares about that-live map is what infects u not the dna-they should have looked for the rna bc that would show if its alive or not. drink milk...get crohn's!
ps: antibiotics aimed at destroying map cure ppl, what more u need?? i have alot more but i dont like writing too much, my hands hurt.
ps: i'd watch out for whole milk if i were u...

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